Acute Pancreatitis Article

Article

Author – Dr Daniel Arbide  Editor – Dr Daniel Arbide

Last updated 09/04/2025

Table of Contents

Introduction

Acute pancreatitis involves inflammation of the pancreas, in conjunction with the inappropriate activation and release of digestive enzymes, notably trypsin, which can damage the pancreas and nearby tissues via autodigestion.

Most commonly caused by gallstones and alcohol, acute pancreatitis has rising incidence, currently 34 per 100,000 people each year (1). It has a wide range of severity, from mild and self-limiting, to very severe, which may be associated with a host of local and systemic complications and require ITU support (2).

Anatomy (3)

This file is licensed under the Creative Commons Attribution-Share Alike 4.0 International license. Author: Cypressvine. https://creativecommons.org/licenses/by-sa/4.0/

 

The pancreas is a glandular organ in the upper abdomen (epigastrium and left hypochondrium) with both endocrine (hormonal) and exocrine (digestive) functions. Macroscopically the pancreas is divided into five parts: uncinate process, head, neck, body and tail. The head, uncinate process and neck lie within the ‘C’ curve of the duodenum, with the neck typically lying at the level of L1, or the transpyloric plane. 

 

Within the pancreas runs the pancreatic duct, which combines with the common bile duct (CBD) in the head of pancreas at the ampulla of Vater, opening into the second (descending) part of the duodenum via the major duodenal papilla. The flow of pancreatic and bile secretions are controlled by the sphincter of Oddi.

 

Relations

  • Posterior to the head and neck of the pancreas lie the aorta and IVC, as well as the portal triad, consisting of the portal vein, hepatic artery and CBD. 
  • The superior mesenteric vessels are closely related to the pancreas and can be seen run posterior to the neck of pancreas and anterior to the uncinate process. 
    • The superior mesenteric artery (SMA) branches from the aorta at L1, runs behind the neck of pancreas and anterior to the uncinate process to supply the embryonic midgut. 
    • The superior mesenteric vein drains blood from the small bowel, runs anterior to the uncinate process and posterior to the neck of pancreas to combine with the splenic vein, forming the portal vein.
  • Anterior to the pancreas is the stomach and pylorus, separated from the pancreas by the lesser sac.
  • The duodenum curves in a recognisable ‘C-shape’ around the neck, head and uncinate process, with the superior mesenteric vessels running over the inferior (or 3rd) part of the duodenum.
  • The transverse mesocolon attaches to the anterior aspect of the pancreas.
  • The spleen is located laterally and posteriorly to the pancreas, connected to the tail within the lieno/splenorenal ligament.

 

Blood supply

  • The body and tail of pancreas are supplied by the splenic artery, arising from the coeliac trunk and running along the superior aspect of the pancreas.
  • The head of pancreas is supplied by the anastomosis between the superior and inferior pancreaticoduodenal arteries. The superior pancreaticoduodenal artery arises from the coeliac trunk at T12, while the inferior arises from the SMA at L1.

Venous drainage of the pancreas is via the splenic and superior mesenteric vein, which combine and drain into the portal vein.

 

Coeliac trunk and branches. Author: Dennis M DePace, PhD. Colorized version of original artwork by Henry VanDyke Carter from Gray’s Anatomy by Henry Gray. This file is licensed under the Creative Commons Attribution-Share Alike 4.0 International license. https://creativecommons.org/licenses/by-sa/4.0/

 

Acini and ducts (4)

 

Microanatomy of the human pancreas. Author: OpenStax College.

This file is licensed under the Creative Commons Attribution 3.0 Unported license. https://creativecommons.org/licenses/by/3.0/

 

Structures of the human pancreas. Publisher: Encyclopaedia Britannica. https://www.britannica.com/science/pancreas#/media/1/440971/68636

 

Acinar cells (pictured above) are the functional units of the exocrine pancreas. They are responsible for the synthesis, storage and secretion of digestive enzymes within the pancreas. It is the premature activation of these enzymes which leads to the onset of acute pancreatitis (4).

Acinar cells form numerous berry-shaped clusters or lobules, termed ‘acini’ (acinus singular). Resembling a bunch of grapes, acini are connected via a network of ducts, first draining into intercalated ducts, which merge to form larger interlobular ducts, eventually draining into the main pancreatic duct, also known as the duct of Wirsung. The accessory pancreatic duct, or the duct of Santorini, drains into the duodenum via the minor papilla superiorly.

In between the acini are the endocrine islets of Langerhans, secreting glucagon (alpha cells), insulin (beta cells) and somatostatin (delta cells).

 

Causes

The aetiology of acute pancreatitis can be remembered by the favourite acronym: I GET SMASHED. Approximately 80% of cases are caused by gallstones and alcohol, which are by far the most common precipitants. 

Gallstones in the CBD can obstruct the pancreatic duct, leading to pancreatic injury, while alcohol directly damages pancreatic tissue. 

Approximately 10% of cases are idiopathic without obvious cause, and the rest are due to the other, rarer causes.

Pathophysiology (2,4,5)

 

Clinical features (2,6)

History 

  • Severe abdominal pain – SOCRATES
  • Classically epigastric pain radiating to the back, exacerbated by movement and relieved on leaning forwards
  • Nausea and vomiting, anorexia, reduced oral intake
  • Any PMH gallstones or alcohol excess?
  • Recent procedures e.g. ERCP?
  • Any new medications started e.g. thiazide diuretics or steroids?
  •  

Examination

  • Observations
    • May show features of hypovolaemia or hypovolaemic shock due to fluid shifts and vomiting e.g. tachycardia, hypotension
    • If superadded infection or concurrent cholangitis may be pyrexial, although can also be due to the normal inflammatory response
  • Epigastric tenderness +/- guarding
  • May be jaundiced if CBD obstructed by gallstone
  • Reduced breath sounds, dullness on percussion may indicate pleural effusion
  • Reduced bowel sounds and abdominal distension may indicate an associated ileus
  • Rarely tetany may be seen due to hypocalcaemia
  • Cullen’s and Grey-Turner’s signs (see below) – indicating haemorrhagic pancreatitis

Cullen’s sign. Source: http://cnx.org/content/m14942/latest/ Author: Herbert L. Fred, MD and Hendrik A. van Dijk This file is licensed under the Creative Commons Attribution 2.0 Generic license. https://creativecommons.org/licenses/by/2.0/

 

Grey-Turner’s sign. Source: http://cnx.org/content/m14904/latest/ Author: Herbert L. Fred, MD and Hendrik A. van Dijk This work is licensed under a Creative Commons Attribution License (CC-BY 2.0). https://creativecommons.org/licenses/by/2.0/

Differentials

There are a wide range of potential differentials to consider for the presentation of acute abdominal pain, including gastrointestinal, renal and urological, vascular, respiratory, and cardiac causes. Diagnosis of acute pancreatitis is made through a combination of history and clinical features, biochemical results and sometimes imaging.

Differentials

You can confirm the diagnosis if at least two of these three criteria are met:

Investigation (2,5,6)

Bedside

  • ECG – may show tachycardia or signs associated with hypocalcaemia e.g. long QT interval.
  • Urine dipstick + pregnancy test in women.
  • Cultures if pyrexial/signs of infection.
  • ABG/VBG – provide lactate and acid-base level in septic patients, respiratory parameters (PO2, PCO2) in patients with suspected respiratory pathology e.g. effusions, ARDS, atelectasis.

Bloods

  • Amylase – diagnostic if >3x upper limit of normal (ULN = ~100), but can be well into the thousands initially. 
  • Not useful as a marker of severity. 
  • Serum lipase is not seen as often but is more accurate with higher sensitivity and specificity. 
  • May be non-specifically raised in other differentials e.g. viscus perforation, DKA, ectopic pregnancy. 
  • In cases of chronic pancreatitis (recurrent acute episodes) bear in mind that amylase/lipase may be lower/below diagnostic threshold due to loss of pancreatic secretory function.
  • WBC + CRP may show raised inflammatory markers, should be serially monitored.
  • Renal profile to check for AKI and monitor renal function.
  • LFTs may indicate underlying biliary pathology e.g. gallstones.
  • Calcium profile – may show hypocalcaemia due to fat necrosis, or hypercalcaemia as a cause of pancreatitis.
  • Clotting screen + G&S – especially useful in haemorrhagic cases, anaemia, or if any invasive intervention planned e.g. ERCP or IR.
  • Glucose – useful for risk scoring and can be used in the assessment of endocrine function.

Imaging (6)

Not generally required for diagnosis, however may be used where there is diagnostic uncertainty, to identify the cause, to rule out differentials or investigate possible complications.

 

Erect CXR

  • Can help identify pulmonary sequelae e.g. pleural effusion, ARDS, and look for pneumoperitoneum if perforation suspected.

AXR

  • Not routinely performed but can demonstrate the ‘sentinel loop sign’ – dilated and prominent loop of small bowel next to the pancreas indicating localised inflammation. Can detect calcified gallstones (15-20% of cases).

Sentinal loop sign in acute appendicitis

Case courtesy of Mohammad Niknejad, Radiopaedia.org, rID: 22034

 

USS abdomen 

  • Required after diagnosis of pancreatitis to assess for underlying cause, typically cholelithiasis, the most common precipitant of pancreatitis.

Acute pancreatitis ultrasound

Case courtesy of Mahmoud Mohie-eldine, Radiopaedia.org, rID: 67452

 

CT AP 

  • Good sensitivity and specificity (~ 90%). Useful when there is diagnostic uncertainty, and for ruling out differentials (e.g. perforation, ischaemia). Can show pancreatic inflammation, oedema and surrounding fat stranding. After several days areas of necrosis (which appear non-enhancing) may develop. 
  • Interval scans may be used days-weeks after the initial attack to assess severity in patients with persistent symptoms, inflammatory response or signs of developing complications, such as fluid collections, necrosis or abscesses.

Necrotising pancreatitis complicated by portal and splenic vein thrombosis

Case courtesy of Henry Knipe, Radiopaedia.org, rID: 48148

 

MRCP

  • MRCP may be useful in cases of diagnostic uncertainty, or where choledocholithiasis or pancreatic stones are suspected e.g. with CBD/pancreatic duct dilatation. Can also be used to identify potentially malignant HPB lesions which may be obstructing, and when planning ERCP.

Acute pancreatitis (MRCP)

Case courtesy of Mohamed AbdelBar, Radiopaedia.org, rID: 76283

 

 

Risk stratification

Several risk-stratification scoring systems exist currently to guide assessment of severity and early ITU/HDU input for the most unwell patients. Examples include APACHE II, Ranson, and the Modified Glasgow-Imrie criteria, the latter of which can helpfully be remembered by the acronym ‘PANCREAS’ as outlined below.

Modified Glasgow-Imrie Criteria slide, taken from Mind The Bleep finals series webinar slides on General Surgery: HPB. Created by Daniel Arbide.

Management (2,5,6)

  • Initially A-E approach acutely.
  • Aggressive fluid resuscitation with crystalloids (typically Hartmann’s or Plasmalyte) is critical due to significant fluid shifts.
    • Strict fluid input/output monitoring with catheterisation.
  • Control pain with strong analgesia (opioids) is usually required, with antiemetics. 
      • PCA may be used if cannot tolerate oral intake due to vomiting, or if pain is very severe.

 

  • NG/Ryles tube in severe vomiting.
  • Early involvement of nutrition/dietetics team – may need parenteral nutrition if enteral route not possible (e.g. in ileus), or NG/NJ tube feed supplementation. 
  • Enteral nutrition is preferred wherever possible and associated with better outcomes. 
    • Patients will be in a catabolic state and need adequate calories to recover. 
    • May need Creon if evidence of exocrine insufficiency (faecal elastase).

 

  • Monitor carefully for developing complications which may progress to SIRS and multi-organ failure. 
    • Involvement of ITU/HDU in severe pancreatitis where appropriate e.g. for haemodynamic or respiratory support. 
    • CT imaging can detect and monitor later complications e.g. fluid collections, abscesses.

 

  • Fluid collections and pancreatic necrosis are typically left for several weeks to become walled off before intervention is considered – they can then be drained or resected.
  • Serial monitoring of CRP and electrolytes including calcium, magnesium, renal profile.

 

  • Antibiotics not routinely indicated unless evidence of superadded infection, infected pancreatic necrosis, abscess formation, pyrexia etc.

 

  • ERCP indicated in gallstone pancreatitis with concurrent cholangitis or obstructing CBD stone.
  • Definitive management e.g. cholecystectomy, referral to alcohol services. 
    • Cholecystectomy may be performed during the same admission or delayed until at least 6 weeks after resolution.

Complications (2,5,6,9)

Acute pancreatitis complications slide, taken from Mind The Bleep finals series webinar slides on General Surgery: HPB. Created by Daniel Arbide.

Systemic

ARDS 

  • Circulating inflammatory mediators and cytokines can cause acute pulmonary injury leading to hypoxaemia.
  • Imaging may show bilateral diffuse pulmonary infiltrates.
  • May require invasive ventilation on ITU.

Pleural effusion and pancreatic ascites

  • Pleural effusion can occur due to inflammatory exudate into the pleura (normal fluid amylase levels).
  • Less commonly, leakage from the pancreatic duct or a pseudocyst can cause accumulation of pancreatic fluid in the peritoneum (ascites) or in the pleura via formation of a pancreatico-pleural fistula. These fluid accumulations will have high amylase content (>1000 U/L) and may present with abdominal pain, distention or breathlessness.

Hypocalcaemia

  • As detailed above, fat necrosis consumes serum calcium by the reaction of released fatty acids with calcium to form chalky deposits.

Hyperglycaemia

  • Occurs due to the destruction of the islets of Langerhans causing  disrupted insulin secretion (especially in chronic pancreatitis).

Sepsis/SIRS/Multi-organ failure

  • Can occur due to translocation of gram-negative bacteria from the gut, and/or inflammatory mediators, resulting in systemic inflammation and infection. Enteral nutrition is a significant protective factor in maintaining gut integrity and preventing this.
  • Can also occur as a result of infected pancreatic necrosis.

Ileus

  • Occurs secondary to inflammation affecting the intestines.

AKI

  • Often caused by hypovolaemia (pre-renal), circulating toxins or severe inflammatory response/sepsis if present.

 

Local

Pancreatic necrosis

  • Typically develops in prolonged or severe pancreatitis where ongoing inflammation leads to infarction and subsequent necrosis of pancreatic tissue. Intervention is delayed until several weeks later when necrosis becomes walled off, and include endoscopic or percutaneous drainage, or sometimes surgical necrosectomy. Can become infected with mortality rates of up to 30% – treated with antibiotics.

Abscess

  • Occurs when peripancreatic fluid collections become infected.
  • Features: pyrexia, persistent symptoms or raised inflammatory markers.
  • Diagnosed on CT and drained by interventional radiology or surgically + antibiotics.

Pseudocysts

  • These are encapsulated collections of fluid that may develop from 4 weeks after the initial episode. Many will resolve by themselves but if they persist can be drained (often endoscopically through the stomach). These are distinct from acute (<4 weeks) peripancreatic fluid collections which can occur and are not encapsulated.

Portal vein thrombosis

  • Release of prothrombotic inflammatory mediators can lead to thrombosis in the portal vein, as well as the splenic and mesenteric veins.

Haemorrhage

  • Protease enzymes e.g. trypsin can erode nearby blood vessels causing bleeding.

Chronic pancreatitis

  • Occurs after recurrent bouts of acute pancreatitis, leading to destruction and scarring of pancreatic functional tissue.
  • This can cause endocrine and exocrine insufficiency with onset of diabetes and Creon requirement.
  • Imaging shows calcification.

Prognosis (6)

Most patients will have mild disease and will improve within a week of conservative management. Those with poor prognostic markers, e.g. high risk scores, presence of SIRS, infected pancreatic necrosis, multiple comorbidities, have significantly increased mortality and morbidity rates, and recovery will inevitably be prolonged.

 

Long term prognosis is dependent on several factors, such as the cause of the pancreatitis, and whether there is progression to recurrent episodes or chronic pancreatitis. Lifestyle factors play a role, with smoking and alcohol conferring a poorer prognosis.

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