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Passive hepatic congestion (congestive hepatopathy) is a common
complication of congestive heart failure and constrictive pericarditis
where elevated central venous pressures are directly transmitted
from the right atrium to the inferior vena cava (IVC) and the hepatic
veins. The liver becomes swollen as the hepatic sinusoids dilate
and engorge to accommodate the backflow of blood leading to blood
stasis and hepatocellular hypoxia. In acute hepatic congestion,
the hepatic veins and the sinusoids are distended with blood secondary
to blood stasis. This congestion can lead to compression of centrilobular
hepatocytes leading to atrophy and necrosis to a variable degree.
The periportal hepatocytes are relatively better oxygenated because
of their proximity to hepatic arterioles and, therefore, experience
less severe hypoxia, typically developing only fatty change. In
chronic passive congestion of the liver, persistent hypoxia prevents
hepatocellular regeneration and initiates fibrosis. In severe, long-standing
hepatic congestion, most commonly associated with heart failure,
there may even be grossly evident hepatic fibrosis (cardiac cirrhosis).
On gross examination, the liver has a “nutmeg” appearance
owing to contrasting reddish (hemorrhagic) centrilobular regions
and yellowish portal regions.
The hepatic changes of congestive hepatopathy may present clinically
with present with hepatomegaly, ascites, jaundice, and abdominal
pain caused by stretching of the liver capsule. Abnormalities of
liver function are generally mild and include elevations of serum
bilirubin, transaminases, alkaline phosphatase, and prothrombin
time.
Patients with passive hepatic congestion may develop a variety
of structural and functional hepatic derangements that can have
distinctive appearances on MRI. The distended IVC and hepatic veins
secondary to increased central venous pressures can be visualized
on cross-sectional imaging. On early dynamic contrast-enhanced MR
images the liver parenchyma can appear inhomogeneous and mottled
with a reticulated-mosaic pattern of low signal intensity contrast
enhancement. Linear and curvilinear regions of low signal intensity
enhancement may be due to delayed enhancement in regions of small
and medium-sized hepatic veins. Larger patchy regions of poor or
delayed enhancement in the periphery of the liver are probably secondary
to the tendency of blood flow to be more stagnant in these regions
in patients with hepatic venous hypertension. Other causes of inhomogeneous
hepatic attenuation on MR images include hepatic venous occlusion
(Budd-Chiari syndrome) and diffuse malignancy. Contrast injected
in a brachial vein may appear earlier in hepatic veins and suprahepatic
IVC than in the portal veins and infrahepatic IVC, reflecting reflux
of contrast from the heart. Non-specific MR findings can include
pleural effusions, pericardial effusions, ascites, cardiomegaly,
and hepatomegaly.
References:
- Semelka, Richard. Abdominal-Pelvic MRI. New York: Wiley-Liss
Inc, 2002. pp. 269, 273-274.
- Cotran RS, Kumar V, and T Collins. Robbins Pathologic Basis
of Disease, 6th Edition. Philadelphia: W.B. Saunders Company,
1999. pp. 116-117.
- Gore RM, Mathieu DG, et al. Passive Hepatic Congestion:
Cross-Sectional Imaging Features. American Journal of Roentgenology.
1994; 162: 71-75.
- Holley HC, Koslin DB, et al. Inhomogeneous Enhancement of
Liver Parenchyma Secondary to Passive Hepatic Congestion: Contrast-Enhanced
CT. Radiology. 1989; 170: 795-800.
- Moulton JS, Miller BL, et al. Passive Hepatic Congestion
in Heart Failure: CT Abnormalities. American Journal of Roentgenology.
1988; 151: 939-942.
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