Imaging Pearls ❯ Liver ❯ Parenchymal Disease
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- “The most common cause of a hyper-attenuated liver is the long-term treatment with amiodarone. This drug has been used very extensively for the management of ventricular arrhythmia and atrial fibrillation. It accounted for 2.4 million prescriptions dispensed to 677,240 patients in the United States during 2020. Amiodarone has a molecular weight of 681 and contains 37.3% iodine. In comparison, the water-soluble contrast agent iothalamate meglumine (Conray 60, Guerbet Company, Paris, France) has 28.2% organically bound iodine. Amiodarone is administered orally or intravenously, and most patients receive it for as long as 5 to 10 years. It is highly lipophilic and metabolized in the liver to its active derivative. This drug has an elimination half-life of 35 to 100 days, thus remains in the body for a prolonged time after its intake has been discontinued.”
Computed tomography of hyper-attenuated liver: Pictorial essay,
Gary G. Ghahremani, Michael E. Hahn, Elliot K. Fishman,
Clinical Imaging, Volume 97,2023,Pages 1-6, - “Adverse effects of amiodarone include thyroid dysfunction in 14%–18% of patients caused by iodine content of the medication, and pulmonary changes due to interstitial fibrosis and pneumonia in about 3% of cases. Approximately 25% of patients receiving amiodarone will have a transient asymptomatic rise of their liver enzyme levels. Amiodarone-induced hepatotoxicity can develop after long-term therapy, causing abnormal liver function tests in 15% to 50% of patients, and hepatitis or cirrhosis in about 3% of cases. LV and Zhao recently performed dual-energy CT of the abdomen in 3 such patients.9 The liver attenuation ranged from 110 to 144 at 100 kVp and from 86 to 104 at 140 kVp, almost double the normal values.”
Computed tomography of hyper-attenuated liver: Pictorial essay,
Gary G. Ghahremani, Michael E. Hahn, Elliot K. Fishman,
Clinical Imaging, Volume 97,2023,Pages 1-6,
- “Wilson’s disease (WD) or hepatolenticular degeneration is a rare, autosomal-recessive inherited disorder of copper metabolism presenting most frequently with either hepatic or neurologic/psychiatric symptomatology. The disease arises from copper accumulation in the liver due to the inability to secrete the copper–ceruloplasmin complex into plasma and free copper into bile.”
Unique CT imaging findings of liver in Wilson’s disease
Weixia Li et al.
Abdom Imaging (2011) 36:69–73 - “Hyperdense nodules on unenhanced CT were observed in 92.31% of our cases (12 in 13 cases), and hypodense nodules on unenhanced CT were seen in 7.69% (one in 13). This finding was found to be in accordance with the data presented by Ko et al. in a case report, in contrast to our findings in a larger study. Both hypodense and hyperdense nodules observed on unenhanced CT may appear as hypodense nodules which become more conspicuous in the portal and/or parenchymal phases. This pattern was also reported previously by Ko and Akhan et al.. Akhan et al. also describe the unique imaging pattern in portal phase as ‘‘honeycomb pattern’’.
Unique CT imaging findings of liver in Wilson’s disease
Weixia Li et al.
Abdom Imaging (2011) 36:69–73 - “We conclude that Wilson’s disease should be considered as one of the leading diagnoses in young patients having hyperdense nodules and a honeycomb pattern not only in the portal and parenchymal phases but also in the pre-contrast scan.”
Unique CT imaging findings of liver in Wilson’s disease
Weixia Li et al.
Abdom Imaging (2011) 36:69–73
- Ascending Cholangitis: Facts
- Due to choledocholithiasis or reflux of bowel contents causing inflammation +/- infection of biliary tree
- Bile duct wall thickening + mucosal enhancement
- Irregular duct arborization
- Intraluminal gas +/- stones
- Liver may show heterogeneous enhancement +/- pyogenic abscesses - Recurrent (“Oriental”) Pyogenic Cholangitis: Facts
- Immigrants from impoverished Asian countries
- Massive dilation of IHBDs and common duct
- Filled with gas, pus, stones
- Will lead to liver abscesses + failure unless surgically corrected - Hepatic Amebic Abscess: facts
- Usually solitary hypodense/hypoechoic lesion
- Thick capsule; not septate
- Especially common in poor Hispanic immigrants
- Does not need to be aspirated or drained!
- Blood tests + medical Rx are effective - Passive Hepatic Congestion: Facts
- Swelling of liver may stretch capsule, cause pain
- Distended hepatic veins + IVC
- Retrograde opacification on early phase CECT
- Patchy enhancement of liver parenchyma - Polycystic Disease:
Autosomal Dominant
- Many cysts of varying size
- Often results in massive hepatomegaly
- Intracyst hemorrhage is common
- May have associated cysts in kidney, pancreas, etc.
- Often have positive family history
- But minimal effect on liver function - Biliary Hamartomas
(von Meyenberg complex)
- Multiple small (<15 mm) low attenuation lesions
- Helps to distinguish from cysts + polycystic liver disease
- Some change in size or disappear after IV contrast
- Due to enhancement of fibrous nodules in periphery
- These also are echogenic on sonography
- Associated with;
- Renal cysts or fibrosis
- Congenital hepatic fibrosis - Biliary Hamartomas: Facts
- Bile duct adenoma, von Meyenburg complex
- Benign proliferation of bile ductules and stroma
- Small (1-10 mm), few to innumerable
- “never” > 15 mm diameter
- Probably a common cause of small low density lesions
- Common in pts with polycystic disease (liver + kidneys) - Biliary Cystadenoma
- Large, solitary, complex multiseptate cystic mass
- Should be considered malignant or premalignant
- Much less common than other cystic masses
- Almost exclusively in women - Caroli disease
- Multiple cystic dilations of bile ducts
- “Central dot” sign
- Portal vein branch
- Surrounded by ectatic bile duct
- Communication with ducts is key feature
- MRCP or ERCP confirms Dx
- Often coexists with other fibropolycystic diseases of liver + kidneys
- E.g., congenital hepatic fibrosis
- Autosomal recessive polycystic kidney disease
- Cirrhosis
- Chronic liver damage leading to fibrosis and nodular regeneration
- Most common causes:
- Alcoholism
- Hepatitis C
- Hepatitis B
- Biliary cirrhosis
- Metabolic Cirrhosis
- Primary Sclerosing Cholangitis - Cirrhosis
- CT Findings:
- Heterogeneous liver texture
- Surface nodularity
- High density nodules in the liver on non-contrast images
- Caudate Hypertrophy
- Transverse caudate width : right lobe width
- > 0.65
- Segmental hypertrophy of segments II and III
- Segmental atrophy of segments VI, VII, and IV
- Enlarged gallbladder fossa
- Enlarged periportal space
- Peribiliary Cysts - Iron Deposition
- Hemochromatosis (“primary”)
- Autosomal recessive
- Liver, Pancreas, Heart
- Cirrhosis, “bronze” diabetes
- Hemosiderosis (“secondary”)
- Transfusions or hemolysis
- Liver, Spleen - Iron Deposition
- CT:
- Liver denser than spleen and muscle
- Similar appearance with some drugs (amiodarone) and glycogen storage disease - Iron Deposition
- MR:
- Low signal on T2 and T1
- Liver and spleen lower in T1 signal compared to muscle
- Signal drop-out on in-phase GRE - Sarcoid
- Commonly involves liver, but rarely causes symptoms
- Multiple nodules in the liver and spleen
- Periportal involvement
- Hepatomegaly and splenomegaly
- Look for lymphadenopathy and lung disease
- Can lead to cirrhosis chronically - Passive Hepatic Congestion
- Reflux of contrast into dilated IVC and hepatic veins
- Can be seen with forceful injections in normal patients
- Heterogeneously enhancing liver
- “Mottled” or “Nutmeg” liver
- Poor enhancement of peripheral liver due to stasis of blood flow
- Hepatomegaly and ascites - Hepatic Infarction
- Uncommon due to dual blood supply of the liver
- Usually hepatic arterial occlusion + portal vein abnormality
- Causes:
- Liver Transplant, Iatrogenic, Hypercoagulability, infection, vasculitis - Hepatic Infarction
- CT Findings:
- Usually wedge shaped, peripheral, and low attenuation
- Can be rounded or irregularly shaped
- Can evolve into bile lakes
- Gas can be seen in both sterile and infected infarcts - Portal Vein Thrombosis
- Causes:
- Cirrhosis and Portal Hypertension
- Slow flow and stasis in portal vein combined with hypercoagulability
- 1% of patients with cirrhosis develop portal vein thrombosis
- Malignancy
- Hypercoagulable States
- Iatrogenic
- Unknown in 1/3 of cases - Portal Vein Thrombosis
- CT Findings:
- Filling defect in the vein
- Thrombus should show no enhancement
- Thread-and-streak sign: Tumor thrombus
- Arterial hyperenhancement in the thrombus
- Chronically, mural thickening along the periphery of the vein with calcification
- Cavernous transformation - Malignant Versus Benign Portal Vein Thrombosis
- Malignant portal vein thrombus
- 35% of patients with HCC
- Poor prognosis and high rates of recurrence
- Liver transplant is contraindicated
- Systemic chemotherapy only real option
- Liver transplant still potentially an option with bland thrombus
- Cirrhosis
Chronic liver damage leading to fibrosis and nodular regeneration
Most common causes:
- Alcoholism
- Hepatitis C
- Hepatitis B
- Biliary cirrhosis
- Metabolic Cirrhosis
- Primary Sclerosing Cholangitis - Cirrhosis
CT Findings:
1. Heterogeneous liver texture
2. Surface nodularity
3. High density nodules in the liver on non-contrast images
4. Caudate Hypertrophy
- Transverse caudate width : right lobe width
- > 0.65
5. Segmental hypertrophy of segments II and III
6. Segmental atrophy of segments VI, VII, and IV
7. Enlarged gallbladder fossa
8. Enlarged periportal space
9. Peribiliary Cysts - Special Cases
1. Primary Sclerosing Cholangitis:
- Pseudotumoral enlargement of caudate
- DDX: Budd-Chiari Syndrome, PSC, and portal vein thrombosis
- Extensive periportal lymphadenopathy
2. Primary Biliary Cirrhosis
- “Lace-like fibrosis” with prominent regenerative nodules - Iron Deposition
1. Hemochromatosis (“primary”)
- Autosomal recessive
- Liver, Pancreas, Heart
- Cirrhosis, “bronze” diabetes
2. Hemisiderosis (“secondary”)
- Transfusions or hemolysis
- Liver, Spleen - Iron Deposition
1. CT:
- Liver denser than spleen and muscle
- Similar appearance with some drugs (amiodarone) and glycogen storage disease
2. MR
- Low signal on T2 and T1
- Liver and spleen lower in T1 signal compared to muscle
- Signal drop-out on in-phase GRE - Sarcoid
1. Commonly involves liver, but rarely causes symptoms
2. Multiple nodules in the liver and spleen
- Periportal involvement
- Hepatomegaly and splenomegaly
3. Look for lymphadenopathy and lung disease
4. Can lead to cirrhosis chronically
- Nonalcoholic Fatty Liver Disease (NAFLD): Facts
Common cause of chronic liver disease
- Usually asymptomatic, mild elevation of aminotransferase levels
- Common in diabetics, obese (metabolic syndrome)
- Affects 15-25% of American adults (10% of kids) - Nonalcoholic steatohepatitis (NASH)
- Subtype of NAFLD (25% of those w steatosis)
- Carries risk of progressive liver disease, cirrhosis
- Can only be diagnosed by Bx, not imaging
– (can’t distinguish NAFLD from NASH) - “CASH”: ChemoRx-associated steatohepatitis
- Common cause of liver dysfunction in cancer patients
- Associated with various agents
- May mask liver metastases on CT
- Liver injury may limit other therapeutic options (e.g., partial resection, ablation)
- Federle - Iron Deposition in the Liver: Facts
Hemochromatosis:
- Common autosomal recessive disorder, ? absorption of iron
- Deposited in hepatocytes, pancreas, heart, etc
- Leads to cirrhosis, HCC, “bronze” diabetes
- “Primary” = pancreatic involvement
Hemosiderosis:
- Due to hemolysis, transfusions
- Iron deposition in liver (RES), spleen
- “Secondary” = spleen
- Steatosis (Fatty Infiltration of the Liver)
CT Findings
- Decreased density (less than spleen on NC, 25 HU less on CECT)
- Vessels course through undisturbed
- Geographic areas
--Can be rounded (esp ~ ligaments + vessels), resemble metastases - Nonalcoholic Fatty Liver Disease
Common cause of chronic liver disease
- Usually asymptomatic, mild elevation of aminotransferase levels
- Common in diabetics, obese (metabolic syndrome)
- Affects 15-25% of American adults (10% of kids) - Nonalcoholic steatohepatitis (NASH)
- Subtype of NAFLD (25% of those w steatosis)
- Carries risk of progressive liver disease, cirrhosis
- May soon be #1 cause of cirrhosis + HCC in USA
- Can only be diagnosed by Bx, not imaging
- (can’t distinguish NAFLD from NASH) - “CASH”: ChemoRx-associated steatohepatitis
- Common cause of liver dysfunction in cancer patients
- Associated with various agents
- May mask liver mets on CT
- Liver injury may limit other Rx options (e.g., partial resection, ablation) - Diffuse Disease that May Simulate Fatty Liver
Diffuse tumor
- Lymphoma > mets > diffuse HCC
Diffuse infection
- Especially in AIDS (viral, mycobacterial, fungal, etc)
Diffuse acute liver injury
- Severe hepatitis
- Tylenol OD, mushroom poisoning
- Radiation hepatitis - Iron Deposition in the Liver
Hemochromatosis:
- Common autosom recess disorder, absorption of iron
- Deposited in hepatocytes, pancreas, heart, etc
- Leads to cirrhosis, HCC, “bronze” diabetes
- “Primary” = pancreatic involvement
Hemosiderosis:
- Due to hemolysis, transfusions
- Iron deposition in liver (RES), spleen
- “Secondary” = spleen - Iron Deposition
CT:
- Liver much denser than spleen, muscle
- DDx: amiodarone Rx, glycogen storage disease, (Wilson’s disease – not!)
MR:
- Marked downward signal on T2 + T1WI
- T1WI: liver + spleen much darker than muscle
- Signal “drop-out” on in-phase GRE (opposite of steatosis) - Sarcoidosis of the Liver
- Periportal involvement
- Can simulate or lead to cirrhosis
- Hepatomegaly, splenomegaly, periportal SI on T2WI
- Multifocal liver/splenic nodules
- Lung disease +/ or nodes (chest + abdomen) - Focal Lesions in the Cirrhotic Liver
Cysts, hemangiomas, focal fat, confluent fibrosis
- Can usually be diagnosed accurately
Hemangiomas shrink and become sclerosed in cirrhotic liver
- Often not identified in advanced cirrhosis
Focal fat
- Key is out-of-phase MR (focal sign dropout)
Brancatelli et al. Radiology 2001; 219: 69-74 - Confluent Hepatic Fibrosis
(Focal Confluent Fibrosis)
Present in ~ 30% of advanced cirrhosis
- > 50% of PSC
Most common in anterior + medial segments
- Usually wedge-shaped lesion
80% have focal volume loss
- Capsular retraction, crowded vessels
Low density on NCCT
- Delayed persistent enhancement
- Can simulate tumor