Acute Pancreatitis

An acute inflammatory process of the pancreas.

Epidemiology

  • Occurs in 56.5/100,000/year (i.e. 0.05%)
  • It has significant mortality- 10-15%
    • <1% in mild; up to 11% in sterile severe cases; up to 25% in infective severe; up to 50% if organ failure for >48hrs

Aetiology

  • Most cases are associated with either gallstones or alcohol excess
  • The remainder can be
    • a complication of ERCP investigation
    • trauma (either accidental or surgical)
    • drugs (there are many drugs that are associated with acute pancreatitis- steroids; azathioprin)
    • rarer causes include infection (mumps); hereditary (gene mutations in CFTR (cystic fibrosis)); other causes of obstruction e.g. tumours; autoimmunity; hypercalcaemia (almost always secondary to hyperparathyroidism); hypothermia; hyperlipidaemia

Presentation

  • History
    • Classically with severe, continuous, boring, sudden-onset pain in the epigastric/ left upper quadrant region
      • Generalised pain and signs of peritonism may indicate severe disease
      • The pain can often radiate to the back; is worse when lying flat
      • In alcohol-related pancreatitis, the onset may be more gradual and occur 6-12 hours after a binge.  Gall-stone related pancreatitis is usually very sudden.
    • Nausea/vomiting
  • Examination
    • Fever is important (may be an early sign of SIRS); Hypotension
    • Abdominal tenderness (may be localised or generalised)
    • Abdominal distension (leakage of fluid into the retroperitoneum in trying to dilute enzymes-> abdominal contents pushed forward)
    • Cullen’s sign (a bluish discolouration around the umbilicus) or Grey-Turner’s sign (the same in the flank)
      • NB these are usually late signs
    • Look for signs of rarer causes e.g. hyperlipidaemia

Investigations

  • Bloods
    • Serum amylase >3x the normal (normal reference range is 30-110U/l; so anything above 300U/l is suggestive; most cases of clear acute pancreatitis will be around 600-800)
      • NB Amylase can also be raised in mesenteric ischaemia; appendicitis; malignancy; macroamylasaemia etc
    • Serum lipase (if available)- more sensitive/specific
    • CRP- often raised but may be low in drug induced pancreatitis
    • Calcium- check for hypocalcaemia (even though its rare)
    • LFTs- raised Alk Phos/bilirubin are suggestive of gallstone disease
    • FBC and U&Es should be done to check for any abnormalities that may require management
  • Imaging
    • Whilst these patients may get abdo x-ray/ CXR/ USS (e.g. may show gall stones), these may not be entirely helpful and the key imaging required is a CT abdo, which will show the extent/severity of disease. 
      • NB A CT is only really justified in patients with (mod-)severe disease
  • Grading Severity
    • General
      • Mild
        • No organ failure and no local/systemic complications (i.e. problem free recovery)
      • Moderately severe
        • Organ failure that resolves within 48 hours
        • Local/systemic complications without persistent organ failure
      • Severe
        • Persistent organ failure (>48 hours)
        • Single or multiple organs
    • Scoring systems
    • Glasogw
    • A score ❤ indicates mild disease; >=3 more severe disease
    • The RANSON Criteria is another scoring system that also includes developments within the first 48 hours (e.g. fall in haematocrit; rise in urea; base deficit; fluid loss; etc.)
    • The Apache II Score is often used in critically ill patients to predict mortality and severity of disease.  It is often used in patients with acute pancreatitis to assess severity.

Management

  • Mild cases can often be managed on a general ward with simple fluid resuscitation and conservative management
    • Antibiotic treatment is only indicated if there are signs of infection
    • Pain control
  • Severe disease may require more intensive management in ICU/HDU
    • Essentially still fluid resuscitation and supportive tx
    • Likely enteral nutrition
    • Surgery is only ever indicated when there is infection/necrosis

Complications

  • Occur in around 15-20%
  • Local complications
    • Pancreatic necrosis (necrotizing pancreatitis) +/- infections
      • Inflammatory mediators released in acute pancreatitis induce thrombosis and haemorrhage leading to pancreatic necrosis.  Necrosis also affects the surrounding tissues (particularly fat) and can spread retroperitoneally behind the colon and into the small bowel mesentery
      • The necrosed tissue commonly becomes infected by bacteria from the gut
    • Pseudocyst
      • Ischaemia and inflammation of the pancreas causes disruption of the pancreatic ducts.  This leads to collections of pancreatic fluid in so called pseudocysts.
        • NB there aren’t always connections between the duct and pseudocysts
    • Abscess
      • Pancreatic abscess usually follows an infections of a limited area of pancreatic necrosis and may develop several weeks after initial infection.
    • Fistulae
      • to the peritoneal cavity (ascites); pleural cavity (pleural effusion); bowel; skin (more common after intervention)
    • Vascular problems
      • Pre-hepatic portal hypertension (involving splenic vein to cause segmental portal hypertension)
      • Erosion and haemorrhage of the pancreatic, splenic or peri-pancreatic arteries or veins
      • Formation of an arterial pseudoaneurysm (i.e. one that does not involve all the layers of the vessel)
  • Systemic complications
    • SIRS

Prognosis

  • About one third of patients can develop diabetes, maldigestion/malabsorption
    • Creon is important if pancreatic function is significantly impaired
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