Passive hepatic congestion is caused by stasis of blood within the liver parenchyma due to compromise of hepatic venous drainage.

It is a common complication of congestive heart failure and constrictive pericarditis, wherein elevated central venous pressure is directly transmitted from the right atrium to the hepatic veins because of their close anatomic relationship (Fig. 1). The liver becomes tensely swollen as the hepatic sinusoids dilate and engorge to accommodate the backflow of blood. A variety of structural and functional hepatic derangements develop that have distinctive appearances on sonograms, CT scans, and MR images. Pathophysiology Hepatocytes are highly sensitive to even short periods of ischemic trauma and can be injured by a variety of cardiacinduced circulatory derangements, including arterial hypoxia, acute left-sided heart failure with a fall in cardiac output, and central venous hypertension [1]. In acute might-sided heart failure, the hepatic veins distend and the sinusoids become congested because of stasis of blood. Compression, atrophy, and necrosis of centrilobulam hepatocytes occur to a variable degree, and mild centrilobulam fatty infiltration may ensue. In chronic passive congestion, persistent hypoxia prevents hepatocellulam regeneration and causes fibrous tissue bands from adjoining centrilobulam areas to join and encircle relatively normal portal tracts, eventually leading to the development of cardiac cirrhosis. Hepatic Venous and Inferior Vena Caval Reflux When a bolus of contrast material injected IV reaches the failing might atrium, it may flow directly into the inferior vena cava and hepatic veins rather than flow normally into the might ventricle [3]. The elevated central venous pressure permits retrograde opacification and enhancement of the infenor vena cava and hepatic veins on contrast-enhanced CT scans (Fig. 3A) and gradient-echo MR images (Fig. 3B). Increased Portal Venous Pulsatility Normal portal venous flow seen on Doppler sonograms is rather steady and continuous except for a mild increase during expiration (Fig. 4A). In patients with passive hepatic congestion, the energy of the elevated pressure from the right atrium and hepatic veins is transmitted directly via the dilated hepatic sinusoids into the portal vein. This causes portal venous blood flow to become pulsatile because the liver no longer prevents changes in central venous pressure from reaching the portal circulation [4, 5] (Fig. 4B). Abnormal pulsations in the portal vein are also observed in patients with tricuspid regurgitation (Fig. 4C). The valvulam leak may cause an increase in the vascular impedance of the portal circulation at the presinusoidal level, particularly during ventricular end systole. This can impede the antegrade flow of blood in the portal vein, leading to monophasic antegrade flow with a peak velocity in ventricular diastole and gradual diminution of velocity throughout ventricular systole or even reversed flow in ventricular systole [6]. These patterns of portal flow are characteristic of severe tricuspid insufficiency and suggestive of congestive heart failure [6].

Liven dysfunction In the setting of congestive heart failure is thought to result from a combination of decreased hepatic blood flow, elevated hepatic venous pressure, and diminished arterial oxygen content [4]. The net effect is hepatocellulan hypoxia. Hepatic changes are manifested clinically as hepatomegaly, ascites, jaundice, and abdominal pain caused by stretching of the liven capsule. Abnormalities of liver function generally are mild and include elevations of serum bilirubin, transaminases, alkaline phosphatase, and pnothrombin time. On gross examination, the liven has a nutmeg appearance owing to contrasting reddish (hemorrhagic) centnilobular regions and yellowish portal regions. Microscopic changes indude variable degrees of compression, atrophy, and necrosis of centrilobular hepatocytes with engongement of adjacent sinusoids. Mild centrilobular fatty infiltration is often seen but is minimal in degree and not a prominent feature. To our knowledge, this abnormal hepatic enhancement on CT has not been reported previously. All seven patients showed a pattern of mottled parenchymal attenuation identifled only during the vascular phase of bolus contrast administration. We speculate that the underlying cause of the CT abnormalities is an alteration in intrahepatic hemodynamics. Hepatic venous outflow is impaired in passive congestion, producing relative stasis of blood in hepatic sinusoids. This, in turn, may impede antegrade blood flow from the portal and hepatic arterial circulation and delay uniform enhancement of the liver. The relative roles of arterial and portal flow are uncertain. With time, more complete hepatic perfusion and extravasculan equilibration would diminish the mottled appearance. Only with rapid scanning and bolus contrast administration can this transient inhomogeneity in hepatic attenuation be shown. Further study is needed to better elucidate the mechanisms that account for these CT findings. Retrograde hepatic venous opacification on the initial bolus scans is also a transient finding that we consider indicative of elevated night heart pressure. The recognition of this finding led us to suspect that the hepatic attenuation differences reflected a hemodynamic abnormality within the liver. Cardiomegaly, pleural effusions, and ascites are ancillary CT findings of congestive heart failure, but these findings are nonspecific. Congestive heart failure is acommon clinical problem, and probably here we have selected a small group of patients with relatively marked right heart failure and hepatic venous congestion. Further study is needed to define the frequency with which such attenuation abnormalities are detected in patients with elevated right heart pressure, as well as the relationship of such CT findings to clinical abnormalities of liver function. Fatty infiltration of the liver, although generally more diffuse in distribution, may on occasion lead to a mottled hepatic attenuation [6]. Density alterations caused by subtotal fatty infiltration should be evident on all scans and not only during the period of maximal contrast enhancement. In addition, the extent of fatty infiltration that accompanies passive congestion generally is slight.