Acute Pancreatitis

Question 1

Epidemiology

Answer 1

Increasing incidence

30 per 100000 in UK

Mortality between 5-30%

Question 2

How can it be distinugished from chronic?

Answer 2

In acute tehre is limited damage to the secretory function of the gland

There is no gross structural damaged

However repeated episodes of acute pancreatitis can lead to chronic pancreatitis

Question 3

Aetiology

Answer 3

Commonly gallstone disease or excess alcohol

Less commonly GET SMASHED

Gallstones

Ethanol

Trauma

Steroids

Mumps

Autoimmune

Scorpion venom

Hypercalcaemia

ERCP

Drugs like azathioprine, NSAIDs or diuretics

Question 4

Pathogenesis of acute pancreatitis

Answer 4

There is a premature and exaggerated activation of digestive enzymes within the pancreas

The pancreatic inflammatory response leads to increase in vascular permeability and subsequent fluid shifts

Enzymes are released into systemic circulation and lead to autodigesetion of fats called fat necrosis

Blood vessels can also be digested leading to retriperitoneal space haemorrhage.

Fat necrosis can cause release of free fatty acids that react with serum calcium and causes hypocalcaemia.

Question 5

Clinical features

Answer 5

Sudden onset of severe epigastric pain that can radiate through to the back

N+V

Question 6

Examination findings

Answer 6

Epigastric tenderness +/- guarding

Can have haemodynamic instability

Question 7

Less common signs

Answer 7

Cullen’s sign (Bruising around umbilicus)

Grey Turner’s sign (bruising in the flank)
These are due to retroperitoneal haemorrhage

There might also be tetany from hypocalcaemia.

Can also have obstructive jaundice if there are gallstones

Question 8

Dx

Answer 8

AAA

Renal calculi

Chronic pancreatitis

Aortic dissection

Peptic ulcer disease

Question 9

Lab tests

Answer 9

Routine bloods

Serum amylase

LFTs

Serum lipase

Question 10

Lab test findings

Answer 10

Serum amylase 3x the upper limit of normal (does not correlate with severity)

LFTs with ALT >150U/L has a positive predictive value of 85% for gallstones as underlying cause

Serum lipase is more accurate for acute pancreatitis as it remains elevated longer than amylase.

Question 11

When else might serum amylase be elevated?

Answer 11

Bowel perforation

Ectopic pregnancy

DKA

However usually not 3x the upper limit

Question 12

Risk scoring

Answer 12

modified Glasgow criteria

Question 13

Explain modified glasgow criteria

Answer 13

Assesses the severity within the first 48h of admission

3 or more positive factors should be considered to have severe pancreatitis and a high-dependency care referral is warranted.

Question 14

Mnemonic for modified glasgow criteria

Answer 14

PANCRES

pO2 <8kPa

Age >55

Neutrophils >15x10^9/L

Calcium <2mmol/L

Renal function (Urea >16mmol/L)

Enzymes LDH>600U/L or AST >200U/L

Albumin <32g/L

Sugar (serum) >10mmol/L

Question 15

Other risk scorers

Answer 15

APACHE II Score

Ranson criteria

Balthazar score

Question 16

Imaging

Answer 16

Abdo USS might be done if cause is unknown

AXR can be done but is not routinely done so

CT may be required if initial assessment and ix prove inconclusive.

Question 17

AXR findings

Answer 17

CAn show a sentinel loop sign = Dilated proximal bowel loop adjacent to the pancreas

This is secondary to localised inflammation

Question 18

What can contrast-enhanced CT show?

Answer 18

If performed within 48h of initial presentation it can show…

Pancreatic oedema and swelling

Non-enhancing areas suggestive of pancreatic necrosis

Question 19

When should CT scan for assessment of severity be done?

Answer 19

Only performed 6-10 days after admission in patients with features of persistent infalmmatory response or organ failure.

Question 20

Mainstay treatment

Answer 20

There is no curative management

Mainstay is supportive measures and treating any underlying cause

Question 21

What does supportive tx include?

Answer 21

IV fluid resus + O2 if needed (balanced crystalloid should be used)

NG tube if a lot of vomit

Catheterisation to accurately monitor urine output and start a fluid balance shart.

Opioid analgesia

Question 22

Where should all patients with severe acute pancreatitis be managed?

Answer 22

In a high dependency unit or intensive therapy unit

Question 23

What might be used as prophylaxis vs infection?

Answer 23

Broad-spectrum antibiotics like imipenem,

This is in cases of confirmed pancreatic necrosis

Question 24

Treatment of gallstones in acute pancreatitis

Answer 24

Once condition has stabilised

Early laparoscopic cholecystectomy

Question 25

Systemic complications

Answer 25

Tend to occur within days of initial onset

DIC

ARDS

Hypocalcaemia

Hyperglycaemia

Question 26

Local complications

Answer 26

Pancreatic necrosis

Pancreatic pseudocyst

Question 27

Explain pancreatic necrosis

Answer 27

The ongoing inflammation can lead to ischaemic infarction.
This should be suspected in persistent systemic inflammation for more than 7-10 days after onset.

Question 28

Confirmation of diagnosis of pancreatic necrosis

Answer 28

CT imaging

Question 29

Treatment of pancreatic necrosis

Answer 29

Pancreatic necrosectomy either open or endoscopic

However the intervention should be delayed until walled-off necrosis has developed which is generally 3-5 weeks after onset of symptoms.

Question 30

When should pancratic necrosis be suspected?

Answer 30

Persistent systemic inflammation for more than 7-10 days

Since pancreatic necrosis is prone to infection -> Clinical deterioration and raised infection markers should warrant suspicion of pancreatic necrosis as well.

Question 31

Diagnosis of infected pancreatic necrosis

Answer 31

Fine needle aspiration of the necrosis

Question 32

What is a pancreatic pseudocyst

Answer 32

A collection of fluid containing pancreatic enzymes, blood and necrotic tissue.

They can occur anywhere within or adjacent to the panceares.

Most commonly seen in the lesser sac and obstructing the gastro-epiploic foramen by inflammatory adhesions.

Question 33

Why are they called pseudocysts?

Answer 33

Because they lack an epithelial lining, instead they have a vascular and fibrotic wall.

They typically form weeks after AP episode.

Question 34

When are pseudocysts found?

Answer 34

Usually incidentally on imaging

They can also present with symptoms of mass effect like biliary obstruction or gastric outlet obstruction.

They are also prone to haemorrhage or rupture and can become infection

Question 35

Treatment of pseudocysts

Answer 35

50% will resolve by themselves so conservative is usually first line

If they have been present for long than 6 weeks they are unlikely to resolve by themselves.

Treatment is then surgical debridment or endoscopic drainage often into the stomach.

Question 36

When should antibiotics be used in acute pancreatitis

Answer 36

As prophylaxis in cases of confirmed pancreatic necrosis