Chronic Pancreatitis

Background/Pathophysiology

  • Chronic pancreatitis is a chronic, irreversible, inflammation and/or fibrosis of the pancreas, often characterised by disabling pain and progressive endocrin and exocrine insufficiency.
  • It was initially thought that chronic pancreatitis involved a distinct process from acute pancreatitis.
    • Acute pancreatitis involves a neutrophilia, oedema and raised serum pancreatic enzymes
    • Chronic pancreatitis involves a lymphocytic inflammation, fibrosis and calcification, often without raised serum pancreatic enzymes
      • It is thought that chronic pancreatitis occurs in people who have an altered immune response to the inflammation of acute pancreatitis
        • Obstruction or Reduction in bicarbonate excretion
        • Alcoholic damage can cause protein deposition in the ductular structures of the pancreas (not seen in acute episodes)
  • It is most common in men 40-50 years old
  • There are thought to be 2 different pathological subtypes of chronic pancreatitis: small duct and large duct pancreatitis.
    • NB Either can be associated with all aetiologies, and they may actually represent part of a spectrum of disease (i.e. same process)
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Aetiology
  • Alcohol
    • 70-90% of cases
    • Exact mechanism uncertain
      • ?Increased protease secretion from acinar cells and decreased secretion of bicarbonate/fluid by ductal cells.
        • Resulting mixture obstructs the ductal lumen and causes upstream acinar atrophy and fibrosis.
      • ?Increased oxidative stress
    • NB Liver cirrhosis and chronic pancreatitis rarely occur together
  • Autoimmune
    • 5-6% of cases
    • 2 types (type 1 & 2)
      • Type 1 is more common in East cf 2 in the Western world
    • Presentation similar to alcoholic pancreatitis but can be asymptomatic
    • NB IMPORTANTLY, autoimmune chronic pancreatitis is steroid-responsive and may be reversible if caught early
    • Increased gGT/IgG4 and autoantibodies a.g. antinuclear antibody and rheumatoid factor
    • Associated with other autoimmune conditions e.g. rheumatoid arthritis, Sjogrens syndrome, primary biliary cirrhosis, primary sclerosing cholangitis and IBD
  • Hereditary
    • Rare, autosomal dominant condition mostly due to a mutation in the cationic trypsinogen gene (PRSS1)
      • Interferes with inactivation of trypsin, allowing active trypsin to autodigest the pancreas
    • Tend to present in young adults/adolescents (i.e. <20 years)
    • Associated with pancreatic cancer also
  • Idiopathic
    • Diagnosis by exclusion but accounts for up to 15% of cases
    • Thought to be due to a number of factors
      • ?Hypersensitivity to alcohol
      • Genetic factors
      • ?Trauma
  • Drugs
    • NB Usually cause more of a recurrent acute pancreatitis scenario which can develop into a chronic pancreatitis
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  • Smoking is an independent risk factor
  • Other rare causes include metabolic disorders (hypertriglyceridaemia, hypercalcaemia); trauma; cystic fibrosis; iatrogenic (ERCP); radiotherapy
Presentation
  • Typical presentation is of recurrent/chronic epigastric pain that radiates to the back
    • Often very severe and dull (may require opiate analgesia); commonly precipitated by eating
    • Lasts several hours at a time
    • Associated with nausea and vomiting
  • Other symptoms include:
    • Reduced appetite; weight loss
    • Steatorrhea
      • Loose, greasy, fatty, foul-smelling stool that are difficult to flush
      • May present as incontinence
  • On examination,
    • Epigastric tenderness
    • May be signs of chronic alcohol excess e.g. liver stomata
      • Jaundice may be present either as a result of concomitant liver disease or stone disease
      • Finger clubbing (more likely to be secondary to steatorrhea)
  • Patients may also present with hyperglycaemia (due to endocrine dysfunction)
Investigation
  • Blood tests
    • FBC- WBC count is often normal
    • LFTs may be abnormal if there is coexistant liver disease or obstruction of the intra-pancreatic bile duct
    • U&E
    • NB serum amylase is usually normal in chronic pancreatitis and does not warrant investigation unless investigating a differential diagnosis
  • Secretin stimulation test
    • Secretin is usually released by the small intestine in the intestinal phase (III) in response to a decrease in intestinal pH as food enters the duodenum
      • It acts on the pancreas to release bicarbonate-rich digestive juices
      • Tests involves administering secretin and measuring (endoscopically or in conjunction with ERCP) the release of pancreatic juices
    • A test will be positive if 60% of the exocrine pancreas is damaged
  • Serum trypsinogen and urinary D-xylose or faecal elastase if malabsorption (diarrhoea, steatorrhoea, weight loss) is present
  • Imaging
    • CT may show calcification of the pancreas
    • Endoscopic USS is becoming increasingly used
  • Pancreatic biopsy is the gold standard
    • Lymphocytosis, fibrosis and focal necrosis with plugs of precipitated proteins
Management
  • Pain management
    • paracetamol + NSAID +/- opiates (depending on severity)
  • Malabsorption
    • Creon and lipase
    • May also require PPI or H2 antagonist to increase their absorption
  • Ocreotide (somatostatin analogue)
    • Decreases pancreatic activity and CCK levels
    • Useful in patients with persisting pain due to pancreatitis
  • ERCP may be used to decompress blocked pancreatic ducts
  • Surgery (Rarely done in cases with intractable pain or severe malabsorption problems)
    • Decompression/drainage (e.g. removal of pseudocysts)
    • Local resection
    • Pancreatodueodenectomy
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