Pancreatitis

Introduction

Pancreatitis is inflammation of the pancreasacute pancreatitis can return to normal after resolution of the episode, conversely chronic pancreatitis, is continuing inflammation with irreversible structural changes.

Acute Pancreatitis

Aetiology

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  I GET SMASHED:

  • S - Steroids
  • M - Mumps
  • A - Autoimmune - e.g. SLE
  • S - Scorpion bites (rare!)
  • H - Hypercalcaemia, hypothermia, hyperlipiaemia
  • E - ERCP
  • D - Drugs - e.g. azathiaprin

90% of acute pancreatitis cases are caused by alcoholgallstones, post-ERCP or idiopathic. (Davidson, 2014 p890)

Pathogenesis

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 tachycardiahypotension and be oliguricAbdominal 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. 

Diagnosis