Acute pancreatitis

Last revised by Rohit Sharma on 27 Sep 2023

Acute pancreatitis (plural: pancreatitides) is an acute inflammation of the pancreas and potentially life-threatening.

Two subtypes of acute pancreatitis are described in the Revised Atlanta Classification 1

The demographics of patients affected by acute pancreatitis reflect the underlying cause, of which there are many (see Pathology below).

The diagnosis of acute pancreatitis is usually based on clinical criteria or a combination of clinical and radiographic features 1

Two of the following three criteria are required for the diagnosis 1:

  • 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

Classical clinical features include 3:

  • acute onset of severe central epigastric pain (over 30-60 min)

  • poorly localized tenderness and pain

  • exacerbated by supine positioning

  • radiates through to the back in 50% of patients

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

A normal amylase level (normoamylasaemia) in acute pancreatitis is well-recognized, especially when it occurs on the ground of chronic pancreatitis. A normal lipase level has also been reported (<10 case reports) but is extremely rare 16.

(Rare) signs of hemorrhage 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 leads to inflammation of the pancreatic tissue, disruption of small pancreatic ducts, and 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.

See: causes of pancreatitis (mnemonic)

The role of imaging is manifold: 

  • to clarify the diagnosis when the clinical picture is confusing

  • to assess severity (e.g. 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, ultrasound is useful for the follow-up of specific abnormalities, such as fluid collections and pseudocysts.

Radiographs are insensitive for evidence of acute pancreatitis: many patients have normal exams. Moreover, none of the signs is specific enough to establish the diagnosis of pancreatitis.

Abdominal radiographs may demonstrate:

Chest radiographs may demonstrate:

The main role of ultrasound is: 

  • to identify gallstones as a possible cause

  • diagnosis of vascular complications, e.g. thrombosis

  • identify areas of necrosis that appear as hypoechoic regions

  • assessment of clinically similar etiologies of an acute abdomen

In the event of a serendipitously patent acoustic window, typical ultrasonographic features congruent with acute pancreatitis include:

  • increased pancreatic volume with a marked decrease in echogenicity 19 

    • volume increase quantified as a pancreatic body exceeding 2.4 cm in diameter, with marked anterior bowing and surface irregularity 17

    • decreased echogenicity secondary to fluid exudation, which may result in a marked heterogeneity of the parenchyma 18

  • displacement of the adjacent transverse colon and/or stomach secondary to pancreatic volume expansion 20

Abnormalities that may be seen in the pancreas include:

  • typical findings

    • focal or diffuse parenchymal enlargement

    • changes in density because of edema

    • indistinct pancreatic margins owing to inflammation

    • surrounding retroperitoneal fat stranding

  • liquefactive necrosis of pancreatic parenchyma

    • lack of parenchymal enhancement (should ideally be 1 week after symptom onset to differentiate from pancreatic hypoenhancement secondary only to edema)

    • often multifocal

  • infected necrosis

    • difficult to distinguish from aseptic liquefactive necrosis

    • the presence of gas is helpful (emphysematous pancreatitis)

    • FNA helpful

  • abscess formation

    • circumscribed fluid collection

    • little or no necrotic tissues (thus distinguishing it from infected necrosis)

  • hemorrhage

    • high-attenuation fluid in the retroperitoneum or peripancreatic tissues

  • calcification

    • evidence of background chronic pancreatitis

  • retroperitoneal fat necrosis 33

    • low density collection showing minimal heterogeneity

    • mimicking carcinomatosis

  • Dual-energy CT may be able to help better differentiate necrotic debris, hematoma, and areas of viable tissue in cases of necrotizing pancreatitis. In hemorrhagic pancreatitis, virtual non-contrast images can depict hematoma and differentiate it from parenchymal enhancement on contrast-enhanced images. It also improves the detection of non-calcified gallstones and isoattenuating cholesterol stones which may be the causative factor in the patient's pancreatitis 21.

Dual-energy CT dual-phase protocols with virtual non-contrast reformats can also offer lower radiation doses than conventional triple-phase CT imaging of the pancreas 21.

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

Diffusion-weighted imaging shows hyperintense signal of the involved parenchyma with decreased ADC values 28,29

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 the 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

The 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 2012 revised Atlanta classification attempts to establish uniformity in reporting for both clinical practice and research 8.

General imaging differential considerations include:

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Cases and figures

  • Figure 1: gross pathology
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  • Case 1
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  • Case 2: complicated by portal vein thrombosis
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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: necrotizing pancreatitis
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  • Case 7
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  • Case 8: necrotizing pancreatitis
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  • Case 9
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  • Case 10: post ERCP infected pancreatitis
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  • Case 11: involving pancreatic tail
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  • Case 12
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  • Case 13
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  • Case 14: L-asparaginase induced
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  • Case 15
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  • Case 16: post ERCP pancreatitis
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  • Case 17
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  • Case 18
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  • Case 19: necrotizing pancreatitis
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  • Case 20: necrotizing pancreatitis with ANCs
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  • Case 21: necrotizing pancreatitis
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  • Case 22: with infected necrosis
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  • Case 23: interstitial edematous pancreatitis
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  • Case 24
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  • Case 25: on top of pancreas divisum
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  • Case 26
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  • Case 27
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  • Case 28
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  • Case 29: with hepatic hydatid cyst
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  • Case 30
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  • Case 31: necrotizing pancreatitis
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  • Case 32
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  • Case 33: focal acute pancreatitis
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  • Case 34
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  • Case 35
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  • Case 36
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  • Case 37
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  • Case 38: Acute pancreatitis (MRCP)
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  • Case 39: with acute fluid collections
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  • Case 40
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