Hepatic Steatosis ( Fatty Liver)
Definition
Accumulation of increasing amount of triglycerides within hepatocytes
Best diagnostic clue
- Preservation of normal hepatic architecture
- Presence of normal vessels coursing through fatty infiltration
- Decreased signal intensity of liver on T1W out of phase gradient-echo images
- Focal, multifocal, or diffuse
- Lobar, segmental, or wedge shaped , Common along hepatic vessels, ligaments, and
- fissures
- Geographic/wedge shape
- Multifocal spherical lesions may simulate metastasis or primary tumor
Variable imaging features depend on
○ Amount of fat deposited in liver
○ Distribution of fat within liver: Focal vs. diffuse
○ Presence of associated hepatic disease
• Grayscale ultrasound
Diffuse fatty infiltration
- liver echogenicity : Increased , more echogenic than kidney
- Liver size : enlarged , changes shape as volume of infiltration increase .
- poor visualization of diaphragm
- Hepatic veins : blurred Margins , due to increased refraction and scattering of sound
- portal vein : Loss of echogenic walls
- US grading of steatosis is subjective and prone to interobserver variation
- Hyperechoic nodule
- multiple confluent hyperechoic lesions
- No mass effect, with vessels running undisplaced through lesion
- Wedge-shaped lobar/segmental distribution
Focal fatty sparing
- Hypoechoic area within echogenic liver
- No mass effect
- Due to direct drainage of hepatic flow into systemic circulation
- Next to gallbladder bed (drained by cystic vein)
- Segment 4, anterior to portal bifurcation (drained by aberrant gastric vein)
CT Findings
Non contrast CT
- Decreased attenuation of liver compared to spleen :
- Steatosis: Liver at least 10 HU less than spleen, or absolute liver attenuation < 40 HU
- Focal nodular fatty infiltration:Low attenuation
- Common location: Adjacent to falciform ligament
- Due to nutritional ischemia at vascular watershed
Contrast Enhanced CT
- Normal vessels course through fatty infiltration
- Dual-energy CT: Steatosis accentuated on lower kVp sequence
- Attenuation measurements and comparisons are less reliable than NECT
- On venous phase or delayed CECT, steatotic liver is usually > 35 HU less dense than spleen
MR Findings
• T1 in-phase GRE (chemical shift): Increased signal intensity of fatty liver vs. spleen
• T1 out of phase GRE: Decreased or loss of signal intensity of fatty liver
• T1 C+ out of phase GRE: Paradoxical decreased signal intensity of liver
• Short T1 inversion recovery (STIR): Fatty areas are low signal intensity
Differential Diagnosis
Steatohepatitis
• Diabetic fatty liver, alcoholic hepatitis, nonalcoholic steatohepatitis (NASH)
• Fatty liver + inflammatory change, fibrosis, and necrosis
• Smooth surface, decreased plasticity
• Hepatic veins show disjointed network-like appearance with blurred outline
• Increasing fibrosis and scarring
Fatty Cirrhosis
• Dense, firm liver
• Hypertrophied left caudate lobe/atrophy of right lobe
• Heterogeneous, hyperechoic parenchyma
• Rarefaction of hepatic veins
Hemangioma
• Typically well-defined, hyperechoic nodule
• Posterior acoustic enhancement
Metastases or Lymphoma
• Hyperechoic metastases may simulate focal steatosis
• Confluent or infiltrative tumor distorts vessels and bile ducts
• Diffuse lymphoma infiltration may be indistinguishable from normal liver or steatosis
PATHOLOGY
• Etiology
Metabolic derangement
• Associated abnormalities
○ Non Alcoholic SteatoHepatitis
– Subset of nonalcoholic fatty liver disease: Strong association with metabolic syndrome
– Seen in patients with hyperlipidemia and diabetes
– May lead to "cryptogenic" cirrhosis
• Fat deposition in liver due to
○ Ethanol: Increased hepatic synthesis of fatty acids
○ Carbon tetrachloride/high-dose tetracycline: Decreases hepatic oxidation/utilization of fatty acids
○ Starvation, steroids, and alcohol
– Excessively mobilizes fatty acids from adipose tissue
○ Segmental fatty infiltration: Where glycogen is depleted from liver
– Decreased nutrients and insulin → decreased glycogen
– Due to underlying mass, Budd-Chiari syndrome, or tumor thrombus
○ Focal steatosis or sparing: Due to variations in hepatic venous drainage
Staging, Grading, & Classification
• Sonographic grading for diffuse steatosis
○ Mild: Minimally increased parenchymal echogenicity and normal-appearing intrahepatic vessel walls
○ Moderate: Further increased parenchymal echogenicity causing decreased resolution of intrahepatic vessel walls
○ Severe: Markedly increased parenchymal echogenicity causing inability to resolve intrahepatic vessel walls
• Nonalcoholic fatty liver disease (NAFLD)
○ Includes nonalcoholic fatty liver (NAFL) and NASH
○ May progress to cirrhosis and hepatocellular carcinoma
○ Risk factors: Obesity, sedentary lifestyle, diet, type II diabetes, metabolic syndrome
CLINICAL ISSUES
○ Asymptomatic, but often with abnormal liver function tests .
○ Hepatomegaly in obese or diabetic patient
○ Alcoholics with acute injury: RUQ pain, tender hepatomegaly
• Lab data
○ Asymptomatic: Normal/mildly elevated Liver Function tests.
○ Alcoholic and NASH: May have markedly abnormal Liver Function tests.
• Diagnosis Biopsy and histology
○ Distinguish simple steatosis from steatohepatitis
○ Sampling error
○ MR Elastography: Emerging noninvasive means for staging fibrosis and differentiating simple steatosis and NASH
• Epidemiology
○ Most common cause of chronic liver disease in Western countries
○ 50% of patients with diabetes mellitus, > 50% of alcoholics; 80-90% of obesity
○ Seen in 25% of nonalcoholics
○ Increasing in prevalence with epidemic of obesity and metabolic syndrome
Natural History & Prognosis
• Alcoholics: Gradual disappearance of fat from liver after 4-8 weeks of adequate diet and abstinence from alcohol
• Resolves in 2 weeks after discontinuation of parenteral hyperalimentation
• Steatohepatitis may progress to acute/chronic liver failure
• Steatosis is synergistic with viral hepatitis
Treatment
• Removal of alcohol or offending toxins
• Correction of metabolic disorders
• Lipotropic agents (like choline) when indicated
DIAGNOSTIC CHECKLIST
• Rule out other liver pathologies that may mimic focal or diffuse steatosis
• Key on all imaging modalities is presence of normal vessels coursing through fatty infiltration
patient with acute alcoholic hepatitis shows moderate steatosis as diffusely increased echogenicity of hepatic parenchyma along with poorly delineated intrahepatic vascular margins
MR Findings
• T1 in-phase GRE (chemical shift): Increased signal intensity of fatty liver vs. spleen
• T1 out of phase GRE: Decreased or loss of signal intensity of fatty liver
• T1 C+ out of phase GRE: Paradoxical decreased signal intensity of liver
• Short T1 inversion recovery (STIR): Fatty areas are low signal intensity
Differential Diagnosis
Steatohepatitis
• Diabetic fatty liver, alcoholic hepatitis, nonalcoholic steatohepatitis (NASH)
• Fatty liver + inflammatory change, fibrosis, and necrosis
• Smooth surface, decreased plasticity
• Hepatic veins show disjointed network-like appearance with blurred outline
• Increasing fibrosis and scarring
Fatty Cirrhosis
• Dense, firm liver
• Hypertrophied left caudate lobe/atrophy of right lobe
• Heterogeneous, hyperechoic parenchyma
• Rarefaction of hepatic veins
Hemangioma
• Typically well-defined, hyperechoic nodule
• Posterior acoustic enhancement
Metastases or Lymphoma
• Hyperechoic metastases may simulate focal steatosis
• Confluent or infiltrative tumor distorts vessels and bile ducts
• Diffuse lymphoma infiltration may be indistinguishable from normal liver or steatosis
PATHOLOGY
• Etiology
Metabolic derangement
- Poorly controlled DM (50%), obesity, hyperlipidemia
- Severe hepatitis and protein malnutrition
- Parenteral hyperalimentation, malabsorption
- Pregnancy, trauma, inflammatory bowel disease
- Cystic fibrosis, Reye syndrome
- Hepatotoxins: Alcohol (> 50%), carbon tetrachlorides, phosphorus
- Drugs :Tetracycline, amiodarone, corticosteroid / Salicylates, tamoxifen, calcium channel blockers
• Associated abnormalities
○ Non Alcoholic SteatoHepatitis
– Subset of nonalcoholic fatty liver disease: Strong association with metabolic syndrome
– Seen in patients with hyperlipidemia and diabetes
– May lead to "cryptogenic" cirrhosis
• Fat deposition in liver due to
○ Ethanol: Increased hepatic synthesis of fatty acids
○ Carbon tetrachloride/high-dose tetracycline: Decreases hepatic oxidation/utilization of fatty acids
○ Starvation, steroids, and alcohol
– Excessively mobilizes fatty acids from adipose tissue
○ Segmental fatty infiltration: Where glycogen is depleted from liver
– Decreased nutrients and insulin → decreased glycogen
– Due to underlying mass, Budd-Chiari syndrome, or tumor thrombus
○ Focal steatosis or sparing: Due to variations in hepatic venous drainage
Staging, Grading, & Classification
• Sonographic grading for diffuse steatosis
○ Mild: Minimally increased parenchymal echogenicity and normal-appearing intrahepatic vessel walls
○ Moderate: Further increased parenchymal echogenicity causing decreased resolution of intrahepatic vessel walls
○ Severe: Markedly increased parenchymal echogenicity causing inability to resolve intrahepatic vessel walls
• Nonalcoholic fatty liver disease (NAFLD)
○ Includes nonalcoholic fatty liver (NAFL) and NASH
○ May progress to cirrhosis and hepatocellular carcinoma
○ Risk factors: Obesity, sedentary lifestyle, diet, type II diabetes, metabolic syndrome
CLINICAL ISSUES
○ Asymptomatic, but often with abnormal liver function tests .
○ Hepatomegaly in obese or diabetic patient
○ Alcoholics with acute injury: RUQ pain, tender hepatomegaly
• Lab data
○ Asymptomatic: Normal/mildly elevated Liver Function tests.
○ Alcoholic and NASH: May have markedly abnormal Liver Function tests.
• Diagnosis Biopsy and histology
○ Distinguish simple steatosis from steatohepatitis
○ Sampling error
○ MR Elastography: Emerging noninvasive means for staging fibrosis and differentiating simple steatosis and NASH
• Epidemiology
○ Most common cause of chronic liver disease in Western countries
○ 50% of patients with diabetes mellitus, > 50% of alcoholics; 80-90% of obesity
○ Seen in 25% of nonalcoholics
○ Increasing in prevalence with epidemic of obesity and metabolic syndrome
Natural History & Prognosis
• Alcoholics: Gradual disappearance of fat from liver after 4-8 weeks of adequate diet and abstinence from alcohol
• Resolves in 2 weeks after discontinuation of parenteral hyperalimentation
• Steatohepatitis may progress to acute/chronic liver failure
• Steatosis is synergistic with viral hepatitis
Treatment
• Removal of alcohol or offending toxins
• Correction of metabolic disorders
• Lipotropic agents (like choline) when indicated
DIAGNOSTIC CHECKLIST
• Rule out other liver pathologies that may mimic focal or diffuse steatosis
• Key on all imaging modalities is presence of normal vessels coursing through fatty infiltration
patient with acute alcoholic hepatitis shows moderate steatosis as diffusely increased echogenicity of hepatic parenchyma along with poorly delineated intrahepatic vascular margins