Acute Pancreatitis Flashcards
Diagnosis of acute pancreatitis
Elevation of serum amylase
Cause of AP
Alcohol Gallstones Trauma Drugs Viruses Autoimmune
How does a primary insult lead to AP
It leads to a release of activated pancreatic enzymes
this results in autodigestion
What is released in auto digestion and what does it cause
Pro-inflammatory cytokines and reactive oxygen species
Causes oedema, fat necrosis and haemorrhage
Clinical features of AP
- Abdominal pain which may radiate to the back
- Vomiting
- Pyrexia
- Tachycardia
- Hypovolaemic shock
- Oliguria
- Jaundice
- Paralytic Ileus - nerve./ muscle dysfunction disrupting normal intestinal muscle contraction (constipation and bloating)
- Retroperitoneal haemorrhage - Grey Turner’s (bruising of flanks) or Cullen’s Signs (oedema, bruising around umbilicus)
- Hypoxia
- Hypocalcaemia
- Hyperglycaemia
- Effusions
Blood tests for AP
Amylase / Lipase - high FBC - leucocytosis U&E's - disturbance CRP - high (organ failure) Glucose - elevated LFTs: ALP, AST, ALT, bilirubin Calcium - hypocalcaemia cause Coagulation screen
Imaging
AXR (ileus)
CXR (pleural effusion)
Abdo USS
CT contrast
How is severity assessed in AP
Glasgow Criteria:
- Score > 3 = severe pancreatitis
within 48 hours of admission :
- White cell count
- blood glucose
- blood urea
- AST
- LDH
- Serum albumin (low)
- Serum calcium (low)
- Arterial PO2 (low)
How is AP generally managed
Analgesia IV fluids Blood transfusion if Hb low Catheter NG tube Oxygen Insulin - if needed Ca supplements - if needed Nutrition
How is pancreatic necrosis specifically managed
CT guided aspiration and antibiotics +/- surgery
How is gallstones in AP specifically managed
EUS or MRCP and cholecystectomy
How would an abscess complication be managed
Antibiotics and drain
How would pseudocyst complication be diagnosed and managed
USS or CT
- <6cm should resolve
- Endoscopic drainage or surgery if persistent pain
What is a pseudocyst
Fluid collection without an epithelial lining
persistent hyperamylasaemia and / or pain