Congestive hepatopathy includes a spectrum of hepatic derangements that can occur in the setting of right-sided heart failure (and its underlying causes). If there is subsequent hepatic fibrosis, the term cardiac cirrhosis may be used. The condition rarely occurs due to non-cardiac causes (e.g. renal arteriovenous malformation).
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Pathology
Etiology
Congestive hepatopathy resulting from passive hepatic congestion is caused by the stasis of blood within the liver parenchyma because of compromised hepatic venous drainage. Prolonged exposure to elevated hepatic venous pressure may lead to liver fibrosis and cirrhosis.
Underlying conditions include 7-9:
congenital heart disease, especially those treated with a Fontan procedure
Markers
If paracentesis is performed, the serum ascites albumin gradient (SAAG) will be equal to or above 1.1 g/dl, consistent with ascites due to portal hypertension. Elevation of total serum bilirubin can occur in up to 70% of patients with congestive hepatopathy 1.
Radiographic features
Most (80%) patients will have hepatomegaly and severe cases have peripheral edema, ascites and/or pleural effusions 7.
Ultrasound
Sonographic findings are generally non-specific when used in isolation but may contribute to a clinical picture when putative cause and effect (i.e. heart failure and liver disease) are shown to co-exist. 2D/B-mode ultrasound may reveal the following features 13:
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cirrhosis with portal hypertension
decreased hepatic size with nodularity and altered echogenicity
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portosystemic shunts
color flow Doppler of the portal vein extending to the hepatic edge may suggest recanalization of the umbilical vein
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venous dilation
left renal vein diameter >1.5 cm
portal vein diameter >1.3 cm
superior mesenteric vein >1.0 cm
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cardiac chamber enlargement and/or dysfunction
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left ventricular systolic or diastolic dysfunction
decreased cardiac index
right and/or left atrial enlargement
valvular stenosis or regurgitation
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dilated (>2.1 cm) inferior vena cava
more specific for elevated filling pressures when lacking respiratory variation (<50%)
elevated filling pressures in the absence of structural cardiac disease may (rarely) imply constrictive pericarditis
Doppler studies may demonstrate:
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increased hepatic arterial resistance (RI >0.7)
resistive index (RI) generally between 0.55 and 0.7
this change may be obfuscated by portal hypertension-related shunting, which classically results in a decreased RI
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pulsatility of the hepatic venous Doppler waveform
prominent a wave and v wave
tricuspid regurgitation may diminish or reverse the S wave
pure right ventricular dysfunction will have a preserved S/D relationship with the amplitude of the S wave > D wave
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elevated cardiac filling pressures
pulsed-wave Doppler of the tricuspid regurgitant jet showing an elevated right ventricular systolic pressure (RVSP)
pulsed wave doppler of the right upper pulmonary vein showing high-velocity AR (atrial reversal) waves with low S/D ratio
pulsed wave doppler of the mitral valve inflow showing restrictive filling
CT
reticular enhancement pattern, similar to nutmeg liver in Budd-Chiari syndrome 10
zonal enhancement pattern
arterial-enhancing (i.e. hypervascular) nodules, which may represent focal nodular hyperplasia (more commonly) or hepatocellular carcinoma (especially in the setting of cirrhosis) 8,10
reflux of intravenous contrast into the IVC and hepatic veins 12
Differential diagnosis
For CT appearances of a nutmeg liver, consider:
hepatic veno-occlusive disease (sinusoidal obstruction syndrome)
shunting through vascular malformations - e.g. hereditary hemorrhagic telangiectasia 17
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