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Acute pancreatitis is an acute inflammatory process that results
from the exudation of fluid containing activated proteolytic enzymes
into the pancreatic parenchyma and peripancreatic tissues. Alcoholism
and choledocholithiasis are the two most common causes of acute
pancreatitis. Other etiologies include hereditary (e.g. familial
pancreatitis, cystic fibrosis), idiopathic, trauma (e.g. blunt abdominal
trauma, postoperative), bacterial, viral or parasitic infection,
metabolic (e.g. hyperlipidemia, uremia, hypercalcemia), poisons
and toxins, drugs (e.g. immunosuppressives, thiazide diuretics,
antimicrobials, steroids), vascular (vasculitis [e.g. SLE, TTP,
malignant hypertension], shock, hypoperfusion), and mechanical (e.g.
pancreas divisum). Despite underlying etiology, the end result is
an acute inflammation of the pancreas that leads to an escape of
activated proteolytic enzymes from the pancreatic ducts leading
to tissue injury, inflammation, necrosis, and in some cases infection.
Symptoms include severe epigastric pain that radiates to the back
(95% of patients), nausea and vomiting (75-85%) and fever (50%).
Patients also have associated elevations in pancreatic enzymes,
especially amylase and lipase.
Pathologically acute pancreatitis is characterized by a spectrum
of morphologic features, which may be patchy or diffuse. In mild
pancreatitis edema predominates, producing so called “edematous”
or “interstitial pancreatitis.” There is scattered peripancreatic
fat necrosis without parenchymal or acinar necrosis. In severe pancreatitis,
extensive pancreatic and peripancreatic fat necrosis, parenchymal
necrosis, and hemorrhage occur. Pancreatitis frequently results
in complications including acute fluid collections within and around
the pancreas, pseudocysts, pancreatic abscesses, hemorrhage, and
infected necrosis. Pancreatic abscesses usually occur greater than
four weeks after the onset of pancreatitis and represent an infection
of an acute fluid collection or of a pancreatic pseudocyst. A discrete
wall of fibrous tissue and granulation tissue is seen around the
abscesses. Infected necrosis represents seeding of areas of necrosis
with bacteria to form a suppurative infection. Unlike an abscess,
areas of infected necrosis do not have a discrete enclosing wall.
The presence of infected necrosis confers a poor prognosis because
it is an unusual complication of severe pancreatitis.
MR imaging features of acute pancreatitis reflect the pathologic
changes seen in the disease, therefore, representing the severity
of the pancreatitis. In uncomplicated, mild acute pancreatitis the
signal intensity features of the pancreas can resemble that of normal
pancreatic tissue. The normal pancreas is high in signal intensity
on pre-contrast T1-weighted fat-suppressed images and enhances in
a normal uniform fashion on immediate post-gadolilinum images reflecting
a normal capillary blush. The diagnosis of acute pancreatitis on
MR images relies on the presence of morphologic and/or signal intensity
changes. The acutely inflamed pancreas shows either focal or diffuse
enlargement, which may be subtle. As the extent of pancreatitis
becomes more severe, the pancreas develops a heterogeneous appearance
on pre-contrast T1-weighted fat suppressed images and enhances in
a more heterogeneously, diminished fashion on immediate post-gadolimium
images.
The complications of acute pancreatitis are well visualized on
cross-sectional MR imaging. Peripancreatic fluid collections
result from pancreatic edema, areas of fat necrosis, and extravasated
pancreatic enzymatic secretions. These fluid collections appear
as low-signal intensity strands of fluid or fluid collections in
a background of high-signal intensity fat on non-contrast or immediate
post-gadolinium T1-weighted spoiled gradient echo (SGE) images.
Because of the presence of blood or protein within these fluid collections,
T1-weighted images can also demonstrate a heterogeneous signal intensity
within these fluid collections. Breathing independent single shot
T2-weighted images employing fat suppression are also effective
at showing small-volume high-signal fluid in a background of intermediate
to low-signal pancreas and low-signal fat. Hemorrhagic fluid
collections appear as high-signal intensity areas on T1-weighted
fat-suppressed images. The extent of pancreatic necrosis has been
considered an important prognostic indicator in patients with acute
pancreatitis. Dynamic gadolinium enhanced T1-weighted SGE images
may be useful for this determination because MRI is very sensitive
in detecting the presence or absence of gadolinium enhancement.
Pseudocysts rarely form before three-four weeks after presentation
of acute pancreatitis and are also seen in chronic pancreatitis.
MRI images acquired in multiple planes permit determination of pseudocyst
location in relation to various organs and structures. Unlike fluid
collections, pseudocysts are encapsulated by a discrete wall, which
generally shows marked enhancement. Simple pseudocysts are low in
signal intensity or signal void in a background of normal signal
intensity pancreatic tissue on both SGE and T1-weighted fat suppressed
images. On T2-weighted images, simple pseudocysts are relatively
homogeneous and high in signal intensity. Pseudocysts that
are complicated by necrotic debris, hemorrhage, or infection have
heterogeneous signal intensity on T2-weighted images. Additionally,
MR images should be surveyed for evidence of a cause for pancreatitis
such as choledocholithiasis and the presence of gallstones or biliary
anomalies should be noted.
References:
- Semelka RC. Abdominal-Pelvic MRI. New York: Wiley-Liss
Inc, c2002. pp. 453-461.
- Matos C, Cappeliez O, et al. MR Imaging of the Pancreas:
A Pictorial Tour. Radiographics. 2002; 22: e2.
- Outwater E.K. and E.S. Siegelman. MR Imaging of Pancreatic
Disorders. Topics in Magnetic Resonance Imaging. 1996; 8(5):
265-289.
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