Acute pancreatitis
Updates to Article Attributes
Acute pancreatitis refers to acute inflammation of the pancreas and is a potentially life threatening condition. Imaging is often required to not only confirm the diagnosis but also to guide treatment.
Epidemiology
The demographics of patients affected by acute pancreatitis reflects the underlying cause. Causes include:
- alcohol abuse: most common cause of chronic pancreatitis
- gallstone passage/impaction: most common cause of acute pancreatitis (up to 15% could develop pancreatitis)
- metabolic disorders
- hereditary pancreatitis (autosomal dominant) SPINK-1 gene mutation 5
- hypercalcemia
- hyperlipidemia (types 1 and 5)
- malnutrition
- trauma : most common cause in children
- blunt abdominal trauma
- surgery
- endoscopic retrograde cholangiopancreatography (ERCP) 7
- penetrating ulcer
- malignancy
- pancreatic adenocarcinoma
- lymphoma
- infection
- viral: mumps, coxsackie, hepatitis, infectious mononucleosis, AIDS
- parasitic: Ascariasis 5, Clonorchis
- structural
- toxins
- scorpion bites
- spider bites (some)
- idiopathic: 20% of cases of acute pancreatitis
- drugs: steroids, tetracycline, frusemide, azathioprine, thiazides, L-asparaginase and many others
- others
Clinical presentation
Acute pancreatitis is generally diagnosed clinically. Classical features include 3:
- gradual development 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.
Signs of haemorrhage include:
- Cullen sign - periumbilical bruising
- Grey-Turner sign - flank bruising
Pathology
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 not withstanding, 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
(collections(are defined by presence or absence ofenzyme-rich pancreatic juicenecrosis )-
necrosis absent:
- acute
: resolve spontaneously in 50% of cases; may be intrapancreatic, anterior pararenal space, lesser sac, or extend anywhere inperipancreatic fluid collections (APFCs) (in theabdomenfirst 4 weeks),into solid organs, or even into the chest -
in the remaining 50% of cases, thesepseudocysts (encapsulated fluid collectionsprogress to pseudocystsafter 4 weeks),
- acute
-
necrosis absent:
- acute necrotic collections (ANCs) in first 4 weeks),
- walled-off necrosis (WON;encapsulatedcollections after 4 weeks).
-
necrosis absent:
-
pseudocyst formation
- a round or oval, encapsulated pancreatic fluid collection encased by a distinct fibrous capsule
- requires at least 4 weeks to develop
- about 50% will spontaneously resolve, whereas the remainder will require catheter or surgical drainage.
- liquefactive necrosis of pancreatic parenchyma
- morbidity and mortality increase dramatically when necrosis is present
- may become secondarily infected (emphysematous pancreatitis)
- abscess - peripancreatic abscess
- 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 peritoneal cavity
Radiographic features
Role of imaging is either to clarify the diagnosis when the clinical picture is confusing, to assess severity (Balthazar score), to determine prognosis, or to detect complications.
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
- indistinctness of the margins of the gland owing to inflammation
- surrounding retroperitoneal stranding
- liquefactive necrosis of pancreatic parenchyma
- lack of parenchymal enhancement
- often multifocal.
- infected necrosis
- difficult to distinguish from aseptic liquefactive necrosis
- 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
May be used to monitor patient's progress:
- diagnosis of vascular complications, ie. thrombosis
- identify gallstones
- hypoechoic lesions may indicate necrotic change
Treatment and prognosis
Prognosis for acute pancreatitis varies according to severity. Overall mortality is 5-10% per attack 3. Ranson's criteria are useful in prognosticating.
The newly revised Atlanta classification system makes the scene for a new international classification system, trying to uniform reporting for both clinical practice and research 8.
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.
Ultrasound or CT directed aspiration biopsy may be needed to confirm the presence of pancreatic abscess. Image-directed catheter placement is an alternative to surgical drainage of pancreatic fluid collections.
Differential diagnosis
General imaging differential considerations include
- pancreatic ductal adenocarcinoma
- autoimmune pancreatitis
- peptic ulcer disease with posterior perforation
- pancreatic lymphoma (diffuse pattern)
See also
-<a title="Cullen sign" href="/articles/cullen-sign">Cullen sign</a> - periumbilical bruising</li>- +<a href="/articles/cullen-sign">Cullen sign</a> - periumbilical bruising</li>
-<a title="Grey-Turner sign" href="/articles/grey-turner-sign">Grey-Turner sign</a> - flank bruising</li>- +<a href="/articles/grey-turner-sign">Grey-Turner sign</a> - flank bruising</li>
-<li>pancreatic fluid collections (collections of enzyme-rich pancreatic juice)<ul>-<li>acute: resolve spontaneously in 50% of cases; may be intrapancreatic, anterior pararenal space, lesser sac, or extend anywhere in the abdomen, into solid organs, or even into the chest</li>-<li>in the remaining 50% of cases, these fluid collections progress to pseudocysts</li>- +<li>pancreatic fluid collections (are defined by presence or absence of necrosis )<ul>
- +<li>necrosis absent:<ul>
- +<li>acute peripancreatic fluid collections (APFCs) (in the first 4 weeks),</li>
- +<li>pseudocysts (encapsulated fluid collections after 4 weeks),</li>
- +</ul>
- +</li>
- +<li>necrosis absent:<ul>
- +<li>acute necrotic collections (ANCs) in first 4 weeks),</li>
- +<li>walled-off necrosis (WON;encapsulated<br>collections after 4 weeks).</li>
- +</ul>
- +</li>
References changed:
- 9. Thoeni R. The Revised Atlanta Classification of Acute Pancreatitis: Its Importance for the Radiologist and Its Effect on Treatment. Radiology. 2012;262(3):751-64. <a href="https://doi.org/10.1148/radiol.11110947">doi:10.1148/radiol.11110947</a> - <a href="https://www.ncbi.nlm.nih.gov/pubmed/22357880">Pubmed</a>
Image 7 CT (C+ portal venous phase) ( update )
Image 11 CT (C+ arterial phase) ( update )
Image 21 CT (C+ portal venous phase) ( update )
Image 24 CT (C+ portal venous phase) ( update )
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