Pancreatitis (Acute) Flashcards

1
Q

What is acute pancreatitis?

A

Acute pancreatitis refers to inflammation of the pancreas.

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2
Q

How does acute and chronic pancreatitis differ?

A

It can be distinguished from chronic pancreatitis by its limited damage to the secretory function of the gland, with no gross structural damage developing. Repeated episodes of acute pancreatitis can eventually lead to chronic pancreatitis.

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3
Q

What are the risk factors for acute pancreatitis?

A

‘GET SMASHED’:

  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune disease, such as SLE
  • Scorpion venom (a rare and unlikely cause in most countries)
  • Hypercalcaemia
  • Endoscopic retrograde cholangio-pancreatography (ERCP)
  • Drugs (azathioprine, NSAIDs or diuretics)
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4
Q

Briefly describe the anatomy of the biliary tree

A
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5
Q

Briefly describe the pathophysiology of acute pancreatitis

A

Each cause risk factor will trigger a premature and exaggerated activation of the digestive enzymes within the pancreas. The resulting pancreatic inflammatory response causes an increase in vascular permeability and subsequent fluid shifts (often termed “third spacing”).

Enzymes are released from the pancreas into the systemic circulation, causing autodigestion of fats (resulting in a ‘fat necrosis’) and blood vessels (sometimes leading to haemorrhage in the retroperitoneal space). Fat necrosis can cause the release of free fatty acids, reacting with serum calcium to form chalky deposits in fatty tissue, resulting in hypocalcaemia.

Severe end-stage pancreatitis will eventually result in partial or complete necrosis of the pancreas.

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6
Q

What are the clinical features of acute pancreatitis?

A

Patients will classically present with a sudden onset of severe epigastric pain, which can radiate through to the back, with nausea and vomiting.

On examination, there is often epigastric tenderness, with or without guarding. In severe cases, there may be haemodynamically instability, due to the inflammatory response occurring.

Less common signs that are often described are Cullen’s sign and Grey Turner’s sign, representing retroperitoneal haemorrhage. Tetany may occur from hypocalcaemia (secondary to fat necrosis) and, in select cases, gallstone aetiology may also cause a concurrent obstructive jaundice.

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7
Q

What is Cullen’s Sign?

A

Cullen’s sign: bruising around the umbilicus.

Representing retroperitoneal haemorrhage.

Shown as A.

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8
Q

What is Grey Turner’s Sign?

A

Grey Turner’s sign: bruising in the flanks.

Representing retroperitoneal haemorrhage.

Shown as B.

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9
Q

What is shown in picture A and B?

A

A= Cullen’s Sign

B= Grey Turner’s Sign

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10
Q

What investigations should be ordered for acute pancreatitis?

Note: laboratory investigations

A

Routine blood tests, as per investigation of any acute abdomen, are required. Specifically for acute pancreatitis, it is important to consider:

  • Serum amylase
  • LFTs
  • Serum lipase
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11
Q

Why investigate serum amylase?

A

Diagnostic of acute pancreatitis if 3x the upper limit of normal.

Amylase can also be marginally raised in pathologies such as bowel perforation, ectopic pregnancy or diabetic ketoacidosis.

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12
Q

Why investigate LFTs?

A

Assess for any concurrent cholestatic element to the clinical picture.

Patients with acute pancreatitis noted that an alanine transaminase (ALT) level >150U/L has a positive predictive value of 85% for gallstones as the underlying cause.

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13
Q

Why investigate serum lipase?

A

A raised serum lipase is more accurate for acute pancreatitis (as it remains elevated longer than amylase), yet it is not available or routinely performed in every hospital.

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14
Q

What investigations should be ordered for acute pancreatitis?

Note: imaging

A

An abdominal ultrasound scan may be requested if the underlying cause is unknown; it is typically used to identify any gallstones (as a potential underlying cause) and any evidence of duct dilatation.

Whilst not routinely performed for acute pancreatitis, an AXR can show a ‘sentinal loop sign’.

A contrast-enhanced CT scan may be required if the initial assessment and investigations prove inconclusive.

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15
Q

How does acute pancreatitis appear on AXR?

A

Presents as sentinel loop sign. This is a dilated proximal bowel loop adjacent to the pancreas, which occurs secondary to localised inflammation. A CXR should be undertaken to look for pleural effusion or signs of ARDS.

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16
Q

How does acute pancreatitis present on contast enhanced CT scan?

Note: after 48 hours

A

If performed after 48hrs from initial presentation, it will often show areas of pancreatic oedema and swelling, or any non-enhancing areas suggestive of pancreatic necrosis.

17
Q

What is shown on the contrast enhanced CT scan?

A

Pancreatitis on Axial CT Scan (A) Localised oedema around the pancreas (B) Extensive fluid collections around the pancreas.

18
Q

Briefly describe the treatment for acute pancreatitis

A

There is no curative management for acute pancreatitis, so supportive measures are the mainstay of treatment. Treat any underlying cause as necessary (e.g. urgent ERCP and sphincterotomy for gallstones) where appropriate.

Supportive measures include:

  • Intravenous fluid resuscitation and oxygen therapy as required
  • Nasogastric tube if the patient is vomiting profusely
  • Catheterisation to accurately monitor urine output and start a fluid balance chart (due to the potential for rapid third space losses)
  • Opioid analgesia
19
Q

Where are patients with acute pancreatitis supposed to be managed?

A

Current UK guidelines state that all patients with severe acute pancreatitis should be managed in a high dependency unit or intensive therapy unit (although this is often impractical).

20
Q

When is antibiotic therapy needed for acute pancreatitis?

A

A broad-spectrum antibiotic, such as imipenem, should be considered for prophylaxis against infection in cases of confirmed pancreatic necrosis.

21
Q

If there is an underlying cause causing acute pancreatitis, when should this be addressed?

A

Treating the underlying cause should be addressed, once the patient has been stabilised.

For those caused by gallstones, early laparoscopic cholecystectomy is advised, whilst those secondary to alcohol excess should ensure they have access to the appropriate services made.

22
Q

What are the systemic complications of acute pancreatitis?

A

The systemic complications of acute pancreatitis tend to occur within days of the initial onset:

  • Disseminated Intravascular Coagulation (DIC)
  • Acute Respiratory Distress Syndrome (ARDS)
  • Hypocalcaemia
  • Hyperglycaemia
23
Q

Why is hypoglycaemia a complication of acute pancreatitis?

A

Fat necrosis from released lipases, results in the release of free fatty acids, which react with serum calcium to form chalky deposits in fatty tissue.

24
Q

Why is hyperglycaemia a complication of acute pancreatitis?

A

Secondary to destruction of islets of Langerhans and subsequent disturbances to insulin metabolism.

25
Q

What are the local complication of acute pancreatitis?

A
  • Pancreatic necrosis
  • Pancreatic pseudocyst
26
Q

What is pancreatic necrosis? How is pancreatic necrosis diagnosed?

A

Ongoing inflammation eventually leads to ischaemic infarction of the pancreatic tissue, hence such progression should be suspected in patients with evidence of persistent systemic inflammation for more than 7-10 days after the onset of pancreatitis.

Any suspected pancreatic necrosis should be confirmed by CT imaging and treatment will often warrant pancreatic necrosectomy (open or endoscopic).

27
Q

When should pancreatic necrosis be suspected in a a patient?

A

Pancreatic necrosis is prone to infection and should be suspected if there is a clinical deterioration in the patient associated with raised infection markers (or from positive blood culture or changes of low density within the pancreas on CT).

Definitive diagnosis of infected pancreatic necrosis can be confirmed by a fine needle aspiration of the necrosis.

28
Q

What are pancreatic pseudocysts?

A

A pancreatic pseudocyst is a collection of fluid containing pancreatic enzymes, blood, and necrotic tissue; they can occur anywhere within or adjacent to the pancreas, however are usually seen in the lesser sac obstructing the gastro-epiploic foramen by inflammatory adhesions..

They are typically formed weeks after the initial acute pancreatitis episode. They lack an epithelial lining, therefore termed pseudocyst, and instead have a vascular and fibrotic wall surrounding the collection.

29
Q

How do pancreatic pseudocysts present?

A

Pseudocysts may be found incidentally on imaging or can present with symptoms of mass effect, such as biliary obstruction or gastric outlet obstruction. They are prone to haemorrhage or rupture, and can become infected.

30
Q

Briefly describe the management of pancreatic pseudocyst

A

About 50% will spontaneously resolve, hence conservative management is usually the initial treatment of choice. Cysts which have been present for longer than 6 weeks are unlikely to resolve spontaneously. Treatment options include surgical debridement or endoscopic drainage (often into the stomach).

31
Q

What are the differential diagnoses of acute pancreatitis?

A

There are a wide variety of causes of an acutely painful abdomen, as discussed elsewhere. However causes specifically resulting in abdominal pain that radiates through to the back include abdominal aortic aneurysm, renal calculi, chronic pancreatitis, aortic dissection or peptic ulcer disease.

32
Q

What scoring system is used to assess the severity of acute pancreatitis?

A

Glasgow Criteria.

33
Q

Briefly describe the Glasgow Criteria for assessing the severity of acute pancreatitis

A

The modified Glasgow criteria is used to assess the severity of acute pancreatitis within the first 48 hours of admission. Any patient scoring with ≥3 positive factors within the first 48hrs should be considered to have severe pancreatitis and a high-dependency care referral is warranted.

Helpfully, the mneumonic to remember the score is PANCREAS:

  • pO2 <8kPa
  • Age >55yrs
  • Neutrophils (/WCC) >15×109/L
  • Calcium <2mmol/L
  • Renal function (Urea) >16mmol/L
  • Enzymes LDH>600U/L or AST>200U/L,
  • Albumin <32g/L
  • Sugar (blood glucose) >10mmol/L