Nambi
Nallasamy, HMS III
Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
Bob is a 39 yo
M with a h/o:
chronic pancreatitis
s/p
distal pancreatectomy
&
splenectomy
pancreatic pseudocyst
past EtOH
abuse
HTN, DM, and hypercholesterolemia
He presented to the ED with:
new back pain, confusion, fatigue, weakness, abd
discomfort, and fever
Extensive past EtOH
use (started drinking in 7th
grade, 30 beers/night in his 20s)
Has been abstinent since 2001 per his record
Alcoholic pancreatitis, s/p
distal pancreatectomy
10 yrs ago
ARDS with hx
tracheostomy
Splenic
hematoma splenectomy
Chronic abd
pain since splenectomy, on methadone
and oxycodone
Portal vein thrombosis with partial occlusion
Asthma
Depression
Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
Alcohol abuse
Cigarette smoking
Hereditary Pancreatitis (AD, 80%
penetrance)
Onset before 20, often before 5
Ductal
obstruction
Strictures 2/2 trauma, pseudocysts, calcific
stones, or tumors
Tropical pancreatitis (possible SPINK1
mutation relation)
CF gene mutation
Chronic inflammation of the pancreas leads to:
Destruction of pancreatic acini
fibrosis
Pancreatic duct dilation and irregularity 2/2 formation
of intraductal
protein plugs and calcifications
▪
Protein plugs serve as nidus
for calcification within inter‐
and
intra‐lobular ducts
▪
Ductal
epithelial lesions result scarring and obstruction of
ducts inflammatory changes and cell loss
▪
Protein plugs consist primarily of GP2, a glycosyl
phsphatidylinositol
anchored protein that is cleaved from the
zymogen
granule membrane and secreted into pancreatic
juice
Abdominal pain
Typically epigastric, radiating to the back
Worse 15‐30 minutes after eating
May become continuous as course progresses
Pacreatic
insufficiency
Fat malabsorption
Diabetes
Normal serum amylase and lipase
concentrations
ERCP
Dilated, beaded, and tortuous pancreatic duct
Abd
Plain Film
Punctate
calcific
densities scattered throughout pancreas
Abd
CT
Punctate
calcifications throughout pancreas (found in 30‐60%
of pts)
MRI
Irregularity of the pancreatic duct
Atrophic pancreas
MRCP
Tortuosity
of the pancreatic duct
Irregularity in caliber of the pancreatic duct
Note the punctatepunctate
calcifications calcifications throughout the
pancreas
Axial C‐
Abd
CT
Lieberman’s eRadiology
http://eradiology.bidmc.harvard.edu
Bob’s abdominal CT does not
demonstrate the punctate
calcifications commonly seen in
chronic pancreatitis
It does, however demonstrate
a different findingdifferent finding, which shall
be discussed later
Axial C‐
Abd
CT
BIDMC PACS
Pancreatic pseudocyst
formation
Renal cyst formation
Bile duct or duodenal obstruction
Pancreatic ascites
or pleural effusion
Splenic
vein thrombosis
Pseudoaneurysms
US
Anechoic fluid collection within the head of the
pancreas with enhanced through transmission
Abd
CT
Homogeneous fluid density collection in the head
of the pancreas
Collection does not enhance with contrast
MRI
Homogeneous water intensity mass
Area of decreased attenuation
corresponding to pancreatic pancreatic
pseudocystpseudocyst
on non‐contrast CT
No evidence of intracystic
hemorrhage
Axial C‐
Abd
CT
BIDMC PACS
Area of increased attenuation
corresponding to pancreatic pancreatic
pseudocystpseudocyst
that does not
enhance with contrast.
No air pockets seen to indicate
infection of the pseudocyst.
Axial C+ Abd
CT
BIDMC PACS
Pseudocyst
Abscess
True cyst
Benign cystic neoplasm
Malignant primary cystic neoplasm
Liver metastasis
Pseudocyst
vs. True Cyst:
Pseudocyst
is technically not a cyst – the wall consists of
granulation and/or fibrous tissue (2/2 inflammation)
Pancreatic pseudocyst
results from passage of inflammatory
fluid into the omental
bursa
True cyst has a wall that consists of a clearly defined epithelial
cell layer
Renal Cyst Renal Cyst (likely 2/2 chronic
pancreatitis) measuring 42.17
mm in diameter.
Sagittal
FRFSE T2‐Weighted L‐
Spine MRI
(FRFSE, FR‐FSE) Fast
Relaxation Fast
Spin Echo
sequence
provides high
signal
intensity
of fluids, even with
short TR.
BIDMC PACS
Acute on Chronic Pancreatitis
Acute cholecystitis
Muscle strain
Pyomyositis
Myonecrosis
Perforated duodenal ulcer
Bowel obstruction
Bowel infarction
Aortic dissection
Renal Colic
Appendicitis
Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
Elevated LFTs, AST > ALT (787 : 285)
Indicative of acute pancreatitis 2/2 EtOH
use
Points to relapse of EtOH
use, which patient
denies
CK > 22,000
Leukocytosis
Concern for epidural abscess given urinary
retention, intermittent complaints of saddle
anesthesia
Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidemia
Drugs (azothioprine, diuretics)
Sensitization of acinar
cells to CCK‐induced
premature activation of zymogens
Potentiation
of the effect of CCK on the
activation of transcription factors, NF‐kappa B
and activating protein‐1
Generation of toxic metabolites such as
acetaldehyde and fatty acid ethyl esters
Activation of pancreatic stellate
cells by
acetaldehyde and oxidative stress increased
production of collagen and other matrix proteins
RUQ Abdominal pain
Can last for days
Can occur 1‐3 days after an alcohol binge
Fever
Tachycardia
Elevated serum amylase
Rises within 6‐12 hours of onset
Often elevated for 3‐5 days
First serum amylase in this patient obtained 3 days
after admission and was normal
Abd
Plain Film
“splenic
cut off sign”
–
paucity of air in the colon distal to the
splenic
flexure due to functional spasm of the descending colon
2/2 spread of pancreatic inflammation to the area
Sentinel loop in LUQ
Abd
CT
Edema of pancreas
Fat stranding surrounding the pancreas
Fluid collection(s) within pancreas
Gas in the pancreas or retroperitoneum
MRI
Offers ability to delineate fluid collections as acute, necrotic,
abscess, hemorrhage, or pseudocyst
Focal fluid collections and ascites
Pseudocyst
formation
Pancreatic abscess
Pancreatic necrosis
Peripancreatic
hemorrhage
Biliary
obstruction
Pseudoaneurysm
formation
Portal Vein Thrombosis
Abberant
Air
Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
Non‐enhancing region within
portal vein on CT indicating
likely portal vein thrombosisportal vein thrombosis
Axial C+ Abd
CT
BIDMC PACS
Acute on Chronic Pancreatitis
Acute cholecystitis
Muscle strain
Pyomyositis
Myonecrosis
Perforated duodenal ulcer
Bowel obstruction
Bowel infarction
Aortic dissection
Renal Colic
Appendicitis
DessicationDessication
of the L4‐L5
intervertebral
disc
Sagittal
L‐Spine T1‐weighted
MRI
BIDMC PACS
Increased signal seen in the
multfidusmultfidus
and quadratusquadratus
lumborumlumborum
muscles
Axial T2‐Weighted L‐Spine MRI
BIDMC PACS
Increased signal seen in the
multfidusmultfidus
and quadratusquadratus
lumborumlumborum
muscles
Axial T1‐Weighted MRI with
Post‐Processing
BIDMC PACS
EdemaEdema
of paraspinal
musculature extending from
T12 to L4/5.
Dependent edema Dependent edema in deep
dorsal subcutaneous soft
tissues – can be seen in supine
patients
Sagittal
STIR (Short Tau
Inversion Recovery) L Spine
MRI
BIDMC PACS
Reason for study:
Evaluation for epidural abscess, pyomyositis, myonecrosis, discitis, vertebral
osteomyelitis
Reason for IV contrast:
To evaluate for enhancing abscess walls, hypervascular
masses, hyperemia
Findings:
Increased STIR signal within R paraspinal
musculature
With contrast, patchy enhancement of R multifidus, longissimus, and
quadratus
luborum
muscles
Normal signal within bone
Normal vertebral body height, signal and sagittal
alignment
Impression:
No evidence of osteomyelitis, discitis, septic arthritis, or epidural abscess
No drainable fluid collection
Findings indicate myonecrosis
vs. pyomyositis
without frank abscess
formation
Our Patient
Imaging Chronic Pancreatitis
Lab Findings
Imaging Acute Pancreatitis
Imaging of Our Patient
Putting it all Together
Acute‐onset damage of the right paraspinal
muscle
(indicated by elevated CK at admission) with subsequent
dramatic symptomatic improvement and normalization of
CK
Abn
signal in paraspinal
muscles on MR concerning for
pyomyositis
vs. myonecrosis
No fluid collections or abscess formation seen
Initially treated empirically with abx, but clinical course pointed
away from infection
No evidence of inflammatory myositis
per Rheumatology
Possibile
etiologies of his myonecrosis:
Myonecrosis
in setting of diabetes
Rhabomyolysis
in setting of pramipexole
use
Trauma
Epidemiology
Usually affects patients with long‐standing poorly controlled DM with pre‐
existing microvascular
complications (e.g. retinopathy, nephropathy, or
neuropathy)
Lab Findings
Elevated CK
Can be accompanied by leukocytosis
(35%)
MRI Features
High intensity of the involved muscle (on T2‐weighted sequences)
Subcutaneous edema
DDx
Pyomyositis
(S. aureus)
Spontaneous gangrenous myositis
(Strep)
Clostridial
myonecrosis
DVT
Intramuscular hematoma
Neoplasm
This patient is a particularly poor historian.
Even when not acutely ill, is taken care of by his
mother
The patient’s past tendencies raised clinical
suspicion of EtOH
relapse given lab values
indicative of acute pancreatitis
Imaging allowed team to overcome these
limitations, and point toward myonecrosis
rather than infection
Shortened the patient’s hospital stay
Reduced antibiotic usage
Dr. Gillian Lieberman, Clerkship Director
Emily Hanson, Education Coordinator
Larry Barbaras, Webmaster
Slide Number 1
Slide Number 2
Slide Number 3
Slide Number 4
Slide Number 5
Slide Number 6
Slide Number 7
Slide Number 8
Slide Number 9
Slide Number 10
Slide Number 11
Slide Number 12
Slide Number 13
Slide Number 14
Slide Number 15
Slide Number 16
Slide Number 17
Slide Number 18
Slide Number 19
Slide Number 20
Slide Number 21
Slide Number 22
Slide Number 23
Slide Number 24
Slide Number 25
Slide Number 26
Slide Number 27
Slide Number 28
Slide Number 29
Slide Number 30
Slide Number 31
Slide Number 32
Slide Number 33
Slide Number 34
Slide Number 35
Slide Number 36
Slide Number 37
Slide Number 38
Slide Number 39