Sonography of Diffuse Liver Disease
Transcript of Sonography of Diffuse Liver Disease
Sonography of Diffuse Liver
Disease
Mitchell E. Tublin, M.D.
Professor of Radiology
Vice Chair of Clinical and Academic Affairs
Section Chief: Abdominal Imaging
University of Pittsburgh
School of Medicine
Diffuse Liver Disease
• Clinical manifestations often subtle…. or absent
• Patient history helpful….sometimes
• Pattern of LFT abnormality sometimes helpful….. but often not
Diffuse Liver Disease: Ultrasound
• US: premier modality for screening of diffuse liver disease, elevated LFTs
• Findings may be subtle, or nonspecific
• Clinical correlation, “second look sonography” improves sensitivity/specificity
• Look for changes in
– echotexture
– echogenicity
– contour
Diffuse Liver Disease: Ultrasound
• Our goals
• Discuss clinical manifestations, diagnostic clues of spectrum of diffuse liver diseases
– NAFLD (nonalcoholic fatty liver disease)
– Cirrhosis and mimics
– Hepatitis
• Describe innovative ultrasound techniques for identifying and quantifying disease
• Demonstrate practical tips…
Nonalcoholic fatty liver disease
• Fatty infiltration and inflammation common complication of ETOH abuse
• Nonalcoholic fatty liver disease (NAFLD) described in 1980
• Spectrum of metabolic fatty liver diseases
– Steatosis
– Nonalcoholic steatohepatitis (NASH)
– Cirrhosis
• Complex pathophysiology: “lipotoxicity” and oxidative stress
Nonalcoholic fatty liver disease
• Epidemiology/risk factors
– Obesity (central>>overall)
– DM type 2
– Dyslipidemia (↑ triglyc, cholesterol) → metabolic syndrome
– Surgical intervention/extensive SB resection
– Exogenous, endogenous steroids
– Medications (tamoxifen, methotrexate, HAART)
– TPN, starvation, rapid weight loss
Nonalcoholic fatty liver disease
• Obesity epidemic
• NAFLD prevalence in United States (sono, MR spectrometry, liver enzymes): 22-45%
• Histologic progression to cirrhosis: 32-37%
• Public health nightmare
NAFLD: initial assessment
• Scoring systems: clinical and biochemical markers (LFT ratios, DM, HTN, age…)
• Maybe CT, DECT, MR, MRS, MRE….
• Ultrasound still primary imaging screen
• In ideal world:
– Quantify fat
– Detect NASH
– Grade Fibrosis
Steatosis: Swollen, “ballooned” hepatocytes
NASH: steatosis and lobular inflammation. Perisinusoidal
collagen (trichrome)Brunt, Modern Pathology, 2007
NASH to Cirrhosis: 4 years
NASH to Cirrhosis:
Pre biopsy ultrasound
Fatty infiltration: ultrasound
• Grades
– “Mild”: ↑ liver echogenicity
– “Moderate”: ↑↑ echogenicity, “slightly” impaired visualization of vessels, diagphragm
– “Severe”: ↑↑↑ echogenicity, beam attenuation – obscured vessels, posterior liver, diaphragm
Mild Moderate
Severe
Fatty infiltration: ultrasound
• Issues
– Qualitative assessment, operator dependent Poor sensitivity
• Mild fatty infiltration (<30%)
• Morbid obesity
– Patchy fat
– Steatosis vs. NASH vs. early Cirrhosis
• Pearls
– Optimize TGC
– Look for sparing
Fatty infiltration: ultrasound
• Quantification attempts
– Traditional image-based analysis: hepatorenal index
– Raw radiofrequency data
• Speed of sound
• US backscatter, attenuation coefficients
• Controlled-attenuation parameter (Fibroscan)
• Shear wave dispersion
• Not ready for prime time
– Reproducibility, validation
– Fat vs. Fibrosis
Obesity
No fatty infiltration Fatty infiltration
Patchy fat
Minimal fat
62 female, HTN, dyslipidemia, obesity, ↑↑↑
AST, ALT. Sono: severe fat
BX: 80% macrovesicular steatosis, chronic
steatohepatitis, mild periportal fibrosis
Cirrhosis: Ultrasound
• End result of chronic liver injury: cell death, fibrosis, regeneration (nodules, nodules, nodules…)
• Micronodular vs macronodular: pattern often not helpful (or detected)
• Ultrasound used to screen for liver injury/fibrosis
Cirrhosis: Ultrasound features
• Volume distribution
–Early (or primary biliary) cirrhosis: large liver
–Advanced cirrhosis: small liver
–Relative enlargement of left lobe, caudate
–Posterior, medial segment atrophy
–Confluent fibrosis: capsular retraction
Small liver
Big caudatePost seg atrophy
Big lateral seg
Cirrhosis: Ultrasound features
• Coarse echotexture
– Subjective
– Beware of infiltrating tumor (HCC, metastases), bad technique, marginal equipment
• Nodular surface
– Easiest to assess when ascites present
– Lateral segment: linear probe (?)
Hepatic Kaposi sarcoma
Adenoca: unknown primary
Cirrhosis
Hepatic sarcoid
ETOH,
jaundice:
“R/O
cirrhosis”Pearl 1
• Refractive shadows
• Sound refracted by
tissues of different
acoustic impedance
• An indirect sign of
isoechoic tumor
PVP
FSE
+ PVT
Pearl 2: Capsular Nodularity in
Cirrhosis
• Present in more advanced cases
• Anterior surface: sagittal view of left
hepatic lobe
• Nodularity may be more apparent on
undersurface of the liver
PBC: Technique & Scanner Upgrade
Cirrhosis: Ultrasound features
• Secondary findings of portal HTN
–Splenomegaly
–Ascites
• Doppler
–Monophasic HV flow
–HA hypertrophy
–Hepatofugal PV flow
–Shunts
Enlarged hepatic artery &
hepatofugal left PV flowMonophasic HV flow
Cavernous
transformationGastric varices
What do these pts all have in common?
Answer: ‘4’
omental caking capsular thickening
implant omental caking
Ascites
1) Cirrhosis
2) Liver Mets
3) HCC
4) Carcinomatosis
Courtesy: Brooke Jeffrey, MD
Pearl 3: Perihepatic
Manifestations of Disease
• Don’t get tunnel vision: evaluate pleural
and perihepatic areas
• Look for causes of ascites: omental and
peritoneal implants
• Look for surface nodules or subtle capsular
thickening
• Remember long DDX of splenomegaly
Offsite imaging center tunnel vision
Prelim: “ascites”
Perfunctory cine loop
Normal: 10 cm
Cirrhosis: 18 cm
Mononucleosis: 19 cm
Sonography of fibrosis
• Traditional imaging doesn’t cut it
–We only identify end stage
fibrosis/cirrhosis
–Lesser degrees of fibrosis now
amenable for therapy (Hep C / NAFLD)
missed
The answer: stiffness assessment and
liver sonoelastography
• Validated, available, requested, reimburseable
• Dedicated SAR workshops on setting up an
elastography practice
• Straightforward, but several pearls (and
pitfalls) learned along the way
• No physics today
Transient elastography vs. ARFI
techniques
• TE (Fibroscan)
• Mechanical impulse
• M, XL probes
• Speed measurement of longitudinal shear
wave
• Not an imaging technique
transducer
explored volume
4 cm
1 cm
Transient Elastography
Point-SWE (pSWE)
• ARFI – Acoustic Radiation Force Impulse
• Transient shear waves
• ROI: 10 x 5 mm2
• Values in m/s or kPa
• QA: IQR/median < 30%
✓ Ultrasound image
✗ No elastography map
Two dimensional-SWE (2D-SWE)
• Multiple ARFI pulse pushes
• Larger ROI than in pSWE
• Values in m/s or kPa
• QA: IQR/median < 30%
✓ Ultrasound image
✓ Elastography map
Normal-mild fibrosis / Metavir F1NAFLD HCV
HCV: (F4) Cirrhosis
NAFLD- (F4) Cirrhosis
Pearl 4: Technique matters
SRU Consensus Statement (Barr et al., Radiology 2015)
Shallow Breath vs. Deep Inspiration
Pearl 5: Many reasons for variability
SRU Consensus Statement (Barr et al., Radiology 2015)
Congestive hepatopathy
ETOH, PVT,
osteomyelitis, possible
ascending cholangitis,
sepsis: “R/O cirrhosis”
Pearl 6: Lots of “In-betweener” Overlap
Two cutoff values (low vs. high risk for advanced fibrosis)
with likelihood ratios advocated (Barr, SRU consensus, Radiology 2015
Pearl 6: Lots of “In-betweener” Overlap
HCV, F2(?) at SWE, BX confirmed F2
Pearl 7: The tough ROI (fat, fibrosis ARFI attenuation)
Acute Hepatitis: Ultrasound
• Clinical diagnosis, but ultrasound may be
performed (pre-LFT evaluation) for eval of
RUQ pain, jaundice
• “Starry sky” liver: increased periportal
echogenicity Kurtz, Radiology, 1980
• Gallbladder wall thickening Juttner, Radiology, 1982
• Nonspecific….and often not present
RUQ pain
Hepatitis: “starry sky” liver
Periportal edema
OLTX Passive congestion
A final important case:
Tylenol overdose
ALT 5K, AST 4K
↓ Hepatic attenuation
but….normal ultrasound?
Fulminant hepatic necrosis
Conclusions
• Despite operator dependence, sono is still primary
imaging screen
• NAFLD is a public health nightmare – we’re often the
first to suggest the DX
• Conventional sonography performs well at extremes
(lots of fat, lots of fibrosis)
– Obesity doesn’t automatically imply steatosis: use internal
controls
– Beware of infiltrating tumor: don’t have tunnel vision
Conclusion
• Grading of steatosis is still subjective
– Validated, reproducible sono based fat quantification
methods needed
• SWE can differentiate between no/minimal and
advanced fibrosis
– Accepted, available, reimburseable
– Easily performed, but technique matters, and many
causes for variability