Multi‐modality Imaging in
Acute Pancreatitis
Marsha Lynch, HMS III
Gillian Lieberman, MD
BIDMC Core Clerkship in Radiology
March 2009
Our Patient R: Introduction
¾52M with 10d history of nausea, vomiting and
abdominal pain.
Patient R: Initial Presentation
PRESENTATION
• WBC 19.1
• ARF: Cr 3.2 (baseline 1.2)
• BG: 235
• Lipase: 2211(0‐60)
• Amylase: 804 (0‐100)
• ALT:10 AST:9 AP:79
• Ca: 7.9 (8.4‐10.2)
• TGs: 511 (0‐149)
PMH
• HTN
• Hyperlipidemia
• Congenital deafness
• Gout
• Obesity
Patient R demonstrates a typical
presentation of acute
pancreatitis
Acute Pancreatitis: Pathophysiology
INFLAMMATION OF THE PANCREAS
• Inappropriate activation of pancreatic enzymes
• Intraparenchymal
and extraparenchymal
extravasation
of enzymes cause autodigestion
of pancreatic
parenchyma and damage to peripancreatic
tissues and
vascular network
• Inflammatory response to this injury out of proportion
to that of other organs to a similar insult
• Inflammatory response causes further damage
– Fluid sequestration, fat necrosis, vasculitis
leading to
occlusions and thrombosis, hemorrhage
Whitcomb, D C, Acute Pancreatitis. N Engl J Med 2006
Balthazar, E J, Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation. Radiology 2002
Acute Pancreatitis: Etiologies
Etiologies of Acute Pancreatitis
Mechanical Gallstones (>45%) , sludge, pancreatic mass, ampullary
stenosis
or
mass ,duodenal stricture or obstruction
Toxic Alcohol (>35%), methanol, steroids/ drugs, scorpion venom
Metabolic Hyperlipidemia, hypertriglyceridemia, hypercalcemia
Trauma Blunt or penetrating, ERCP, s/p
abdominal surgery
Infection Viral (mumps), parasitic, bacterial
Vascular Ischemia, embolism, vasculitis
Congenital Pancreas divisum
Genetic CFTR mutation
Miscellaneous Autoimmune, renal transplant, alpha‐1‐anti‐trypsin deficiency
Adapted from “etiology of acute pancreatitis”; Up-To-Date
Acute Pancreatitis: Epidemiology
• >200,000 US hospital
admission yearly
• 20% have a severe
course
– Associated with systemic
and local complications
and increased mortality
(10‐30%)
• Severe Course
¾ SYSTEMIC
COMPLICATIONS
• Shock
• DIC
• Pulm. Insufficiency/ARDS
¾ LOCAL COMPLICATIONS
• Necrosis
• Abscess
• Pseudocyst
• Pseudoaneurysm
• Splenic
vein thrombosis
Acute Pancreatitis: Severity
Assessment
Severity of acute pancreatitis is commonly assessed using :
1.
Ranson’s Criteria
– 5 clinical signs at presentation and 6 at 48hrs
– ≥
3 associated with severe course (systemic complications and/or
pancreatic necrosis)
2.
APACHE II
– 12 routine physiologic measurement, age and previous health status
– ≥
8 associated with severe course
3.
CT Severity Index (CTSI)
– Based on extent of inflammation and presence of complications on
CT scan.
Let’s briefly review the anatomy
of the pancreas
Pancreas Anatomy
Retroperitoneal organ stretching from
the curvature of the duodenum to the
spleen. Rich arterial supply from
vessels off the celiac artery superiorly
and the SMA inferiorly. Glandular
tissue with both endocrine and
exocrine function.
http://www.fairview.org/healthlibrary/content/pancreas.gif
Pancreas Anatomy: Axial CT View
Image from: PACS, BIDMC
pancreas pancreas
Companion Patient 1: Delayed Phase Axial CT
Acute Pancreatitis
CLINICAL DIAGNOSIS
• Abdominal pain
• Nausea/Vomiting
• Elevated Pancreatic
Enzymes
MANAGEMENT
• Bowel Rest/NPO
• IVF
• Analgesics
http://www.fairview.org/healthlibrary/content/pancreas.gif
The diagnosis of pancreatitis is largely a
clinical one based on physical signs and
symptoms as well as serum levels of
pancreatic enzymes.
What then is the role of Radiology in its
management?
Role of Radiology in Acute Pancreatitis
• Rule out other intra‐abdominal conditions as
cause of abdominal pain or other symptoms
– Bowel obstruction, infarction or perforation; acute cholecystitis;
appendicitis
• Confirm diagnosis and Identify causes (e.g.
gallstones)
• Evaluate and stage local pancreatic morphology
• Identify and manage complications
• Menu of Tests: US, Plain Film, CT, MR
Back to Our Patient R
Patient R: Ranson’s
Criteria
¾ Ranson’s Score ≥ 3 (Threshold)
• At Presentation
– Age > 55
– BG > 200
– WBC > 16,000
– LDH > 350
– ALT > 250
• Within 48 Hours
– Hct
> 10% decrease
– Serum Ca < 8
– Base Def > 4
– BUN > 5 increase
– Fluid Sequestration > 6L
– PaO2
< 60
¾ PATIENT X PRESENTATION
– WBC 19.1
– BG 235
– Age 52
– ALT 10
– LDH 15
We are less concerned about our patient
progressing down an more severe path based
on him having only 2/5 Ranson’s criteria at
presentation.
However, we can use radiology to assess
whether his acute pancreatitis is due to one
of the commonest etiologies: gallstones.
We therefore proceed to abdominal
Ultrasound…
Use of Abdominal Ultrasound in
Acute Pancreatitis
Indicated early in acute pancreatitis
¾ Pros
– Inexpensive
– Excellent for identifying gallbladder pathology, sludge and gallstones
(Most common cause of pancreatitis!)
– Evaluate bile‐duct dilation
– May visualize masses and
follow up of pseudocyst
¾ Cons
– Not optimal for pancreas; retroperitoneal location easily obscured by
bowel gas distension
– Less sensitive for stones in distal CBD
– Limited in early assessment of pancreatitis
Balthazar, E J, Acute Pancreatitis: Assessment of Severity with Clinical and CT Evaluation. Radiology 2002
Patient R Abdominal US: Liver,GB
Image from: PACS, BIDMC
Gallbladder:
anechoic cystic
region with
increased through-
transmission
Liver parenchyma: no gross
intra-hepatic ductal dilitation
Abdominal Ultrasound: RUQ
Patient R Abdominal US: GB
Image from: PACS, BIDMC
Absence of
hyperechoic foci
Non-distended GB with
normal wall thickness
No signs of acute cholecyctitis: lack of gallbladder wall
thickening, pericholecystic fluid or cholelithiasis
Abdominal Ultrasound: RUQ
Happily, our suspicion of gallbladder
pathology as the cause of our patient R’s
acute pancreatitis is now greatly lowered.
So we continue supportive
management with bowel rest, IVF
and analgesics.
On Hospital Day 5…
…our Patient R develops bowel
distension and abdominal pain.
We proceed immediately to
Abdominal Plain Film
Use of Abdominal Plain Film in
Acute Pancreatitis
¾ Pros
– Screen
for/exclude separate or accompanying abdominal process
• Signs of peritonitis or bowel ischemia
– Free air
• Bowel Obstruction
• Ascites
– Inexpensive, readily available and fast
¾ Cons
– Poor visualization of the pancreas and retroperitoneum
• May see calcifications due to chronic process
Patient R:
Abdominal
Plain Film
HD 5
Image from: PACS, BIDMC
residual contrast in asc.
and desc. colon
----- isolated segments of
dilated sm. bowel, up to
3cm luminal diameter
Transverse colon shows no
marked distention but with
no contrast
Abdominal Plain Film: Supine
spasm of the desc.
colon just distal to splenic
flexure
Patient R
Abdominal
Plain Film
HD 5
Image from: PACS, BIDMCAbdominal Plain Film: L Lat Decubitus
Air fluid levels
The presence of distension in the along with
air‐fluid levels concern us for small bowel
obstruction. We decide to closely follow our
patient.
On Hospital Day 6…
Our patient has worsening
abdominal pain and distension. We
quickly perform a repeat abdominal
plain film.
Patient X
Abdominal
Plain Film
HD 6
3.3 cm
8.5 cm
Distended stomach
Increased focal
distension of
small bowel
Abdominal Plain Film: Supine Image from: PACS, BIDMC
Marked distension of
transverse colon, still
with no contrast in
lumen.
arrest of contrast (2 days)
We are certainly more concerned about
obstruction now. Before we continue, let’s
review some possible causes of obstruction in
this patient.
Possible Causes of Bowel
Obstruction in Our Patient R
• Functional
– Focal ileus/Sentinel loops (Transverse colon and
segments of small bowel) due to adjacent
pancreatic inflammatory process
• Mechanical
– Pancreatic mass
• Developing fluid collections or pseudocyst
• GB unseen on U/S
We are more concerned about yet unseen
causes of any mechanical obstruction.
We now proceed to Abdominal CT to further
evaluate the cause of the increasing
abdominal distension and to have a better
look at the inflamed pancreas.
Use of Abdominal CT in Acute
Pancreatitis
¾ Pros
– Readily available and Fast
– Aid in diagnosis and staging of pancreatitis
– Depict,
quantify pancreatic
parenchymal
injury
• Ability to assess the presence or absence of:
– Edema (focal or diffuse)
– Peripancreatic
fluid and inflammation
– Fluid collections
– Pseudocysts
– Necrosis
– Evaluate common bile duct for stones or other obstructions
¾ Cons
– Our Patient R is in ARF and this may be exacerbated by IV contrast
administration
Patient R Delayed‐Phase axial CT:
Supra‐pancreatic fluid collection
Image from: PACS, BIDMC
4x7cm fluid
collection just
superior to
the pancreas
Delayed Phase CT: Axial
Normal vs. Acute Pancreatitis
Images from: PACS, BIDMC
Acute pancreatitis: swollen, edematous gland with
indistinct edges blurred into those of surrounding
structures
Axial Delayed Phase CT: Companion Pt. 1 Axial Delayed Phase CT: Patient R
Normal pancreas: Fluffy, macronodular gland
texture distinct from surrounding organs
Patient R: Abdominal CT ‐
peripancreatic
fat stranding and
patent splenic
vein
peripancreatic fat stranding
patent splenic vein
Axial Delayed Phase CT: Patient RAxial Delayed Phase CT: Patient R
Images from: PACS, BIDMC
Patient R Abdominal CT: Focal
Transverse Ileus
and Arrest of
Contrast
arrest of contrast
adynamic transverse colon
Axial Delayed Phase CT: Patient RAxial Delayed Phase CT: Patient R
Images from: PACS, BIDMC
Patient R Abdominal CT:
Suspicious hyperattenuating
lesion
There is a round
hyperdensity
measuring 1.4cm with
similar attenuation as
the adjacent aorta.
We can also visualize
the IVC posterior and
the GDA adjacent
and just superior to
the lesion.
This could represent:
1.Pseudoaneurysm of
GDA
2.Gallstone
3.Reactive lymph
node.
Image from: PACS, BIDMCDelayed Phase CT: Axial
What Now???
We need to further explore this lesion as our
last study was limited by the lack of both a
non‐contrast and arterial phase.
Luckily, we have another tool in our arsenal.
Use of MR in Acute Pancreatitis
Increasingly used in diagnosis and management of acute pancreatitis
¾ Pros
– Non‐invasive and no use of IV contrast
– Ability to better characterize fluid collections (acute collection vs.
abscess, necrosis, hemorrhage, pseudocyst)
– Ability to delineate pancreatic and bile ducts (detect
choledocholithiasis
missed on U/S ) and other complications
comparable to ERCP
– Greater sensitivity vs. CT in detecting mild pancreatitis
¾ Cons
– Expensive and in many less severe cases not necessary for diagnosis
and management
– Less readily available in non‐tertiary medical centers
Patient R: Abdominal MR
Image from: PACS, BIDMCT2 MRI: flow-void sequence
Our lesion has
high signal
distinct from the
absence of signal
(flow-void
sequence) in the
other three
vessels of
interest: GDA,
IVC and aorta.
In particular, the
lesion is distinct
from the GDA,
significantly
reducing our
suspicion for
pseudoaneurysm.
Patient R: High signal lesion on MR
In this sequence,
gallstones would
demonstrate no
signal and our
lesion is
consistent with a
reactive lymph
node.
Image from: PACS, BIDMCT2 MRI: flow-void sequence
Patient R: Comparison of CT versus
MRI findings
The suspicious lesion on CT was further evaluated on MR and found to
be benign consistent with a reactive lymph nose Images from: PACS, BIDMC
T2 MR: flow-void sequenceDelayed Phase CT: Axial
A word about Pleural Effusions…
Pleural Effusions: a common
complication of Acute Pancreatitis
Approx. 1/3 patients with acute pancreatitis will have will
have abnormal CXRs. The typical findings include
elevated hemidiaphragm, pleural effusions, atelectasis and
in more severe cases ARDS
Patient R: Delayed Phase CT Low lung volumes,
Bibasilar atelectasis and
pleural effusions
Images from: PACS,
BIDMC
Patient R: Frontal CXR
Patient R: Lateral CXR
Patient R: Remaining Course
• HD 6
– Emesis and large BM that largely relieved abdominal pain
• Started on TPN
– Diet slowly advanced until tolerated regular diet
• Continued on supportive measures as labs
normalized and symptoms resolved
• Discharged to Home on HD 16
Patient R Remaining Course cont’d
PRESENTATION
• WBC 19.1
• ARF: Cr 3.2 (baseline 1.0)
• BG: 235
• Lipase: 2211(0‐60)
• Amylase: 804 (0‐100)
• ALT:10 (0‐40)
• AST:9 (0‐40)
• AP:79 (39‐117)
• Ca: 7.9 (8.4‐10.2)
• TGs: 511 (0‐149)
DISCHARGE
• WBC 7.4
• Cr 0.9
• BG: 95
• Lipase: 59*(0‐60)
• Amylase: 50* (0‐100)
• ALT:18
• AST:29
• AP:79*
• Ca: 8.7 (8.4‐10.2)
• TGs: 112 (0‐149)
* Last labs drawn before date of discharge
Summary
• Acute Pancreatitis is a common illness with
many potential highly morbid complications.
• Many cases are diagnosed clinically and
managed supportively with bowel rest,
aggressive fluid administrations and analgesics.
• Radiology plays important role in confirming
diagnoses, evaluating severity and identifying
and managing complications of acute
pancreatitis.
References
• Whitcomb, D C, Acute Pancreatitis. N Engl
J Med
2006;354:2142‐50.
• Balthazar, E J, Acute Pancreatitis: Assessment of
Severity with Clinical and CT Evaluation. Radiology
2002; 223:603–
613
• Textbook of Gastrointestinal Radiology /
[edited by] Richard M. Gore, Marc S. Levine.
London : W. B. Saunders Co., c2000.
• Up-To-Date, ‘Clinical manifestations and
diagnosis of acute pancreatitis’, ‘etiologies of
acute pancreatitis’
Acknowledgements
• Ernest Yeh, MD
• Maria Levantakis, Course Co‐ordinator
• Gillian Lieberman, MD
Multi-modality Imaging in �Acute Pancreatitis
Our Patient R: Introduction�
Patient R: Initial Presentation
Patient R demonstrates a typical presentation of acute pancreatitis
Acute Pancreatitis: Pathophysiology
Acute Pancreatitis: Etiologies
Acute Pancreatitis: Epidemiology
Acute Pancreatitis: Severity Assessment
Let’s briefly review the anatomy of the pancreas
Pancreas Anatomy
Pancreas Anatomy: Axial CT View
Acute Pancreatitis
The diagnosis of pancreatitis is largely a clinical one based on physical signs and symptoms as well as serum levels of pancreatic enzymes. ��What then is the role of Radiology in its management?
Role of Radiology in Acute Pancreatitis
Back to Our Patient R
Patient R: Ranson’s Criteria
We are less concerned about our patient progressing down an more severe path based on him having only 2/5 Ranson’s criteria at presentation.
However, we can use radiology to assess whether his acute pancreatitis is due to one of the commonest etiologies: gallstones.
Use of Abdominal Ultrasound in Acute Pancreatitis
Patient R Abdominal US: Liver,GB
Patient R Abdominal US: GB
Happily, our suspicion of gallbladder pathology as the cause of our patient R’s acute pancreatitis is now greatly lowered.
On Hospital Day 5…
Use of Abdominal Plain Film in Acute Pancreatitis
Patient R: Abdominal �Plain Film�HD 5
Patient R Abdominal Plain Film�HD 5
The presence of distension in the along with air-fluid levels concern us for small bowel obstruction. We decide to closely follow our patient.
On Hospital Day 6…
Slide Number 29
We are certainly more concerned about obstruction now. Before we continue, let’s review some possible causes of obstruction in this patient.
Possible Causes of Bowel Obstruction in Our Patient R
We are more concerned about yet unseen causes of any mechanical obstruction. �We now proceed to Abdominal CT to further evaluate the cause of the increasing abdominal distension and to have a better look at the inflamed pancreas.
Use of Abdominal CT in Acute Pancreatitis
Patient R Delayed-Phase axial CT: Supra-pancreatic fluid collection
Normal vs. Acute Pancreatitis
Patient R: Abdominal CT - peripancreatic fat stranding and patent splenic vein
Patient R Abdominal CT: Focal Transverse Ileus and Arrest of Contrast
Patient R Abdominal CT: �Suspicious hyperattenuating lesion
What Now???�We need to further explore this lesion as our last study was limited by the lack of both a non-contrast and arterial phase.�Luckily, we have another tool in our arsenal.
Use of MR in Acute Pancreatitis
Patient R: Abdominal MR
Patient R: High signal lesion on MR
Patient R: Comparison of CT versus MRI findings
A word about Pleural Effusions…
Pleural Effusions: a common complication of Acute Pancreatitis
Patient R: Remaining Course
Patient R Remaining Course cont’d
Summary
References
Acknowledgements