Acute pancreatitis

• Acute inflammation of the pancreas caused by destructive effect of enzymes released from the pancreatic acini

Causes

• Gallstones (most common), also other things that may obstruct the pancreatic duct system
• Alchohol
• Trauma
• Shock and thromboembolism causing ischaemia
• Mumps, and other viruses such as coxsacchie and Mycoplasma pneumonia
• Autoimmune – PAN
• Scorpion venom
• Hyperlipidaemia, hypercalcaemia, hypothermia
• ERCP and other iatrogenic procedures
• Drugs e.g. thiazides, oestrogens and sulphonamides
• 80% are associated with gallstones or alcohol
• There are also some hereditary forms associated with mutations in genes encoding pancreatic enzymes and their inhibitors

Pathogenesis

• Central to the pathogenesis of acute pancreatitis is the activation of trypsinogen to form trypsin which can then go on to activate other proenzymes involved in autodigestion as well as activating the clotting and complement system as well
• The mechanisms by which activation of pancreatic enzymes may occur are;
  • Obstruction of the bile duct distal to the site of union of the common bile duct and pancreatic ducts resulting in refulx and build up of enzyme rich fluid in the pancreas, resulting in toxic injury to the pancreatic acini and inflammation and oedema
  • Primary acinar cell injury due to viruses, drugs and ishaemia with the release of intracellular proenzymes and lysosomal hydrolases
  • Defective cellular transport with exocrine enzymes being directed to lysosomes rather then being secreted. This results in their activation and release
• The manner by which alcohol causes pancreatitis is unknown. Possibly mechanisms are;
  • Transient increases in pancreatic exocrine secretion
  • Contraction of the Sphincter of Oddi
  • Direct toxic effects on the acinar cells
  • Chronic alcohol digestion results in secretion of a protein rich pancreatic fluid leading to deposition of solid plus within the smaller pancreatic ducts

• Irrespective of the causes of pancreatitis, the loberation of lytic enzymes causes causes necrosis of the normal tissues;
  • Lipases causes fat necrosis. Can result in discoloration of the skin of the abdominal wall (Cullen’s on GreyTurner’s sign)
  • Proteases result in destruction of the lung parenchyma. Endocrine destruction results in hyperglycaemia
  • Elastases and other enzymes can cause vascular damage with haemorrhage into the pancreas or peritoneum. Excessive haemorrhage is known as acute haemorrhagic peritonitis

Morphology

• The basic alterations seen are;
• Vascular leakage causing oedema
• Fat necrosis by lipolytic enzymes
• Acute inflammation
• Proteolytic destruction of the pancreatic substance
• Vascular injury resulting in interstitial haemorrhage
• In the mild forms only the first three features are seen

Clinical

• Severe central abdo pain of sudden onset, often radiating through to the back
• Nausea and vomiting
• Tachycardia
• Fever jaundice
• Ileus
• Shock
• Rigid abdomen
• Discoloration around the umbilicus – Cullen’s sign
• Discoloration around the flanks – Grey Turner’s sign
• Death may occur from shock, ARDS and acute renal failure

Investigations

• FBC – leukocytosis
• Blood sugar – may be raised in severe disease
• LFT’s – increased bilirubin, increased Alk Phos, decreased albumin
• Serum amylase elevated (within first 24hr)
• Serum lipase elevated (after 72-96hr)

Complications

• May be local affecting the pancreas;
  • Pancreatic pseudocyst
  • Abscess formation
• GI – gastric or duodenal erosions, intestinal ileus
• Systemic
  • ARDS
  • Acute renal failure
  • Shock
  • Diabetes mellitus
  • Peritonitis

The pancreas can resolve to normal if the acute pancreatitis resolves