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Diagnostic Ultrasound - Abdomen and Pelvis

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Hepatic Steatosis<br />

Diagnoses: Liver<br />

○ Metabolic derangement<br />

– Poorly controlled DM (50%), obesity, hyperlipidemia<br />

– Severe hepatitis <strong>and</strong> protein malnutrition<br />

– Parenteral hyperalimentation, malabsorption<br />

– Pregnancy, trauma, inflammatory bowel disease<br />

– Cystic fibrosis, Reye syndrome<br />

○ Hepatotoxins:Alcohol (> 50%), carbon tetrachlorides,<br />

phosphorus<br />

○ Drugs<br />

– Tetracycline, amiodarone, corticosteroids<br />

– Salicylates, tamoxifen, calcium channel blockers<br />

• Associated abnormalities<br />

○ NASH<br />

– Subset of nonalcoholic fatty liver disease: Strong<br />

association with metabolic syndrome<br />

– Seen in patients with hyperlipidemia <strong>and</strong> diabetes<br />

– May lead to "cryptogenic" cirrhosis<br />

• Fat deposition in liver due to<br />

○ Ethanol: Increased hepatic synthesis of fatty acids<br />

○ Carbon tetrachloride/high-dose tetracycline: Decreases<br />

hepatic oxidation/utilization of fatty acids<br />

○ Starvation, steroids, <strong>and</strong> alcohol<br />

– Excessively mobilizes fatty acids from adipose tissue<br />

○ Segmental fatty infiltration: Where glycogen is depleted<br />

from liver<br />

– Decreased nutrients <strong>and</strong> insulin → decreased<br />

glycogen<br />

– Due to underlying mass, Budd-Chiari syndrome, or<br />

tumor thrombus<br />

○ Focal steatosis or sparing: Due to variations in hepatic<br />

venous drainage<br />

Staging, Grading, & Classification<br />

• Sonographic grading for diffuse steatosis<br />

○ Mild: Minimally increased parenchymal echogenicity <strong>and</strong><br />

normal-appearing intrahepatic vessel walls<br />

○ Moderate: Further increased parenchymal echogenicity<br />

causing decreased resolution of intrahepatic vessel walls<br />

○ Severe: Markedly increased parenchymal echogenicity<br />

causing inability to resolve intrahepatic vessel walls<br />

• Nonalcoholic fatty liver disease (NAFLD)<br />

○ Includes nonalcoholic fatty liver (NAFL) <strong>and</strong> NASH<br />

○ May progress to cirrhosis <strong>and</strong> hepatocellular carcinoma<br />

○ Risk factors: Obesity, sedentary lifestyle, diet, type II<br />

diabetes, metabolic syndrome<br />

Gross Pathologic & Surgical Features<br />

• Enlarged, smooth capsule, rounded inferior contour<br />

• Soft, yellow, greasy cut surface<br />

Microscopic Features<br />

• Triglyceride accumulation within hepatocyte cytoplasm<br />

• Macrovesicular fatty liver (most common type)<br />

○ Hepatocytes with large cytoplasmic fat vacuoles<br />

displacing nucleus peripherally<br />

○ Alcohol <strong>and</strong> diabetes mellitus<br />

• Microvesicular<br />

○ Fat is present in many small vacuoles<br />

○ Reye syndrome<br />

CLINICAL ISSUES<br />

Presentation<br />

• Most common signs/symptoms<br />

○ Asymptomatic, but often with abnormal liver function<br />

tests (LFTs)<br />

○ Hepatomegaly in obese or diabetic patient<br />

○ Alcoholics with acute injury: RUQ pain, tender<br />

hepatomegaly<br />

• Lab data<br />

○ Asymptomatic: Normal/mildly elevated LFTs<br />

○ Alcoholic <strong>and</strong> NASH: May have markedly abnormal LFTs<br />

• Diagnosis:Biopsy <strong>and</strong> histology<br />

○ Distinguish simple steatosis from steatohepatitis<br />

○ Sampling error<br />

○ MR Elastography: Emerging noninvasive means for<br />

staging fibrosis <strong>and</strong> differentiating simple steatosis <strong>and</strong><br />

NASH<br />

Demographics<br />

• Epidemiology<br />

○ Most common cause of chronic liver disease in Western<br />

countries<br />

○ 50% of patients with diabetes mellitus, > 50% of<br />

alcoholics; 80-90% of obesity<br />

○ Seen in 25% of nonalcoholics<br />

○ Increasing in prevalence with epidemic of obesity <strong>and</strong><br />

metabolic syndrome<br />

Natural History & Prognosis<br />

• Alcoholics: Gradual disappearance of fat from liver after 4-8<br />

weeks of adequate diet <strong>and</strong> abstinence from alcohol<br />

• Resolves in 2 weeks after discontinuation of parenteral<br />

hyperalimentation<br />

• Steatohepatitis may progress to acute/chronic liver failure<br />

• Steatosis is synergistic with viral hepatitis<br />

Treatment<br />

• Removal of alcohol or offending toxins<br />

• Correction of metabolic disorders<br />

• Lipotropic agents (like choline) when indicated<br />

DIAGNOSTIC CHECKLIST<br />

Consider<br />

• Rule out other liver pathologies that may mimic focal or<br />

diffuse steatosis<br />

Image Interpretation Pearls<br />

• Key on all imaging modalities is presence of normal vessels<br />

coursing through fatty infiltration<br />

SELECTED REFERENCES<br />

1. Loomba R et al: Magnetic resonance elastography predicts advanced fibrosis<br />

in patients with nonalcoholic fatty liver disease: a prospective study.<br />

Hepatology. 60(6):1920-8, 2014<br />

2. Borges VF et al: Sonographic hepatorenal ratio: a noninvasive method to<br />

diagnose nonalcoholic steatosis. J Clin <strong>Ultrasound</strong>. 41(1):18-25, 2013<br />

3. Kwon HJ et al: Value of the ultrasound attenuation index for noninvasive<br />

quantitative estimation of hepatic steatosis. J <strong>Ultrasound</strong> Med. 32(2):229-35,<br />

2013<br />

188<br />

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