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Pancreatitis (acute and chronic)

Definition

  • Inflammation of the liver that can be acute, chronic or acute-on-chronic
    • Acute – a previously healthy pancreas that subsequently returns to normal
    • Chronic – ongoing pancreatic inflammation

 

Risk factors

  • High alcohol intake/alcoholism (major risk factor)
  • Gallstones
  • Smoking
  • High serum triglycerides
  • Raised oestrogen levels (natural or hormonal therapy)
  • Family history, including hereditary pancreatitis (PRSS1 mutation)

 

Differential diagnoses

  • Cholangitis
  • Cholecystitis
  • Cholelithiasis
  • Pancreatic cancer
  • Colon cancer
  • MI
  • Pneumonia
  • Peptic ulcer
  • Viral hepatitis

 

Epidemiology

  • Acute pancreatitis
    • 15-42 per 100,000 in the UK
    • Slightly higher in USA
    • Gallstones is major cause in Northern Europe, alcohol is major cause in USA
  • Chronic pancreatitis
    • 3 per 100,000 in the UK
    • 4:1 men:women, average patient age of about 40
  • Both acute and chronic are increasing in incidence

 

Aetiology

  • Acute pancreatitis
    • Biliary tract disease (accounts for approx. 40%), gallstones (including micro-stones) lodging at the sphincter of Oddi
    • Alcohol (accounts for approx. 35%) – alcohol increases digestive enzyme accumulation and release
    • Iatrogenic (accounts for approx. 4%) – result of trauma from ERCP (endoscopic retrograde cholangiopancreatography)
    • Drugs (approx. 2%) – some antibiotics including sulphonamides & tetracycline, oestrogens, furosemide, azathioprine, corticosteroids
    • Abdominal trauma (especially penetrating trauma)
    • Infection
    • Hereditary pancreatitis (accounts for <1%), mutation of PRSS1, which has 80% penetrance, causes increased trypsin activation
    •  Hypercalcaemia
    • Hyperlipidaemia
    • Pancreatic tumour
    • Developmental/structural abnormalities of the pancreas
    • Toxins, including scorpion sting from Tityus trinitatis scorpion of Trinidad
  • Chronic pancreatitis
    • Excess alcohol intake accounts for about 60% of cases – a result of increased viscosity of pancreatic fluid, by increasing protein secretion and decreasing fluid and bicarbonate secretion
    • Idiopathic causes account for about 30% of cases, likely to have polygenic cause
    • Gallstones, hereditary pancreatitis, hypercalcaemia, trauma, drugs, hyperlipidaemia as above
    • Cystic fibrosis – some types are associated with chronic pancreatitis
    • Autoimmune

 

Clinical features

  • Acute pancreatitis
    • Epigastric pain, worsening, radiating to the back (retroperitoneum involvement)
    • Nausea + vomiting
    • If severe, may have tachycardia, hypotension, oliguria
    • History of gallstones, may be accompanied by jaundice or cholangitis
    • Necrotising pancreatitis: Cullen’s sign (periumbilical bruising) and Grey Turner’s sign (flank bruising)
  • Chronic pancreatitis
    • Epigastric pain, radiating to pack
    • Episodic pattern of pain, or may be chronic/constant
    • Alcohol may worsen the pain
    • Anorexia and weight loss associated with pain
    • May be painless
    • Malabsorption, diabetes
    • Jaundice
    • Steatorrhoea

 

Pathophysiology

  • Acute pancreatitis
    • Inflammatory response to premature and increased activation of digestive enzymes in the pancreas
      • Acute rise in intracellular calcium
      • Activation of trypsinogen to trypsin
      • Impaired trypsin degradation by chymotrypsin C
      • Cellular necrosis as a result of enzymatic activity
    • Gallstones occlude pancreatic drainage and cause hypertension of the pancreatic duct, which raises calcium levels, as above
    • Alcohol may alter calcium regulation in pancreatic cells
  • Chronic pancreatitis
    • The same pathophysiology as in acute, but lacking an acute rise in intracellular calcium, the rise of pancreatic enzyme activity has a slower onset, but is likely still linked to raised intracellular calcium
    • Increased protein secretion as a result of prolonged enzyme activity occlude the pancreatic duct à ductal hypertension as in acute
    • Autoimmune chronic pancreatitis (ACP) is an IgG4-related disorder, with raised serum IgG4 levels
      • Eosinophil infiltrate
      • Can be identified by responsiveness to steroids

 

Investigations

  • Acute pancreatitis
    • Serum amylase – very sensitive and quite specific test, especially for acute pancreatitis. May be raised in severe chronic pancreatitis
    • Serum lipase and urinary amylase – remain elevated for longer
    • FBC, with CRP – elevated CRP
    • U&Es, glucose, LFTs, ABG, plasma calcium – for monitoring severity and progression
    • CXR – to rule out other causes, eg peptic ulcer perforation
    • Abdominal ultrasound – to look for gallstones
    • Contrast CT
    • ERCP (endoscopic retrograde cholangiopancreatography) for investigation and removal of stones in the bile duct
    • MRCP (MRI) – good for differentiating between fluid and solid masses
    • Scoring systems such as APACHE (acute physiology and chronic health evaluation) should be used to predict progression and prognosis. Combines physiological and laboratory parameters.
  • Chronic pancreatitis
    • Serum amylase and lipase – may be elevated in severe disease, but may be normal/low
    • Faecal elastase – reduced in chronic pancreatitis
    • Abdominal ultrasound
    • Contrast CT
    • ERCP
    • MRCP – used more than ERCP

 

Management

  • Acute pancreatitis
    • Understand the cause, and treat if necessary – eg gallstone removal
    • Management is generally supportive, escalation to high dependency can be carried out early by using scoring systems such as APACHE
    • Fluid management
    • Prophylactic antibiotics
    • Analgesia, eg tramadol or other opiates, fentanyl. Morphine and diamorphine should be avoided as can worsen pancreatitis by contracting sphincter of Oddi
    • Feeding and nutritional management
    • Anticoagulation for DVT prophylaxis
  • Chronic pancreatitis
    • Alcohol abstinence in drinkers
    • Endoscopic or surgical intervention
    • Pancreatic enzyme replacement
    • PPI (eg omeprazole) or H2 receptor agonist (eg ranitidine) to suppress gastric acid production
    • Tricyclic antidepressants (eg amitriptyline), pregabalin and opiates for chronic pain
    • Insulin therapy for diabetes secondary to chronic pancreatitis

 

Prognosis

  • Acute pancreatitis
    • Most patients make a full recovery, although severe episodes may result in exocrine and endocrine dysfunction, leading to malabsorption and diabetes respectively
    • Complications include:
      • Multiorgan failure from systemic inflammatory response
      • Significant necrosis of the pancreas à infection, which has a higher mortality risk
  • Chronic pancreatitis
    • Increased risk of pancreatic cancer – up to 15% in alcohol related, up to 40% in hereditary pancreatitis
    • Pancreatic pseudocyst are a common complication. May rupture, bleed or become infected. May occlude surrounding tissues, eg duodenum. Surgical interventions have reasonable success, depending on severity
    • Ascites and pleural effusions (with high amylase levels) suggest disruption of the main pancreatic duct, which requires surgical intervention
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