Acute pancreatitis

Acute pancreatitis is an acute inflammation of the pancreas and is a potentially life-threatening condition.

The diagnosis of acute pancreatitis is made by fulfilling two of the following three criteria 8:

  • acute onset of persistent, severe epigastric pain (i.e. pain consistent with acute pancreatitis)
  • lipase/amylase elevation >3 times the upper limit of normal
  • characteristic imaging features on contrast-enhanced CT, MRI, or ultrasound

Imaging is only required to establish the diagnosis if the first two criteria are not met. Imaging is crucial for the detection of complications and to help guide treatment.

There are two subtypes of acute pancreatitis 8

The demographics of patients affected by acute pancreatitis reflects the underlying cause, of which there are many, including: 

See: causes of pancreatitis (mnemonic)

Classical clinical features include 3:

  • acute onset of severe central epigastric pain (over 30-60 min)
  • poorly localised tenderness and pain
  • exacerbated by supine positioning
  • radiates through to the back in 50% of patients

Elevation of amylase and lipase are 90-95% specific for the diagnosis 3.

(Rare) signs of haemorrhage on the physical exam include:

There continues to be debate over the precipitating factor leading to acute pancreatitis, with duct occlusion being an important factor, but neither necessary nor sufficient.

Mechanism notwithstanding, activation of pancreatic enzymes within the pancreas rather than the bowel lead to inflammation of the pancreatic tissue, disruption of small pancreatic ducts and in leakage of pancreatic secretions. Because the pancreas lacks a capsule, the pancreatic juices have ready access to surrounding tissues. Pancreatic enzymes digest fascial layers, spreading the inflammatory process to multiple anatomic compartments.

Complications
  • pancreatic fluid collections are defined by presence or absence of necrosis:
  • liquefactive necrosis of pancreatic parenchyma (e.g. necrotising pancreatitis)
  • pancreatic abscess
    • a presence of infection without significant necrosis
    • extremely rare
    • term not in current use 8
  • vascular complications
    • haemorrhage: resulting from erosion of blood vessels and tissue necrosis
    • pseudoaneurysm: autodigestion of arterial walls by pancreatic enzymes results in pulsatile mass that is lined by fibrous tissue and maintains communication with parent artery
    • splenic vein thrombosis
    • portal vein thrombosis
  • fistula formation with pancreatic ascites: leakage of pancreatic secretions into the peritoneal cavity

The role of imaging is manifold: 

  • to clarify the diagnosis when the clinical picture is confusing
  • to assess severity (Balthazar score) and thus to determine prognosis
  • to detect complications
  • to determine possible causes

Imaging studies of acute pancreatitis may be normal in mild cases. Contrast-enhanced CT provides the most comprehensive initial assessment, typically with a dual phase (arterial and portal venous) protocol. However, US is useful for follow-up of specific abnormalities, such as fluid collections and pseudocysts.

CT

Abnormalities that may be seen in the pancreas include:

  • typical findings
    • focal or diffuse parenchymal enlargement
    • changes in density because of oedema
    • indistinct pancreatic margins owing to inflammation
    • surrounding retroperitoneal fat stranding
  • liquefactive necrosis of pancreatic parenchyma
    • lack of parenchymal enhancement
    • often multifocal
  • infected necrosis
    • difficult to distinguish from aseptic liquefactive necrosis
    • the presence of gas is helpful
    • FNA helpful
  • abscess formation
    • circumscribed fluid collection
    • little or no necrotic tissues (thus distinguishing it from infected necrosis)
  • haemorrhage
    • high-attenuation fluid in the retroperitoneum or peripancreatic tissues
MRI

Contrast-enhanced MR is equivalent to CT in the assessment of pancreatitis.

Ultrasound

The main role of ultrasound is: 

  • to identify gallstones as a possible cause
  • diagnosis of vascular complications, e.g. thrombosis
  • identify areas of necrosis which appear as hypoechoic regions

Treatment is largely supportive, often requiring ICU care in severe cases for respiratory and cardiovascular support and careful management of glucose, calcium, and fluid balance. 

Recommendations include 11:

  • aggressive fluid resuscitation in first 24 hours
  • no need for prophylactic antibiotics
  • enteral feeding strongly preferred over parenteral feeding, especially in severe acute pancreatitis
  • no need for ERCP in acute gallstone pancreatitis unless evidence of ascending cholangitis
  • image-directed catheter placement is an alternative to surgical drainage of pancreatic fluid collections
  • cholecystectomy before discharge in patients with acute pancreatitis and gallstones found on imaging

Prognosis for acute pancreatitis varies according to severity. Overall mortality is 5-10% per attack 3. Various scoring systems exist that attempt to stratify severity (e.g. Ranson's criteria and APACHE II).

The newly revised Atlanta classification (new international classification system), attempts to establish uniformity in reporting for both clinical practice and research 8.

General imaging differential considerations include:

Pancreatic pathology
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Synonyms or Alternate Spellings:
  • Pancreatitis - acute

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Cases and figures

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    Case 1
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    Case 2: complicated by portal vein thrombus
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    Case 3: walled off necrosis
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    Case 4
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    Case 5: resolving
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    Case 6: necrotising pancreatitis
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    Case 7
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    Case 8: necrotising pancreatitis
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    Case 9
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    Case 11: involving pancreatic tail
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    Case 10: post ERCP infected pancreatitis
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    Case 14: L-asparaginase induced
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    Case 16: post ERCP pancreatitis
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    Case 18
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    Case 19: necrotising pancreatitis
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    Case 20: necrotising pancreatitis with ANCs
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    Case 21: necrotising pancreatitis
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    Case 23: interstitial oedematous pancreatitis
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    Case 22: with infected necrosis
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    Case 24
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