Diffuse hepatic steatosis

Diffuse hepatic steatosis

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Diffuse hepatic steatosis

Dr Daniel J Bell and A.Prof Frank Gaillard et al.

Diffuse hepatic steatosis, also known as fatty liver, is a common imaging finding and can lead to difficulties assessing the liver appearances, especially when associated with focal fatty sparing .

On this page:

Article:

  • Terminology
  • Epidemiology
  • Pathology
  • Radiographic features
  • Treatment and prognosis
  • Practical points
  • Related articles
  • References

Images:

  • Cases and figures

Terminology

The term ‘fatty infiltration of the liver’ is often erroneously used to describe liver steatosis. Since fat is intracellular in liver steatosis, and not in the extracellular matrix, using infiltration to describe it is factually incorrect.

Epidemiology

Diffuse hepatic steatosis is common, affecting ~25% of the population. 

Pathology

Hepatic steatosis is due to the abnormal accumulation of lipids, particularly triglycerides within hepatocytes 3,4. These are found in both small and large vesicles. Macroscopically, the liver is enlarged, yellow and greasy. Steatosis can lead to fibrosis and cirrhosis .

Aetiology 

Diffuse hepatic steatosis is often idiopathic. However, it may be associated with 1:

  • alcohol abuse
  • non-alcoholic fatty liver disease (NAFLD)  4, which is associated with

    • insulin resistance / diabetes mellitus
    • obesity
    • dyslipidaemia
  • exogenous steroid intake
  • drugs (amiodarone, methotrexate, chemotherapy e.g. tamoxifen)
  • IV hyperalimentation
  • c hronic hepatitis
  • pregnancy:  acute fatty liver of pregnancy (AFLP)  4
  • metabolic disorders
    • glycogen storage diseases
  • radiation

Radiographic features

General features include:

  • mild hepatomegaly (in ~75%) 5
  • attenuation/signal of liver shifted towards that of fat 
  • focal fatty sparing

    • islands of normal liver tissue within a sea of hepatic steatosis 
    • possibly occur due to regional perfusion differences 2 
    • importantly, compared to intrahepatic masses, fatty sparing has no mass effect with no distortion of vessels 
    • see also focal hepatic steatosis
Plain radiograph

Radiolucent liver sign: liver soft-tissue outline becomes difficult to appreciate 5.

Ultrasound

Steatosis manifests as increased echogenicity and beam attenuation 2,12. This results in:

  • renal cortex appearing relatively hypoechoic compared to the liver parenchyma (normally liver and renal cortex are of a similar echogenicity)
    • increased echogenicity relative to the spleen, when there is parenchymal renal disease
  • absence of the normal echogenic walls of the portal veins and hepatic veins
    • important not to assess vessels running perpendicular to the beam, as these produce direct reflection and can appear echogenic even in a fatty liver
  • poor visualisation of deep portions of the liver
  • poor visualisation of the diaphragm

Sonoelastography : can assess the degree of accompanying fibrosis by measuring tissue stiffness (FibroScan®, acoustic radiation force impulse) 10.

Grading
  • see:  grading of diffuse hepatic steatosis
CT

Steatosis causes reduced liver attenuation . This results in:

  •  low hepatic attenuation compared with spleen on non-contrast imaging
    • non-fatty liver is normally 6-12 HU greater density than spleen 5
    • if the attenuation of the liver is at least 10 HU less than that of the spleen the diagnosis of fatty liver is made 11
    • arterial phase or portal venous phase scans should not be used as the spleen enhances earlier than the liver due to predominant systemic arterial supply. Fatty liver can be diagnosed by contrast-enhanced CT if absolute attenuation is less than 40 HU 15, but this threshold has limited sensitivity 11
  • relatively hyperattenuating intrahepatic vessels
MRI

Requires both in-phase (IP) and out-of-phase (OOP) imaging to be adequately assessed 1. Fatty liver appears:

  • T1: hyperintense
  • T2: mildly hyperintense
  • IP/OOP imaging: signal drop out in fatty liver in out of phase >15%

On IP/OOP imaging the maximum signal loss occurs when there is 50% fatty infiltration of the liver. In situations in which there is >50% fatty infiltration, the out-of-phase sequence paradoxically becomes less hypointense than at 50%. This happens because there are relatively fewer water molecules to cancel out the fat signal. Chemical shift artifact at the parenchyma-vessel interface aids in detecting this situation 13.

Other MRI uses:

  • MR spectroscopy : accurate quantitative non-invasive assessment of hepatic steatosis 8
  • MR elastography: shows promise as a method for assessing accompanying hepatic fibrosis 9
Nuclear medicine
  • Tc99m sulfur colloid 

    • uptake is reduced in fatty liver 5
    • reduced hepatic uptake relative to the spleen (reversal of normal liver:spleen uptake ratio)
    • focal fatty area can simulate a hepatic mass 7
  • Xenon133: accurate quantitative non-invasive assessment of hepatic steatosis 8
  • FDG-PET: liver uptake is not altered by the presence of steatosis 6

Treatment and prognosis

As long as hepatic fibrosis and cirrhosis have not developed, fatty change is reversible with modification of the underlying causative factor, e.g. alcohol, pregnancy, obesity, diet.

Practical points

  • there is potential for missing mild hepatic steatosis on ultrasound if there is concurrent chronic renal disease, which increases the echogenicity of the kidneys; if there is any question that the patient may have a chronic renal disease , comparison of the left kidney with the spleen may be useful
  • a greater echogenicity difference between the right kidney and the liver than between the left kidney and the spleen is indicative of hepatic steatosis 12
  • if the attenuation of the liver on CT is at least 10 HU less than that of the spleen the diagnosis of fatty liver is made 11
  • MRI IP/OOP imaging shows a signal drop out in fatty liver >15%

References

  • 1. Tom WW, Yeh BM, Cheng JC et-al. Hepatic pseudotumor due to nodular fatty sparing: the diagnostic role of opposed-phase MRI. AJR Am J Roentgenol. 2004;183 (3): 721-4. AJR Am J Roentgenol (full text) – Pubmed citation
  • 2. Kato M, Saji S, Kanematsu M et-al. A case of liver metastasis from colon cancer masquerading as focal sparing in a fatty liver. Jpn. J. Clin. Oncol. 1997;27 (3): 189-92. doi:10.1093/jjco/27.3.189 – Pubmed citation
  • 3. Chung JJ, Kim MJ, Kim JH et-al. Fat sparing of surrounding liver from metastasis in patients with fatty liver: MR imaging with histopathologic correlation. AJR Am J Roentgenol. 2003;180 (5): 1347-50. AJR Am J Roentgenol (full text) – Pubmed citation
  • 4. Kumar V, Abbas AK, Fausto N et-al. Robbins and Cotran pathologic basis of disease. W B Saunders Co. (2005) ISBN:0721601871. Read it at Google Books – Find it at Amazon
  • 5. Dähnert W. Radiology Review Manual. Lippincott Williams & Wilkins. (2007) ISBN:0781766206. Read it at Google Books – Find it at Amazon
  • 6. Abele JT, Fung CI. Effect of hepatic steatosis on liver FDG uptake measured in mean standard uptake values. Radiology. 2010;254 (3): 917-24. doi:10.1148/radiol.09090768 – Pubmed citation
  • 7. Khedkar N, Pestika B, Rosenblate H et-al. Large focal defect on liver/spleen scan caused by fatty liver and masquerading as neoplasm. J. Nucl. Med. 1992;33 (2): 258-9. J. Nucl. Med. (link) – Pubmed citation
  • 8. Fabbrini E, Conte C, Magkos F. Methods for assessing intrahepatic fat content and steatosis. Curr Opin Clin Nutr Metab Care. 2009;12 (5): 474-81. doi:10.1097/MCO.0b013e32832eb587 – Pubmed citation
  • 9. Watanabe H, Kanematsu M, Kitagawa T et-al. MR elastography of the liver at 3 T with cine-tagging and bending energy analysis: preliminary results. 2010; doi:10.1007/s00330-010-1800-0 – Pubmed citation
  • 10. Boursier J, Isselin G, Fouchard-hubert I et-al. Acoustic radiation force impulse: a new ultrasonographic technology for the widespread noninvasive diagnosis of liver fibrosis. 2010; doi:10.1097/MEG.0b013e328339e0a1 – Pubmed citation
  • 11. Hamer OW, Aguirre DA, Casola G et-al. Fatty liver: imaging patterns and pitfalls. Radiographics. 26 (6): 1637-53. doi:10.1148/rg.266065004 – Pubmed citation
  • 12. Tchelepi H, Ralls PW, Radin R et-al. Sonography of diffuse liver disease. J Ultrasound Med. 2003;21 (9): 1023-32. Pubmed citation
  • 13. Reeder SB, Sirlin CB. Quantification of liver fat with magnetic resonance imaging. Magn Reson Imaging Clin N Am. 2010;18 (3): 337-57, ix. doi:10.1016/j.mric.2010.08.013 – Free text at pubmed – Pubmed citation
  • 14. Tolman KG, Dalpiaz AS. Treatment of non-alcoholic fatty liver disease. Ther Clin Risk Manag. 2011;3 (6): 1153-63. Free text at pubmed – Pubmed citation
  • 15. Kodama Y, Ng CS, Wu TT, Ayers GD, Curley SA, Abdalla EK, Vauthey JN, Charnsangavej C. Comparison of CT methods for determining the fat content of the liver. (2007) AJR. American journal of roentgenology. 188 (5): 1307-12. doi:10.2214/AJR.06.0992 – Pubmed
Ultrasound – liver
  • ultrasound (introduction)
  • liver ultrasound
    • liver
      • focal
        • hyperechoic liver lesions
        • hypoechoic halo sign / target lesions
        • simple hepatic cyst
        • hepatic haemangioma
        • focal nodular hyperplasia
        • hepatic adenoma
        • hepatic metastases

          • cystic hepatic metastases
        • hepatic abscess
        • periportal hyperechogenicity
        • periportal hypoechogenicity
      • diffuse
        • acute hepatitis
        • cirrhosis
        • hyperechoic liver

          • diffuse hepatic steatosis

            • grading of hepatic steatosis
        • coarsened hepatic echotexture
        • generalised decrease in hepatic echogenicity
        • “starry sky appearance” of the liver
      • hepatic vasculature
        • normal hepatic vein Doppler
        • portal hypertension
        • portal vein thrombosis
        • developed collaterals / portosystemic shunts
      • other
        • hepatic trauma on ultrasound
    • liver transplant
      • hepatic arterial resistive index
    • biliary
      • bile duct dilatation (differential)
      • bile duct wall thickening (differential)
      • choledocholithiasis
      • cholangiocarcinoma
      • Mirizzi syndrome

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Article information

rID: 6853
System: Hepatobiliary
Tag: liver
Synonyms or Alternate Spellings:

  • Diffuse fatty infiltration
  • Diffuse hepatic fatty infiltration
  • Diffuse fatty inflitration of the liver
  • Diffuse steatosis of the liver

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Cases and figures

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    Fatty liver - CECT

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      Gastrointestinal Society Logo

      The Dangers of Non-Alcoholic Fatty Liver Disease

      The Dangers of Non-Alcoholic Fatty Liver Disease GIS 2016-11-30T11:38:50+00:00

      Non-alcoholic fatty liver disease (NAFLD) occurs when a large amount of fat – that isn’t associated with heavy alcohol use – accumulates in the liver (5-10% by weight). In its mildest form, this disease doesn’t cause much trouble, presenting with few (if any) symptoms and complications. NAFLD affects 20-30% of North Americans, but can be treated with lifestyle changes.

       

      Non-Alcoholic Steatohepatitis

      While NAFLD is mostly benign, left unaddressed it can develop into a much more harmful disease-state called non-alcoholic steatohepatitis (NASH), which involves inflammation of the liver. NASH affects 20% of those with NAFLD.1 It occurs when scar tissue (fibrosis) is visible in the liver. Fibrosis can develop into advanced scarring (cirrhosis) or liver cancer. About 20% of those diagnosed with NASH develop cirrhosis, which is a serious problem that can lead to many complications.2 In 2008 and 2009, 12% of British patients waiting for a liver transplant had cirrhosis caused by NASH.5 It can even be deadly: a recent study found that 11% of patients with NASH are at risk of death from liver-related illness.4

       

      A Symptom of Metabolic Syndrome

      Metabolic syndrome is a condition defined by an increase in blood pressure, blood sugar, and/or cholesterol, as well as having excess abdominal fat. NAFLD is so common in individuals with this illness that some researchers believe it is the hepatic manifestation of metabolic syndrome and should become part of the diagnostic criteria. They even suggest the usefulness of ultrasonically-detected NAFLD as a diagnostic tool for metabolic syndrome.3 Having other disorders associated with metabolic syndrome may also make your NAFLD more dangerous. One study found that individuals who had NAFLD along with type 2 diabetes were more likely to die from liver disease than those without diabetes.4 If you are concerned you may have any of these ailments, talk to your physician about being tested.

       

      What Did Your Mother Eat?

      Most new mothers are aware that specific habits during pregnancy, such as tobacco and alcohol consumption, can have a powerful effect on the health of the child. However, the type of food mothers eat can also cause issues. A recent study showed that the children of women who ate a high-fat diet while pregnant were more likely to develop NAFLD when they got older. While the exact mechanism responsible for this is unclear, the researchers have an idea. They believe that most people develop NAFLD in a two-step process. The first step is hepatic insulin resistance or impaired β-oxidation of fatty acids, the second step is inflammation or oxidative stress. The researchers speculate that children who are exposed to high amounts of fatty acids in utero experience this first step before birth, so that all it takes for them to develop NAFLD is some sort of inflammation or oxidative stress. However, pregnant women may be able to prevent this by reducing the overall quantity of fats in their diets and eating more omega-3 fatty acids.1

       

      NAFLD is Treatable

      Although the statistics for this disease are significant, the good thing is that it is treatable. Many studies have looked at possible treatments for NAFLD, and the overarching theme is that treating with diet and exercise, usually to achieve weight loss, is very effective. However, it is important for patients to avoid any drastic weight loss methods; starvation, protein deficiency, and rapid weight loss can cause or worsen NAFLD.2 This is why it is important to follow a healthy regimen to treat NAFLD, rather than opting for surgeries or programs that offer rapid weight loss.5 Consult your general practitioner or a registered dietitian to learn about the right treatment for you.


      First published in the Inside Tract® newsletter issue 192 – 2014
      1. Hughes AN et al. A lipid-rich gestational diet predisposes offspring to non-alcoholic fatty liver disease: a potential sequence of events. Hepatic Medicine: Evidence and Research. 2014;6:15-23.
      2. Canadian Liver Foundation. Fatty Liver Disease. Available at: http://www.liver.ca/liver-disease/types/fatty-liver.aspx. Accessed 2014-09-18.
      3. Tarantino G et al. What about non-alcoholic fatty liver disease as a new criterion to define metabolic syndrome. World Journal of Gastroenterology. 2013;19(22):3375-84.
      4. Stepanova M et al. Predictors of All-Cause Mortality and Liver-Related Mortality in Patients with Non-Alcoholic Fatty Liver Disease (NAFLD). Digestive Diseases and Sciences. 2013;58:3017-23.
      5. Bradford V et al. Lifestyle interventions for the treatment of non-alcoholic fatty liver disease. Hepatic Medicine: Evidence and Research. 2014;6:1-10.

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