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General surgery + HPB - YR3 > Pancreatitis - acute > Flashcards

Pancreatitis - acute Flashcards

1
Q

acute vs chronic definition

A
  • Acute = limited damage to secretory function of pancreas
  • No gross structural damage
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2
Q

Causes of acute pancreatitis

A

IGETSMASHED
* Idiopathic
* Gallstones
* Ethanol - binge
* Trauma
* Steroid use
* Mumps
* Autoimmune eg SLE, sjogrens
* Scorpion bite
* Hypercalcaemia
* ERCP
* Drugs - azathioprine, NSAIDs, diuretics

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3
Q

Pathophys acute pancreatitis

A
  • Each of the causes creates a premature and exaggerated activation of digestive enzymes
  • = pancreatic inflammatory response
  • = increased vascular permeability and fluid shifts (third spacing)

Third spacing fluids –> hypovolaemic shock

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4
Q

What happens in pancreatitis after it’s initiation?

A
  • Enzymes released into systemic circulation
  • Autodigestion of fats = fat necrosis and of blood vessels (can cause retroperitoneal bleeding)
  • Fat necrosis can release fatty acids, react with calcium to form chalky deposits in fat = hypocalcaemia
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5
Q

What is severe end stage pancreatitis?

A

Necrosis - partial or complete

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6
Q

Presentation of pancreatitis - acute

A
  • Sudden
  • Severe
  • Epigastric pain - radiate to back
  • N+V
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7
Q

Signs on exam of acute pancreatitis

A
  • Cullens sign - bruising around umbilicus
  • Grey Turners sign - bruising flanks
  • Tetany from hypocalcaema?
  • If gallstones cause, can be jaundiced too

From retroperitoneal bleeding

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8
Q

differential for acute pancreatitis

A
  • AAA
  • Renal calculi
  • Chronic pancreatitis
  • Aortic dissection
  • PUD
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9
Q

Investigations for acute pancreatitis - bloods

A
  • Serum amylase or lipase (diagnostic if 3x upper limit)
  • LFTs - concurrent cholestatic elements
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10
Q

Imaging for acute pancreatitis

A
  • Abdominal USS - if cause unknown, see if gallstones
  • AXR - sentinal loop sign (dilated loop adjacent to pancreas due to local inflam
  • CXR - pleural effusion or ARDs
  • Contrast enhanced CT - if none of these find cause/inconclusive

BUT severity assessing CT scans should only be done 6-10 days after admi

Only used if persistent inflam/organ failure

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11
Q

What will contrast enhanced CT scan of pancreas show?

A

If done after 48hrs from initial presentation:
* Pancreatic oedema/swelling
* Non-enhancing areas suggestive of pancreatic necrosis

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12
Q

Management acute pancreatitis

A
  • No cure
  • Treat underlying cause eg ERCP if gallstones
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13
Q

Supportive management for acute pancreatitis

A
  • IV fluid resuscitation
  • NG tube - if vomitting profusely for drainage
  • Cathterisation to monitor urine output and fluid balance chart
  • Opioid analgesia
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14
Q

When are abx used for acute pancreatitis?

A
  • If confirmed pancreatic necrosis
  • Broad spec eg imipenem
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15
Q

How to manage severe acute pancreatitis?

A
  • Need to be on HDU or ITU
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16
Q

Scoring system for acute pancreatitis

A
  • Modified Glasglow (Imrie) criteria
  • Within first 48hrs of admission
  • 3 or more –> severe pancreatitis, refer to HDU
17
Q

Modified Glasgow criteria

A

PANCREAS
* pO2 less than 8kpA
* Age older 55
* Neutrophils more than 15
* Calcium less than 2
* Renal function (urea) more than 16
* Enzymes - LDH more than 600 or albumin less 32
* Sugar more than 10mmol/L

18
Q

Complications of acute pancreatitis - systemic

A
  • DIC
  • ARDs
  • Hypocalcaemia - fat necrosis
  • Hyperglycaemia
19
Q

Local complications of acute pancreatitis

A
  • Pancreatic necrosis
  • Psuedocyst
20
Q

Pancreatic necrosis management

A
  • Due to ongoing inflam –> ischaemic infarction
  • persistent systemic inflam for more than 7-10 days after onset = suspect
  • confirm with CT
  • need pancreatic necrosectomy
  • Necrosis can become infected - if raised WCC and deteriorate, then need FNA
21
Q

When is pancreatic necrosectomy done?

A

3-5 weeks after onset of symptoms to ensure walled off necrosis has developed

22
Q

What is pancreatic pseudocyst?

A
  • Collection of fluid containing pancreatic enzymes, blood and necrotic tissue
  • Can occur within or adjacent to pancreas
  • Usually in lesser sac
  • Obstruct the epiploic foramen due to adhesions
23
Q

Progression of pseudocyst

A
  • Form weeks after initial presentation
  • Lack epithelial lining = pseudo
  • Vascular and fibrotic wall
  • Can present as symptoms of mass effect eg biliary obstruction/gastric outlet obstruction
  • Prone to haemorrhage, rupture and can become infected
24
Q

Management psuedocyst

A
  • Conservative initially - 50% resolve
  • Surgical debridement or endoscopic drainage (into stomach) if persist >6 weeks
25
Q

Mechanism of gallstones causing acute pancreatitis

A
  • Blockage of gallstone in CBD near ampulla of vater
  • Pancreatic contents then cannot reach duodenum
  • Proteases then get prematurely activated within pancreatic duct
  • = autodigestion of pancreas
  • = inflammation
26
Q
A

General surgery + HPB - YR3 (38 decks)

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