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