General: Acute Pancreatitis

Question 1

How is acute pancreatitis different from chronic?

Answer 1

Distinguished from chronic pancreatitis by its limited damage to the secretory function of the gland, with no gross structural damage developing

Question 2

Outline the pathophysiology of acute pancreatitis

Answer 2

Premature/exaggerated activation of digestive enzymes within = pancreatic inflammatory response = increase in vascular permeability = fluid loss into the third space (interstitial e.g. peritoneal cavity)

Enzymes released into the systemic circulation = autodigestion of fats (fat necrosis) and blood vessels (haemorrhage in retroperitoneal space)

Fat necrosis = release of free fatty acids, reacting with serum calcium = chalky deposits in fatty tissue = hypocalcaemia.

Severe end-stage pancreatitis = partial or complete necrosis of the pancreas

Question 3

What is the aetiology of acute pancreatitis?

Answer 3

(GET SMASHED)

Gallstones (in ampulla of vater)
Ethanol
Trauma 
Steroids
Mumps
Autoimmune disease (SLE)
Scorpion venom 
Hypercalcaemia 
Endoscopic retrograde cholangio-pancreatography (ERCP)
Drugs = Azathioprine, NSAIDs, Diuretics

Question 4

How does acute pancreatitis present?

Answer 4

Sudden onset severe epigastric pain (can radiate through to the back)

Nausea

Vomiting

Epigastric tenderness

Soft abdomen

Normal bowel sounds

Guarding and rigid abdo

Grey Turner’s Sign (bruising in the flanks)

Cullen’s Sign (bruising around the umbilicus)

Steatorrhea = stools with high levels of undigested fat

Def of fat soluble vits

Question 5

How should acute pancreatitis be investigated?

Answer 5

Serum amylase = acute pancreatitis if 3x the upper limit of normal

LFTs = assess for any concurrent cholestatic element to the clinical picture

Serum lipase = more accurate for acute pancreatitis (as it remains elevated longer than amylase), yet it is not available or routinely performed at every hospital

Abdo US = if cause unknown

Contrast-enhanced CT scan = if bloods inconclusive

Question 6

Explain how acute pancreatitis should be managed

Answer 6

A-E approach 
IV fluids - hartmans
Catheter
Encourage E+D
Early dietician input
Analgesia (PCA)
Glasgow score (PANCREAS - PaO2, age, neutrophil, Ca, renal urea, enzyme LDH/AST, albumin, sugar)
Ix cause (IGETSMASHED - idiopathic, gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion sting, hyperlipidaemia, ERCP, drugs)

If no improvement with conservative Mx = CT (pancreatic necrosis)

Question 7

What are the possible complications of acute pancreatitis?

Answer 7

DIC

Acute Respiratory Distress Syndrome (ARDS)

Hypocalcaemia

Hyperglycaemia = secondary to disturbances of insulin metabolism

Hypovolemic shock and multiorgan failure

Pancreatic necrosis = ongoing inflam = ischaemic infarction of the pancreatic tissue

Pancreatic pseudocyst = collection of fluid containing pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac

Question 8

What is the mechanism by which gallstones cause acute pancreatitis?

Answer 8

Gallstones produced in the gallbladder can block the bile duct, stopping pancreatic enzymes from traveling to the small intestine and forcing them back into the pancreas, the enzymes then begin to irritate the cells of the pancreas, causing the inflammation associated with pancreatitis and the auto digestion of cells

Question 9

There are many rare causes of acute pancreatitis, what are they?

Answer 9

Accidental damage - during a procedure to remove gallstones

Mumps

Measles

Cystic fibrosis

High triglyceride levels in the blood

High Ca

Hereditary disorders of the pancreas

Cigarette smoking

Question 10

Name a scoring system (clinical, radiological) to assess the severity of acute pancreatitis

Answer 10

Modified Glasgow criteria