Imaging of Complications in Acute Pancreatitis: a Pictorial
Review from the Standpoints of Pathogenic Mechanism
Poster No.:
C-1490
Congress:
ECR 2015
Type:
Educational Exhibit
Authors:
T. Wada, T. Tajima, T. Noguchi, T. Masuda, T. Okafuji; Tokyo/JP
Keywords:
Abdomen, Pancreas, Vascular, CT, MR, Catheter arteriography,
Contrast agent-intravenous, Abscess delineation, Embolisation,
Acute, Inflammation, Aneurysms
DOI:
10.1594/ecr2015/C-1490
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Page 1 of 35
Learning objectives
•
To learn the radiologic findings of complications in acute pancreatitis (AP)
from the standpoints of pathogenic mechanisms.
•
To review the CT images of complications in AP according to the extrapancreatic inflammation spread.
•
To understand the role of the CT severity indexes in patients with
complications with AP.
Background
There are various complications in AP, which involves many organs. The pathogenic
mechanisms of complications in AP are, in particular, autodigestion, ischemia and
infection.
Autodigestion by pancreatic digestive enzyme causes pseudocyst, aneurysm and
gastrointestinal perforation. Ischemia occurs because of arterial stenosis, coagulation
disorder and intravascular dehydration, causing pancreatic necrosis (Fig. 3 on page
2), non-occlusive mesenteric ischemia (NOMI) and other organ ischemia.
Autodigestion and ischemia cause infection, such as abscess (Fig. 5 on page 3),
cholangitis and sepsis.
In this exhibit, common and uncommon CT findings of complications in AP according to
the direction of extra-pancreatic inflammation spread and visceral involvement.
Images for this section:
Page 2 of 35
Fig. 3: A 53 year-old male with pancreatic necrosis. Contrast-enhanced CT shows no
enhancement of the parenchyma in the pancreatic body and tail (arrow).
Page 3 of 35
Fig. 5: A 93 year-old female with pancreatic abscess. Contrast-enhanced CT shows the
fluid collection in the pancreas tail, containing air bubbles (arrow). Inflammatory change
in the surrounding fat tissue and wall thickening of the transverse colon are also seen
(arrowhead).
Page 4 of 35
Findings and procedure details
AP is an auto-digestive phenomenon resulting from the inappropriate activation of
digestive enzymes within the pancreas itself. There are various pathogenesis of AP,
such as bile duct stone, alcohol, pancreas divisum, biliary sludge, endoscopic retrograde
cholangiopancreatography (ERCP), hypercalcemia, drugs, infectious agents, genetic
mutation, and so forth [1].
Systemic problems, which are usually seen in severe AP, include skin, thoracic,
hepatobiliary, urological, splenic, vascular and gastrointestinal complications.
Pathogenic Mechanisms
Pathogenic mechanisms of these complications are mainly classified into six types as
follows:
1. Autodigestion: fatty necrosis, pseudoaneurysm, and pseudocyst.
2. Ischemia: pancreatic necrosis, NOMI, hepatic and splenic infarction.
3. Infection: pancreatic abscess, suppurative cholangitis and pneumonia.
4. Organ failure: disseminated intravascular coagulation (DIC), acute respiratory distress
syndrome (ARDS) and diabetes mellitus.
5. Extension of inflammation: paralytic ileus phlegmon and skin complications.
6. Others: portal vein thrombosis and gastroduodenal ulcer.
Imaging of Visceral Involvement of AP
The radiographic findings in AP range from unremarkable in mild disease to localized
ileus of a segment of small intestine (sentinel loop) or the colon cut off sign in more severe
disease (Fig. 1 on page 14). Computed tomography (CT) is an important common
initial assessment tool for AP. CT severity score has been developed based upon the
Page 5 of 35
degree of necrosis, inflammation, and the presence of fluid collections (Fig. 2 on page
14, Fig. 3 on page 15).
Complications in AP may result in local or systemic problems and affect the prognosis.
Systemic problems include skin, thoracic, hepatobiliary, urological, splenic, vascular and
gastrointestinal complications,
Complications in AP, illustrated on imaging, are classified into many types of visceral
involvement as follows:
1.
2.
3.
4.
5.
6.
7.
8.
9.
Pancreas: necrosis, abscess, pancreatic juice leakage, and fatty necrosis
and phlegmon.
Vessels: pseudoaneurysms, rupture of pseudoaneurysms into the
pancreatic duct (hemosuccus pancreaticus), and occlusion of splenic, renal,
superior mesenteric and portal vein.
Gastrointestinal tract: ileus, perforation and NOMI.
Hepatobiliary system: infarction, abscess, portobiliary fistula and fatty liver.
Spleen: pseudocyst, infarct and subcapsular hemorrhage.
Kidney and perirenal space: perirenal fluid collections and acute renal
failure.
Adrenal gland: hematoma and abnormal enhancement.
Skin and soft tissue: classical clinical symptoms such as Grey-Turner's,
Cullen's and Fox's signs.
Thoracic cavity: pleural effusion and mediastinal extension.
Herein we will present the representative types of visceral involvement associated with
AP from the viewpoint of pathogenic mechanisms.
1. Pancreatic Necrosis
Pathogenic Mechanisms
•
•
•
Pancreatic ischemia in the early phase of acute pancreatitis is important in
the development of pancreatic necrosis.
While depletion of intravascular volume has often been assumed to
be the main circulatory defect, an additional disturbance of pancreatic
microcirculation has been demonstrated experimentally.
Possible contributory mechanisms include chemical-induced
vasoconstriction, direct injury of vessel wall, intravascular coagulation
and increased endothelial permeability resulting in pancreatic edema,
hemoconcentration and impaired venous drainage.
Page 6 of 35
•
Pancreatic ischemia as a consequence of these local effects seems to be
responsible for the transition of mild pancreatitis to parenchymal necrosis
[2].
Image Findings
•
•
•
•
Focal or diffuse areas of nonviable pancreatic parenchyma, which usually is
associated with peripancreatic fat necrosis.
Necrosis typically develops early in course of acute pancreatitis.
Fails to enhance on contrast-enhanced CT (Fig. 4 on page 16).
Necrosis and abscess may be indistinguishable [3].
2. Pancreatic Abscess
Pathogenic Mechanisms
•
•
Pancreatic abscesses usually develop in patients with pancreatic
pseudocysts that become infected. They may also form as a result of fibrous
wall formation around fluid collections or penetrating peptic ulcers.
Pancreatic abscess is a late complication of acute necrotizing pancreatitis,
occurring more than 4 weeks after the initial attack. A pancreatic abscess is
a collection of pus resulting from tissue necrosis, liquefaction, and infection
[4].
Image Findings
•
•
A thick-walled fluid collection with gas bubbles or an area of poorly defined
fluid with heterogeneous attenuation is shown on CT.
Confirmation of diagnosis may require aspiration of pus (Fig. 5 on page
17).
3. Pancreatic Juice Leakage
Pathogenic Mechanisms
•
•
Leakage of pancreatic juice is caused by necrosis of pancreatic parenchyma
or pancreatic duct. It is reported that a ductal leakage was first observed
only after 4 days from the onset of pancreatitis.
The end result of leakage of pancreatic juice underneath the pancreatic
capsule or through the capsule into the peripancreatic space is sterile
necrosis, infected necrosis, or rupture into an adjacent hollow structure [5].
Page 7 of 35
Image Findings
•
Pancreatic juice leakage was significantly associated with pancreatic
necrosis. The frequent finding of a pseudocyst or a peripancreatic amylaserich fluid collection in patients with severe acute pancreatitis indicates that
a pancreatic duct disruption or leak may be a common event in the severe
form of this disease [5] (Fig. 6 on page 18).
4. Fatty Necrosis and Phlegmon
Pathogenic Mechanisms
•
•
•
Fatty necrosis is a form of necrosis characterized by the action upon fat by
pancreatic digestive enzymes, namely lipase.
Acute pancreatic phlegmons develop commonly in the setting of acute
pancreatitis as a result of focal damage to the pancreas. Phlegmons consist
of focal tissue necrosis, inflammatory debris, and necrotic fat. Phlegmons
develop within a few days of severe pancreatitis and may persist for several
weeks or months and finally resolve [6].
Intraabdominal fluid collections are the result of the release of activated
pancreatic enzymes which also causes necrosis of the surrounding tissues
including fat.
Image Findings
•
•
•
Pancreatic phlegmon is a noninfected solid mass of inflamed pancreatic and
retroperitoneal tissues. Clinically, a phlegmon may be confused with other
pancreatic masses, especially a pseudocyst.
On CT, phlegmons are illustrated as a mass in the surrounding
peripancreatic fat tissue.
Phlegmons typically present as palpable epigastric masses which are solid on
sonography and CT [7] (Fig. 7 on page 19).
5. Portal Vein Thrombosis
Pathogenic Mechanisms
•
The mechanism is suggested to be either portal venous compression caused
by pseudocyst or abscess, or an imbalance between blood coagulation and
fibrinolysis.
Page 8 of 35
•
Portal phlebitis caused by leakage of pancreatic juice around the portal vein
may also be a factor in the development of portal vein thrombosis (PVT) in
pancreatitis. PVT may be surrounded by the fluid induced by the episode of
pancreatitis [8].
Image Findings
•
•
PVT is described as a defect in the portal vein in contrast-enhanced CT (Fig.
8 on page 20). PVT also may be described as high attenuation lesion in
the portal vein in unenhanced CT.
PVT may include thrombosis of one or more of splenic vein and superior
mesenteric vein.
6. Pancreatic Pseudocyst with Portal Vein Fistula
Pathogenic Mechanisms
•
•
•
•
Pancreatic pseudocyst with portal vein fistula is a rare but important subset
of complications associated with acute or chronic pancreatitis; these patients
present with a pseudocyst fistulizing into the portal vein.
Among the internal pancreatic fistula, there is the fistula to a biliary system,
colon, small intestine, peritoneal cavity, and thoracic cavity other than portal
vein.
As a developmental mechanism, a pancreatic enzyme within the pancreatic
duct and the pseudocyst erodes with portal vein wall, and the pancreatic
juice permeates intraportally, then the PVT is formed [9].
Surgery such as pancreatic resection, surgical decompression with a cystgastrostomy or pancreatojejunostomy, stent placement for the pancreatic
duct or the supportive medical treatment is performed as a treatment.
Image Findings
•
•
The chief image findings are acute pancreatitis and pseudocyst in the
pancreatic head.
The main trunk and its branch of portal vein are filled with fluid collection
showing the attenuation like a pseudocyst. In chronic cases, cavernomatous
transformation may be formed (Fig. 9 on page 21). As a rare complication
of portal vein fistula, disseminated fat necrosis in the subcutaneous tissue,
joints, bone marrow and the liver is reported.
7. Visceral Artery Pseudoaneurysm
Page 9 of 35
Pathogenic Mechanisms
•
•
Pancreatitis with secondary pseudocyst formation is the most common
cause of pancreatic pseudoaneurysms, although they have been known to
occur in the absence of a pseudocyst.
Overall, the splenic artery is the most frequent site of visceral artery
pseudoaneurysms, followed by the hepatic artery [10].
Image Findings
•
•
CT or MR angiography can depict the pseudoaneurysm as a well-delineated
rounded structure originating from the donor artery (Fig. 10 on page 22,
Fig. 11 on page 23, Fig. 12 on page 24).
High-attenuation or high-signal-intensity thrombus may be seen within the
sac on unenhanced CT scans and fat-suppressed T1-weighted MR images.
8. Hemosuccus Pancreaticus
Pathogenic Mechanisms
•
•
•
•
•
Hemosuccus pancreaticus, also known as pseudohemobilia or
Wirsungorrhage is a rare cause of hemorrhage in the gastro-intestinal tract.
It is caused by a bleeding source in the pancreas, pancreatic duct, or structures
adjacent to the pancreas which is connected with the duodenum.
The most common causes are following: 1) rupture of the pseudoaneurysm/
aneurysm of peripancreatic artery into pancreatic duct and 2) bleeding of the
primary intact or aneurysm containing artery to the pancreatic pseudocyst
communicating with the duct.
These kinds of complications may be found mostly in chronic pancreatitis.
The cause of development and subsequent rupture of pseudoaneurysm/
aneurysm or rupture of primary intact peripancreatic artery to the pseudocyst
is continuous thinning and autodigestion of vessel wall by pancreatic enzymes
and cyst induced pressure necrosis.
Mostly, splenic artery is affected, following with decreasing incidence by
gastroduodenal artery, pancreatic-duodenal, hepatic and left gastric artery
[11].
Image Findings
•
Contrast-enhanced CT and CT angiography are useful to determine a
source of bleeding and visualize pseudoaneurysm/aneurysm.
Page 10 of 35
•
Contrast-enhanced CT and angiogram may show the contrast blush
suggestive of active bleeding from the pseudoaneurysm (Fig. 13 on page
25).
9. Suppurative Cholangitis
Pathogenic Mechanisms
•
•
Obstruction of the biliary system due to pancreatitis, stones or tumor may
cause suppurative cholangitis.
Biliary obstruction raises intrabiliary pressure and leads to increased
permeability of bile ductules, permitting translocation of bacteria and toxins
from the portal circulation into the biliary tract [12].
Image Findings
•
There are no definite specific image findings for supprative cholangitis. Bile
duct dilatation, etiology of obstruction, such as stones, mass or bile duct
narrowing, and thickening of the bile duct wall may be found (Fig. 14 on
page 26).
10. Hepatic and Splenic Infarction
Pathogenic Mechanisms
•
•
•
As splenic complications, infarction, subcapsular hematoma, perisplenic fluid
collection, splenic pseudocyst, splenic abscess and splenic vein thrombosis,
are reported [13].
The most frequently cited pathogenic mechanism of splenic infarction is
splenic vein thrombosis, be it by direct extension of the local inflammatory
process, by the hypercoagulability state induced by pancreatitis, or both.
Compression of the splenic artery, inflammation of its wall, or permanent
arterial spasm may be other mechanisms in the development of splenic
infarction [14].
Pathogenesis of hepatic infarct is associated with portal and hepatic vein
thrombosis. The portal vein thrombosis might have also led to secondary
blood flow stasis in the hepatic vein [15].
Image Findings
Page 11 of 35
•
•
•
Splenic infarctions are defined as focal or diffuse hypoattenuating and
hypovascular regions within the spleen (classically manifesting as a wedgeshaped area) [13] (Fig. 15 on page 27).
Perisplenic fluid collections are defined either as poorly delineated fluid
accumulation or well delineated pseudocyst formation alongside the spleen
or in the splenic hilum [13]. In infected case of the perisplenic fluid collection,
wall enhancement and air bubble in the fluid collection can be detected.
Splenic subcapsular hematoma can be associated with severe
pancreatitis. Complications of pseudocysts include intracystic hemorrhage,
intraperitoneal hemorrhage, and mass effect/obstruction.
11. Abnormal Adrenal Enhancement
Pathogenic Mechanisms
•
•
Especially in the patients with severe AP, inflammation within the anterior
pararenal space extends to the perirenal space, and then adrenal gland
involvement of AP can occur.
Exudate including the pancreatic enzymes may infiltrate the perirenal fascia
and affect the adrenal gland.
Image Findings
•
•
•
•
On contrast-enhanced CT, unilateral or bilateral adrenals may show intense
enhancement with increased CT values higher than adjacent inferior vena
cava (Fig. 16 on page 28). These findings can be seen in patients with
severe AP on contrast-enhanced CT. Intense adrenal enhancement has
been reported in association with hypovolemic and septic shock [16]. In
contrast, another appearance of a poorly enhancement in the unilateral
swollen adrenal gland can be seen in AP, indicating the dysfunction of the
left adrenal gland (Fig. 16 on page 28).
Involvement of the juxtarenal spaces and kidneys in AP are well known.
Although delineation of the regions of accumulation of exudate has been
elegantly confirmed with the advent and advance of refined CT [17].
Bollen TL, et al. [16] showed that all the patients with AP who showed
intense bilateral adrenal enhancement on contrast-enhanced CT had early
multiple organ failure and subsequently died. In patients who showed
intense adrenal enhancement on CT, further studies should be necessary to
confirm the observation.
Liu Z, et al. [18] showed that left adrenal gland involvement (LAGI) and
gastric bare area involvement (GBAI) were characteristic CT findings in AP
and could serve as useful prognostic indicators for AP: especially, patients
with LAGI were 7.4 and 13.7 times more likely to have complications and die
than were patients without.
Page 12 of 35
12. Extension to the Skin and Soft Tissue
Pathogenic Mechanisms
•
•
•
•
Acute pancreatitis may extend to skin and soft tissue. Grey Turner's
sign, Cullen's sign and Fox's sign can be rarely observed in severe acute
pancreatitis [19] (Fig. 17 on page 29).
Grey Turner's sign is produced by the spread of hemorrhagic fluid from the
posterior pararenal space to the lateral edge of the quadratus lumborum
muscle and, subsequently, to the subcutaneous tissues via a defect in the
fascia of the flank [19].
Cullen's sign arises from the diffusion of retroperitoneal blood into the
falciform ligament and, subsequently, to the subcutaneous umbilical tissues
via the connective tissue covering of the round ligament complex [19].
Fox's sign is produced by tracking of the fluid extraperitoneally along the
fascia of psoas and iliacus beneath the inguinal ligament until it becomes
subcutaneous in the upper thigh [19].
Image Findings
•
CT show extension of the inflammatory changes in the subcutaneous
tissues of the abdominal wall, umbilical region and inguinal region (Fig. 18
on page 30).
13. Extension to the Thoracic Cavity
Pathogenic Mechanisms
•
•
•
Pancreatitis may be associated with thoracic complications, notably
chronic massive pleural effusion, mediastinal pseudocysts and enzymatic
mediastinitis [20].
Two main causes of pleural effusion are transdiaphragmatic lymphatic
blockage or pancreaticopleural fistulae secondary to leak and disruption
of the pancreatic duct or pseudocyst caused by an episode of acute
pancreatitis. The leak or disruption is more likely to lead to a pleural effusion
if the duct disruption is posteriorly into the retroperitoneum [20].
Mediastinal pseudocysts develop after rupture of the pancreatic duct
posteriorly into the retroperitoneal space. In most cases the pancreatic fluid
enters the mediastinum through the esophageal or aortic hiatus [20].
Image Findings
Page 13 of 35
•
•
Pleural effusions in AP are usually small and occasionally bloody. The
majority of pleural effusions (68%) are leftsided (Fig. 19 on page 31),
22% are bilateral and 10% are right-sided only [20].
Mediastinal pseudocysts are described as a cystic lesion, and the finding
of communicating cystic structures in the upper abdomen confirmed
the diagnosis of pancreatic pseudocysts (Fig. 20 on page 32). A
multimodal approach of multislice CT with multiplanar reformations and
three-dimensional magnetic resonance cholangiopancreatography (MRCP)
are useful.
Images for this section:
Fig. 1: Radiographs seen in the patients with AP. A: sentinel loop sign. B: colon cut off
sign.
Page 14 of 35
Fig. 2: Computed Tomography Severity Index (Balthazar scoring)
Page 15 of 35
Fig. 3: A 53 year-old male with pancreatic necrosis. Contrast-enhanced CT shows no
enhancement of the parenchyma in the pancreatic body and tail (arrow).
Page 16 of 35
Fig. 4: A 59 year-old man with necrotic pancreatitis. A-B: Delayed phase images of
contrast-enhanced CT show poorly enhanced lesions in the body and tail of the pancreas.
C: T2-weighted MR image shows hyperintense lesions in the body and the tail of the
pancreas. D: Fat-saturated T1-weighted MR image shows hyperintense lesions at the
corresponding areas seen in C, indicating the presence of contents of hemorrhage.
Page 17 of 35
Fig. 5: A 93 year-old female with pancreatic abscess. Contrast-enhanced CT shows the
fluid collection in the pancreas tail, containing air bubbles (arrow). Inflammatory change
in the surrounding fat tissue and wall thickening of the transverse colon are also seen
(arrowhead).
Page 18 of 35
Fig. 6: Pancreatic juice leakage seen in a 74 year-old woman with severe AP. A-D:
Contrast-enhanced CT shows a diffusely enlarged pancreas, in consistent with findings
of AP. In the parenchyma of the pancreatic body, a fluid collection is found (arrows). Note
the discontinuity of the main pancreatic duct (arrowhead), indicating the pancreatic duct
disconnection and leakage of the pancreatic juice.
Page 19 of 35
Fig. 7: Phlegmon seen in a 73 year-old man with severe AP. A-B: The early phase images
of contrast-enhanced CT show a poorly enhanced mass in front of the pancreatic body
and tail.
Page 20 of 35
Fig. 8: Portal vein thrombosis seen in a 48 year-old male with AP. Contrast-enhanced CT
(A: axial, B: coronal) shows the diffuse glandular enlargement with inflammatory changes
in the surrounding fat. Thrombosis is seen in the main portal vein (arrow).
Page 21 of 35
Fig. 9: A 62 year-old man with pseudocyst-portal vein fistula and focal fatty changes
in the liver. A-B: Contrast-enhanced CT shows a pseudocyst in the pancreatic head
(arrow). The low-attenuation foci which are similar to cystic contents is shown in the main
trunk and its branches of the portal vein and superior mesenteric vein (arrowheads). C:
MRCP shows a pseudocyst (arrow) communicating with the portal vein. D: Contrastenhanced CT shows multiple hypoattenuating lesions in the caudate lobe and the left
lateral segment (arrowheads), which were subsequently demonstrated the fatty changes
on the chemical shift imaging on MRI (not shown).
Page 22 of 35
Fig. 10: A 55 year-old man with a pseudoaneurysm within a pseudocyst. A: Contrastenhanced CT shows a pseudocyst in the pancreatic head (arrow). An enhancing
structure within the pseudocyst is detected, indicating a pseudoaneurysm of the dorsal
pancreatic artery (arrowhead). B: Angiogram of the superior mesenteric artery reveals the
pseudoaneurysm (arrow). C: Angiogram performed subsequently after embolising the
pseudoaneurysm using microcoils shows disappearance of the pseudoaneurysm. Note
the replaced right hepatic artery is present.
Page 23 of 35
Fig. 11: Double pseudoaneurysms seen in a 74 year-old woman with AP (The same case
presented in Fig. 6). A: Contrast-enhanced CT shows the two pseudoaneurysms in the
accessory left hepatic artery from the left gastric artery (arrows). B: Angiogram of the left
gastric artery reveals the pseudoaneurysms of the accessory left hepatic artery (arrows).
C: She underwent embolization using metallic coils and NBCA via the left gastric artery.
On arteriogram after the TAE, the pseudoaneurysms are not depicted (C).
Page 24 of 35
Fig. 12: Ruptured pseudoaneurysm seen in a 61 year-old man with acute exacerbation
of chronic pancreatitis. He suddenly developed hematemesis. A and B: On axial and
coronal images of contrast-enhanced CT show a cystic mass at the anterior portion of the
pancreatic tail protruding in the greater curvature of the gastric wall. Diffuse calcification is
found in pancreas, indicating a typical findings of the chronic pancreatitis (yellow arrows).
Note the attenuation of the content of the cystic mass is increased, and a small contrast
extravasation is shown at the periphery of the mass. C: The celiac angiography shows
a pseudoaneurysm in the short gastric artery (yellow arrowhead) and extravasation (red
arrowheads). D: He underwent embolization using metallic coils and NBCA. On splenic
arteriogram after the TAE shows disappearance of the pseudoaneurysm.
Page 25 of 35
Fig. 13: A 67 year-old man with hemosuccus pancreaticus developed with melena. A:
Contrast-enhanced CT shows a pseudoaneurysm (arrow) and pseudocyst (arrowhead)
in the pancreas body. B: Angiogram of the dorsal pancreatic artery shows the
pseudoaneurysm (arrow) and the main pancreatic duct (B: arrowhead). C: Angiogram
performed subsequently after embolising the pseudoaneurysm with microcoils shows
disappearance of the pseudoaneurysm. Note the main pancreatic duct is also not
visualized.
Page 26 of 35
Fig. 14: Cholangitis seen in a 41 year-old man with AP. A-B: Axial and coronal
images in the early phase of contrast-enhanced CT. The common bile duct is diffusely
thickened and enhanced. Note the fluid collection surrounding the bile duct within the
hepatoduodenal ligament, indicating the inflammatory process from the pancreatitis in
the pancreatic body and tail.
Page 27 of 35
Fig. 15: A 53 year-old man with hepatosplenic infarcts. After necrotomy for the severe AP.
Early (A) and delayed (B) phase images of contrast-enhanced CT show the unenhanced
areas in the caudate lobe and the spleen, indicating infarcts.
Page 28 of 35
Fig. 16: Abnormal adrenal enhancement seen in patients with AP. A: Abnormal
enhancement in the early phase of contrast-enhanced CT seen in a 71 year-old woman
with severe AP. Intense enhancement is seen in the swollen left adrenal gland, which is
reported an indicator of the adrenal gland dysfunction. B: Abnormal enhancement in the
early phase of contrast-enhanced CT seen in another case of a 71 year-old woman on
the 5th day of severe AP. The periphery of the left adrenal gland is weakly enhanced and
the adrenal parenchyma is poor enhanced, which may indicate the decreased function
of the adrenal gland.
Page 29 of 35
Fig. 17: Photographs of skin complications of AP. A: Grey-Turner's sign. B: Cullen's sign.
Page 30 of 35
Fig. 18: Skin complications in a 52 year-old man with AP. A: Grey-Turner's sign. B:
Cullen's sign. C: Fox's sign.
Page 31 of 35
Fig. 19: Massive pancreatic pleural effusion seen in a 54 year-old man with severe AP.
The left thoracic cavity is filled with the massive pleural effusion. Note the atelectasis of
the left lower lung.
Page 32 of 35
Fig. 20: Mediastinal extension seen in a 54 year-old man with severe AP (The same case
presented in Fig. 19). A-D: Contrast-enhanced CT shows the extension of the pseudocyst
into the lower portion of the middle mediastinal space from the perigastric space.
Page 33 of 35
Conclusion
CT plays an important role in diagnosis, follow-up, treatment policy making and
prognostic value in patients with complications in AP.
Personal information
References
1.
Guo JW, Chun FG, Dong W, et al. Acute pancreatitis: Etiology and common
pathogenesis. World J Gastroenterol 2009; 15(12): 1427-30.
2.
Klar E, Messmer K, Warshaw AL, et al. Pancreatic ischaemia in
experimental acute pancreatitis: mechanism, significance and therapy. Br J
Surg 1990; 77(11): 1205-10.
3.
Marshall JB. Acute pancreatitis. A review with an emphasis on new
developments. Arch Intern Med 1993; 153(10): 1185-98.
4.
Forsmark CE. Pancreatitis. In: Goldman L, Schafer AI, eds. Cecil Medicine.
24th ed. Philadelphia, Pa: Saunders Elsevier 2011; chap 146.
5.
Banks PA1, Bollen TL, Dervenis C, et al. Classification of acute
pancreatitis--2012: revision of the Atlanta classification and definitions by
international consensus. Gut. january/2013; 62: 102-11.
6.
Stanley T Lau, Erik JS, Richard AK, et al. A pancreatic ductal leak should
be sought to direct treatment in patients with acute pancreatitis. Am J Surg
2001; 181(5): 411-15.
7.
Kryvoruchko IA, Honcharova NM, Adreieshchev SA. Pancreatic pseudocysts:
diagnosis and treatment. Klin Khir 2014; 2: 67-72.
8.
Hunter TB, Haber K, Pond GD. Phlegmon of the pancreas. Am J Gastroenterol
1982; 77(12): 949-52.
9.
Hollingshead M, Burke C, Mauro M, et al. Transcatheter thrombolytic
therapy for acute mesenteric and portal vein thrombosis. J Vasc Interv
Radiol 2005; 16: 651-61.
10. Ng TS, Rochefort H, Czaplicki C, et al. Massive pancreatic pseudocyst
with portal vein fistula: Case report and proposed treatment algorithm.
Pancreatology 2014 Nov 28.
11. Potts JR 3rd. Pancreatic-portal vein fistula with disseminated fat necrosis
treated by pancreaticoduodenectomy. South Med J. 1991 May; 84(5): 632-5.
12. Harvey J, Dardik H, Impeduglia T, et al. Endovascular management of hepatic
artery pseudoaneurysm hemorrhage complicating pancreaticoduodenectomy.
J Vasc Surg 2006; 43(3): 613-7.
Page 34 of 35
13. Koren M, Kinova S, Bedeova J, et al. Case report and review: Hemosuccus
pancreaticus. Bratisl Lek Listy 2008; 109(1): 37-41.
14. Kimura Y, Takada T, Kawarada Y, et al. Definitions, pathophysiology, and
epidemiology of acute cholangitis and cholecystitis: Tokyo Guidelines. J
Hepatobiliary Pancreat Surg 2007; 14(1): 15-26.
15. Mortelé KJ, Mergo PJ, Taylor HM, et al. Splenic and perisplenic involvement
in acute pancreatitis: determination of prevalence and morphologic helical CT
features. J Comput Assist Tomogr 2001; 25(1): 50-4.
16. Arenal Vera JJ, Said A, Guerro JA, et al. Splenic infarction secondary to
acute pancreatitis. Rev Esp Enferm Dig 2008; 100(5): 300-3.
17. Masahiro M, Akira Y, Yasuhiro K, et al. Hepatic infarction complicated with
acute pancreatitis precisely diagnosed with gadoxetate disodium-enhanced
magnetic resonance imaging. Intern Med 2014; 53: 2215-21.
18. Bollen TL, van Santvoort HC, Besselink MG, et al. Intense adrenal
enhancement in patients with acute pancreatitis and early organ failure.
Emerg Radiol 2007; 14(5): 317-22.
19. Farman J, Morehouse H, Amis ES Jr, et al. CT of pancreatitis with renal and
juxtarenal manifestations. Clin Imaging 1997; 21(3): 183-8.
20. Liu Z, Yan Z, Min P, et al. Gastric bare area and left adrenal gland
involvement on abdominal computed tomography and their prognostic value
in acute pancreatitis. Eur Radiol 2008; 18(8): 1611-6.
21. Berm J, Bradley EL 3rd. Subcutaneous manifestations of severe acute
pancreatitis. Pancreas 1998; 16(4): 551-55.
22. George WB, Pitchumoni CS. Pathophysiology of pulmonary complications of
acute pancreatitis. World J Gastroenterol 2006; 12(44): 7087-96.
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