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Pancreatitis is a condition involving inflammation of the pancreas. It can be acute or chronic; acute pancreatitis can return to normal after resolution of the episode, conversely chronic pancreatitis, is continuing inflammation, often with irreversible structural changes.

Acute Pancreatitis


Gallstones and alcohol account for the vast majority of episodes. The severity varies from mild self-limiting to extremely severe with extensive pancreatic and peripancreatic necrosis as well as haemorrhage. In its most severe form the mortality can be between 40-50%, as damage can result in the release of is lytic enzymes into the blood, contributing to severe shock and digestion of surrounding tissue. The causes of pancreatitis can be remembered with the acronym GET SMASHED:

  • G – Gallstones
  • E – Ethanol (alcohol!)
  • T – Trauma
  • S – Steroids
  • M – Mumps
  • A – Autoimmune – e.g. SLE
  • S – Scorpion bites (rare!)
  • H – Hypercalcaemia, hypothermia, hyperlipiaemia
  • E – ERCP
  • D – Drugs – e.g. azathiaprin


Necrosis >> Autolysis >> Infection >> Pseuodycyst
A theory suggests that the final common pathway has marked in intracellular calcium which → activation of intracellular proteases. There is evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells. In severe inflammation, it becomes swollen and haemorrhagic. Proteases digest the walls of blood vessel → blood extravasation; amylase is released into the blood (but is a non-specific diagnostic marker). Released lipases (better diagnostic marker) cause fat necrosis within abdomen and subcutaneous tissue, can → discolouration of skin (Grey Turner’s sign). The released fatty acids can bind Ca2+ can → hypocalcaemia.Concomitant destruction of adjacent islets can → hyperglycaemia and thus cause Type  II diabetes. Also, formation of abscesses and cysts within the pancreas or adjacent tissues can occur.Infection secondary to pancreatic tissue damage does not always occur. Not all cases of infection lead to cyst / pseudocyst formation.
Pulmonary failure in acute pancreatitis is believed to be caused by circulating activated digestion enzymes (e.g. trypsin, phospholipase A2, etc.) leading to a loss of surfactant, atelectasis and irritation eventually leading to ARDS and pleural effusion. Cardiac depression and breakdown of the blood brain barrier can also occur in severe AP and are possibly due to the same etiology.

Clinical features

Upper abdominal pain, normally beginning in the epigastrium accompanied by nausea and vomiting. As inflammation spreads in peritoneal cavity pain → more intense, involvement of the retroperitoneum frequently → back pain. In severe cases the patient may have tachycardia, hypotension and be oliguric. Abdominal examination may show widespread tenderness with guarding; also reduced/absent bowel sounds. Also periumbilical bruising (Cullen’s sign) and Grey Turner’ sign (flank bruising) if present show severe necrotising pancreatitis. Left sided pleural effusion, if present, is indicative of poor prognosis.


  • Blood tests will show raised serum amylase (may be many times norm level, important indication of pancreatic inflammation), lipase, also with raised urinary amylase. Amylase is not prognostic, nor is the level related to the degree of tissue damage Lipase levels are more specific and may relate to the level of tissue damage, but levels do not rise until up to 8 hours after the onset of symptoms.
  • CXR to exclude gastroduodenal perforation, which also ↑ serum amylase. May show gallstones or pancreatic calcification.
  • Ultrasound scan (USS) → find gallstones (biliary cause of pancreatitis), may also sow pancreatic swelling and necrosis.
  • Contrast-enhanced spiral CT → assess extent of pancreatic necrosis + to detect complications such as abscess dev, fluid collection and pseudocyst formation.
  • MRI (MRCP) assesses degree of pancreas damage and finds gallstones, can differentiate between fluid and solid inflammation.
  • ERCP (Endoscopic Retrograde Cholangiopancreatography) used to look at pancreatic duct for inflammatory fibrosis or tumours, and pancreatic juice can be collected and biochemically examined.
  • Operative biopsies or needle aspiration cytology under USS.
  • APACHE (acute physiology and chronic health evaluation score) is a means of assessing the severity of a wide spectrum of illness, adjusted for age + obesity and other health problems, has a high sensitively as early as 24 hours after symptom onset. A score of >8 indicates severe disease
  • The Glasgow scoring system can also be used to asses the severity and prognosis of pancreatitis. The modified version of the score can be remembered with the acronym PANCREAS:
  • PO2 Oxygen < 60mmHg or 7.9kPa
  • Age > 55
  • Neutrophilia White blood cells > 15
  • Calcium < 2 mmol/L
  • Renal Urea > 16 mmol/L
  • Enzymes Lactate dehydrogenase (LDH) > 600iu/L Aspartate transaminase (AST) > 200iu/L
  • Albumin < 32g/L
  • Sugar Glucose > 10 mmol/L


  • Replace lost fluids (IV) and a urinary catheter might be necessary
  • Nasogastric suction to prevent abdominal distension and vomitus and hence ↓ risk of aspiration pneumonia. Continuous oxygen administration may be necessary, depending on sats.
  • Prophylactic antibiotics, broad spectrum e.g. cefuroxime or aztreonam ↓ infection complications
  • Analgesia, pethidine and tramadol administered under patient control system
  • Enteral nutrition, via nasojejunal tubes.
  • In patients with multiorgan failureventilation and renal support, mortality rate >80%.
  • Complications of acute pancreatitis:
    • Within the first week, the morbidity and mortality reflect the systemic inflammatory response, which in turn results in multiple organ failure. After this, the prognosis is related to the extent of pancreatic necrosis. Extensive necrosis (> 50%) is associated with high risk of further complications, which frequently need surgical intervention. Infection of the necrotic pancreas can lead to sepsis, resection of infected areas of pancreas may be needed. Some fluid collections will be surrounded by granulation tissue → pseudocyst, larger ones (> 6cm) may become infected or → intraperitoneal bleeding, thus need to be drained surgically.

Prognosis – The vast majority of patients with mild or moderate acute pancreatitis will make a full recovery. Severe acute pancreatitis patients may become pancreatically insufficient with respect to exocrine (malabsorption) and endocrine function (diabetes).


Chronic Pancreatitis


In MDCs alcohol accounts for the vast majority (60-80%) of cases (either repeated acute episodes or chronic). Also, it may result from a rare inherited autosomal dominant trait, associated with aminoaciduria or hyperparathyroidism, or cystic fibrosis due to CFTR problems → mucus problems. Or obstruction of the pancreatic duct (benign of malignant) or due to a congenital abnormalities such as pancreas divisum.


Possibly, due to inappropriate activation of enzymes within the pancreas, this has been demonstrated in the case of hereditary pancreatitis, where genetic abnormalities of cationic trypsinogen and its inhibitory proteins have led to unopposed trypsin activity within the pancreas. Chronic alcohol intake is also believed to the level of trypsinogen relative to its inhibitor, and human trypsinogen has a tendency to auto-activate → unopposed activity → damage pancreas.  It is believed that the intrapancreatic enzyme activityprecipitation of proteins within the pancreatic duct lumen in the form of plugs. These form a starting point for calcification and also → ductal hypertension → further pancreatic damage. Cytokine activation and oxygen stress → perpetuate this process, via inflammation.  Clinical features Pain: usually epigastric often radiating through into the back, it may be episodic. Exacerbations may follow further alcohol excess. During periods of abdominal pain, weight loss may be severe. Malabsorption and diabetes by develop due to exocrine and endocrine insufficiency respectively. Jaundice secondary to common bile duct obstruction, may be a feature in a small number of patients.


  • ERCP (Endoscopic Retrograde Cholangiopancreatography) often shows distorted pancreatic ducts due to scar tissue resulting from chronic inflammatory process.
  • X-Ray of upper abdomen often reveals flecks of calcification due to previous fat necrosis.
  • Serum amylase and lipase levels are elevated.
  • Faecal elastase levels will be abnormal in the majority of patients.
  • PABA and pancreolauryl tests
  • USS and contrast enhanced spiral CT, MRI with MRCP (magnetic resonance Cholangiopancreatography), which has replaced ERCP are used as in diagnosis of acute pancreatitis
  •  Endoscopic ultrasound


Combination of NSAIDs and opiate (tramadol) for pain relief. Trycyclic antidepressants e.g. amitriptyline are used for chronic pain. Oral pancreatic enzyme supplements reduce pancreatic stimulation (by -ve feedback) and hence intensity of pain. Pain does improve over time, after 6 to 10 years, 60% of patients are pain free. For patients with debilitating pain, surgical intervention is an option, with duct drainage and limited resection which can relieve pain in 80% of patients, but mortality of 5%. Endoscopic techniques can be used to improve pancreatic drainage. An acid suppressor (H2-receptor antagonist or PPI) is also given, to compensate for decreased bicarbonate secretion. Despite this, a proportion of patients continue to malabsorb, due to inadequate mixing of pancreatic supplements with the food as well as the low pH in the duodenum.

Pancreatic enzyme supplements – pancreatin

Pancreatin consists of protease, lipase and amylase, which are inactivated by gastric acid and by heat. Supplements, therefore, must be taken with food (but not mixed with very hot food), and either concurrently with gastric acid suppression therapy (e.g. with cimetidine, H2-receptor antagonist or a proton pump inhibitor) or as enteric-coated formulations. Pancreatin preparations in clinical use are of porcine origin. Dosage is adjusted according to the size, frequency and consistency of stools.

Unwanted effects include irritation of the mouth and perianal skin, nausea, vomiting and abdominal discomfort. Some higher-strength formulations should be avoided in children under 15 years of age with cystic fibrosis, since they have been associated with the formation of large-bowel strictures. Thus, the amount of pancreatin given has to be balanced with the side effects. For example, to reduce the side effects, the amount of pancreatin given has to be reduced; which in turn means the amount of total dietary fat consumed has to also be reduced, to avoid steatorrhoea.


Same as acute pancreatitis, pseudocyst formation etc. Also, formation of ascites, accumulation of serous fluid in the peritoneal cavity and occasionally pleural effusions.


Passage of fat in large amounts in the faeces (up to 30 mmol per 24 hours), due to failure to digest and absorb it, is associated with pancreatic insufficiency. This will usually improve with pancreatic enzyme supplements, e.g. pancreatin, and a low fat diet.


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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