Passive hepatic congestion, also known as congested liver in cardiac disease or congestive hepatopathy, describes the stasis of blood in the hepatic parenchyma due to impaired hepatic venous drainage, which leads to the dilation of central hepatic veins and hepatomegaly. If there is subsequent hepatic fibrosis, cardiac cirrhosis may develop. Passive hepatic congestion is a well-studied result of acute or chronic right heart failure.

Clinical presentation

Symptoms of right heart failure dominate the clinical findings in these patients. Mild right upper quadrant abdominal pain has been reported to be the result of hepatomegaly and stretching of the hepatic Glisson capsule ¹. Asymptomatic elevation of serum liver enzymes may also occur ⁴. 

Pathology

Elevated hepatic venous pressure and decreased hepatic venous flow cause hypoxia in hepatic parenchyma and eventual diffuse hepatocyte death and fibrosis. This results in micronodular cirrhosis, indistinguishable from cirrhosis produced by other causes ².

Aetiology

All forms of heart disease (congenital or acquired) are linked to passive hepatic congestion. 

Most common causes of passive hepatic congestion ^4-7:

• congestive heart failure

• restrictive cardiomyopathy

• constrictive pericarditis

• right-sided valvular disease involving the tricuspid or pulmonary valve

• pulmonary-related right heart failure, e.g. pulmonary hypertension

• congenital heart disease, especially those treated with a Fontan procedure

Radiographic features

Most (80%) patients will have hepatomegaly and severe cases have peripheral oedema, ascites and/or pleural effusions ⁵.

Ultrasound

Early in the course of the disease, the main abnormality is enlargement of the right hepatic lobe. Normally the right hepatic vein measures <6 mm and, in these patients, its mean is ~9 mm ^ref. 

• real-time B-Mode

  • hepatomegaly +/- cirrhosis +/- findings of portal hypertension ^ref

  • dilated (>2.1 cm) inferior vena cava ^ref

    • 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

  • dilated hepatic veins ^ref

    • normal: 5.6 to 6.2 mm

    • mean diameter: 8.8 mm (in passive congestion) 

    • increases up to 13 mm with pericardial effusion

• colour Doppler

  • spectral velocity pattern (lVC and hepatic veins)

    • loss of normal triphasic flow pattern

    • spectral signal may have an "M" shape

    • flattening of Doppler waveform in hepatic veins

    • to-and-fro motion in hepatic veins and IVC

• 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

• 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

• spectral velocity pattern (portal vein)

  • increased pulsatility of the portal venous Doppler signal

• cardiac chamber enlargement and/or dysfunction

  • left ventricular systolic or diastolic dysfunction

    • decreased cardiac index

  • right ventricular dysfunction

  • right and/or left atrial enlargement

  • pleural effusion

  • valvular stenosis or regurgitation

• sonographic pulmonary oedema

CT

• early enhancement of dilated IVC and hepatic veins due to contrast reflux from the right atrium into IVC ⁹

• heterogeneous, mottled and reticulated mosaic parenchymal pattern with areas of poor enhancement, similar to nutmeg liver in Budd-Chiari syndrome ⁸

• peripheral large patchy areas of poor/delayed enhancement

• periportal low attenuation (perivascular lymphoedema) 

• arterial-enhancing (i.e. hypervascular) nodules, which may represent focal nodular hyperplasia (more commonly) or hepatocellular carcinoma (especially in the setting of cirrhosis) ^7,8

• ascites

• hepatomegaly

Chest images may show cardiomegaly and pericardial and pleural effusion ⁴. 

MRI

Macroscopically CT and MRI are able to depict cirrhotic changes as non-specific findings.

• T1 C+ (Gd)

  • liver enhancement pattern: reticulated mosaic pattern of low signal intensity linear markings which become more homogenous in 1-2 minutes.

  • hepatic veins and suprahepatic IVC: early enhancement due to reflux from the atrium 

  • portal vein: diminished, delayed or absent enhancement

• fast low-angle shot (FLASH) contrast-enhanced MRI: early reflux of contrast into dilated hepatic veins and IVC

• T2: periportal high signal intensity (periportal oedema) 

• MR angiography: slow or absent antegrade flow within IVC

Differential diagnosis

General imaging differential considerations include ^ref:

• Budd Chiari syndrome

• acute viral hepatitis

• hepatic veno-occlusive disease

• portal venous emboli

• shunting through vascular malformations, e.g. hereditary haemorrhagic telangiectasia

See also

• congestive hepatopathy