939

Passive Hepatic Congestion Heart Failure: CT Abnormalities

in

Jonathan S. Moulton1 Bradley L. Miller Gerald D. Dodd III Doan N. Vu

Using

bolus-enhanced

CT, we encountered

an unusual

constellation

of findings

in

seven patients with clinical evidence of right heart failure. These included retrograde hepatic venous opacification on the early bolus scans and a diffusely mottled pattern of hepatic enhancement seen only during the vascular phase of contrast administration.
Ancillary CT findings include cardiomegaly, pleural effusions, ascites, and intrahepatic perivascular radiolucency. We believe that these CT abnormalities are caused by passive

hepatic congestion. This pattern of abnormal hepatic enhancement represents a potential pitfall in the use of dynamic bolus-enhanced CT for the detection of focal hepatic masses. Recognition of passive hepatic congestion as a possible cause of mottled hepatic enhancement on CT may help explain clinical abnormalities of liver function in patients with heart failure and prevent confusion with other disease processes that produce

abnormalities

of hepatic attenuation.

CT with bolus
widely used abnormalities

IV contrast

enhancement

and dynamic

scanning

techniques

is

for the detection of focal of hepatic attenuation

liver lesions [1]. On contrast-enhanced CT, may also be produced by hemodynamic

disturbances,

such as hepatic

venous

thrombosis,

which

affect

the delivery

of

contrast material to the liver [2, 3]. enhancement is important in order to the liven. We encountered a peculiar hepatic of contrast material into the hepatic heart failure and passive congestion patients form the basis of the report.

Recognition of these patterns of abnormal avoid confusion with neoplastic disease within enhancement pattern accompanied by neflux veins in seven patients who had congestive of the liver. The CT findings in these seven

Subjects and Methods

Between June i

987 and March 1988, seven patients

were identified

on the basis of an
for evidence mottled
inferior

unusual constellation of CT findings. The medical records were reviewed congestive heart failure and liver dysfunction. Two primary CT abnormalities were present in all patients: (1) a diffusely
of hepatic enhancement and (2) evidence of retrograde opacification of the

of

pattem
cava

vena

(IVC) and hepatic veins (Figs. 1-3). Diffusely inhomogeneous

hepatic enhancement

was noted

Received May 23, 1988; accepted after revision July 6, 1988. I All authors: Department of Radiology, University Hospital,

45267-0742. Moulton. 0361 -803x/88/1

American

234 Goodman St., Cincinnati, OH Address reprint requests to J. S.

only during the first several minutes of contrast administration, during the phase of maximal vascular enhancement. This inhomogeneous enhancement pattern faded quickly on scans through the inferior aspect of the liver performed after the vascular phase of contrast administration. Delayed postcontrast scans in three patients revealed homogeneous hepatic attenuation. All segments of the liver, including the caudate lobe, were involved.

Reflux of contrast
of these vessels

material into the IVC and hepatic veins was seen as dense opacification
several scans; enhancement of the hepatic parenchyma occurred

on the first

AJR 151:939-942,

November 51 5-0939

1988

only on subsequent scans (Figs. 1 and 2). Additional CT findings included cardiomegaly
pleural effusion in five patients. In two

in all seven
a thin

patients,
rim of

along

with

ascites
was

and
seen

Roentgen

Ray Society

patients,

radiolucency

940

MOULTON

ET AL.

AJR:151,

November1988

scans in 54-year-old woman with and refractory congestive heart failure. A, Early bolus-enhanced scan shows dense retrograde hepatic venous opacification (arrows). LV = left ventricle. B, Scan obtained during vascular phase of bolus enhancement shows diffusely mottled hepatic enhancement. A = ascites. 30-mm delayed CT scan (not shown) revealed homogeneous hepatic attenuation.
ischemic cardiomegaly

Fig. 1.-CT

Fig. 2.-Bolus-enhanced CT scans in 44-yearold woman with severe congestive heart failure, abdominal pain, and jaundice. Autopsy performed 2 weeks after CT scan revealed severe passive hepatic congestion. A, Dense retrograde hepatic

venous opaclfihepatic enhance-

cation (arrow). B, Diffusely inhomogeneous ment.

Fig. 3.-A and B, Bolus-enhanced CT scans in two different patients with chronic right heart failure show diffusely mottled enhancement of liver parenchyma. Pertinent findings on other slices included cardiomegaly, retrograde inferior vena caval and hepatic vein enhancement, and pleural effusions.

surrounding and IVC.

the intrahepatic

portions

of the hepatic and portal veins

signs and symptoms suggested cause of congestive heart failure alcohol-related in three patients. right heart pressure was present

In all seven patients, the clinical chronic congestive heart failure. The was ischemic in four patients and Hemodynamic evidence of elevated

in all four patients

studied

within

patients who were studied with echocardiography

1 month of CT scanning. All six and radionuclide

ventriculography had abnormalities of cardiac function. Liver function tests were obtained in six of the seven patients. All showed mild-tomoderate elevation of serum bilirubin, alkaline phosphatase, and transaminases. Three patients were evaluated for hepatitis-B infection, and all three studies were negative. Pathologic evaluation of the liver was performed in two patients, who died 12 days and 4 months, respectively, after CT scanning.

Gross examination

revealed both livers to have a nutmeg appearance,

AJR:151,

November1988

HEPATIC

CONGESTION

IN HEART

FAILURE

941

consistent

with

passive Minimal

congestion.

Microscopically, infiltration

both

livers

showed centrilobular congestion and necrosis consistent with severe

passive congestion. one patient.
Indications for CT

elevated night heart pressure. The recognition of this finding led us to suspect that the hepatic attenuation differences

centrilobularfatty

was seen in

Four men and three women (age range, 36-79 years) were studied.
scanning included evaluation of possible obstruc-

reflected a hemodynamic megaly, pleural effusions,

of congestive on hepatic heart failure, CT scans

abnormality within the liver. Cardioand ascites are ancillary CT findings

but these findings are nonspecific.

tive jaundice (four patients), new-onset ascites (one patient), fever of unknown origin (one patient), and possible retroperitoneal hemorrhage (one patient). All patients were studied on a GE 9800 CT scanner (Milwaukee, WI) with 1 0-mm contiguous axial sections or

Koslin et al. [5] recently They attributed

described

perivasculan

radiolucency
heart failure.

in patients

with congestive

10-mm

sections

with 20-mm

table incrementation.

Scanning

was

this finding to perivascular lymphedema. We encountered this feature in only two of our seven patients. All seven patients in this series were identified first on the
basis of their CT findings, problem, which were retrospectively corre-

performed during administration

of 150 ml of 60% diatrizoate meg-

lumine via a mechanical injector (Angiomat; Liebel-Flarsheim, Cincinnati, OH). Contrast material was administered through a superficial
vein

lated

with

the clinical

data.

Congestive

heart

failure

is a

in the upper extremity.

Scanning was begun

An initial bolus of 50 ml administered

at the level of the diaphragmatic

at

common failure needed

clinical and

and probably

1 .5 mI/sec was followed by a sustained infusion of 100 ml at 0.7 ml/

sec. dome

a small group

approximately

administration. Routine scan time was 2 sec with an interscan delay of 16 sec. Nine to 1 6 scans were made through the liver in 2.5-4 mm. Delayed scans (1 0-60 mm after contrast administration) were obtained in three patients.

30 sec after the start of contrast

of patients with hepatic venous congestion. Further study is to define the frequency with which such attenuation abnormalities are detected in patients with elevated right heart
pressure, as well as the relationship clinical abnormalities of liver function. of such CT findings to

here we have selected relatively marked right heart

Fatty infiltration
in distribution,

Discussion

attenuation
infiltration

of the liver, although generally more diffuse on occasion lead to a mottled hepatic [6]. Density alterations caused by subtotal fatty
may be evident on all scans and not only during

should

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,
stretching

Liven dysfunction

the period of maximal

contrast

enhancement.

In addition,
passive

the

extent of fatty infiltration that accompanies tion generally is slight. For these reasons,

conges-

that fatty infiltration is responsible seen in our patients.

we do not believe for the density alterations

ascites,

jaundice,

and abdominal

pain caused

by

generally transaminases,

of the liven capsule. Abnormalities of liver function are mild and include elevations of serum bilirubin,
alkaline phosphatase, and pnothrombin time.

Another reported cause of inhomogeneous hepatic attenuation is hepatic venous occlusion (Budd-Chiari syndrome)

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,

[2, 3, 7]. The clinical and pathologic features of Budd-Chiari syndrome are similar to those of passive hepatic congestion [8]. Characteristic CT findings in Budd-Chiari syndrome indude nonvisualization or thrombosis of the hepatic veins and a patchy pattern of hepatic enhancement. Prominent enhancement within the caudate lobe and central portions of the liven, with relatively decreased enhancement peripherally, has been described; this pattern may reverse on delayed scans. These enhancement abnormalities have been attributed to slow on reversed venous outflow. portal flow in regions of impaired

Hepatic venous enhancement was a prominent feature in our patients, in contrast to the lack of venous opaciflcation
seen in Budd-Chiari syndrome. In addition, central
the

the

inhomoge-

neous enhancement
tire liven diffusely,
caudate-lobe asymmetrically sparing. owing

pattern
without
This

described
may reflect

here involved
tendency and

the enon
hefor

prominent

enhancement

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 admin-

patic vein thrombosis

to affect
to variations

various
in the

regions
duration

of the liver
extent

istration 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

of venous occlusion and the development of collaterals [3]. Patients with hepatomegaly and abnormalities of liver function often are evaluated by CT to detect neoplastic disease. Diffuse malignancy is a further diagnostic consideration when inhomogeneous hepatic attenuation is identified. Neoplastic
disease was excluded pathologically

on on clinical

follow-up

in all patients in this series. Liver biopsy or serial CT examinations may be needed to make this distinction in some cases. Furthermore, focal hepatic lesions may be obscured on their

942

MOULTON

ET AL.

AJR:151,

November1988

extent

underestimated

by superimposed

density

alterations

REFERENCES
1 . Zeman RK, Clements

due to hemodynamic abnormalities. If our observations can be corroborated by further study, recognition of this pattern of hepatic enhancement may help

prevailing

methods

LA, Silverman PM, at al. CT of the liver: a survey of for administration of contrast material. AJR

1988;150:107-109

explain clinical abnormalities of liver function in patients with heart failure. More importantly, such hemodynamically related abnormalities of liver enhancement represent a potential pitfall in the use of dynamic-bolus CT for the detection of focal hepatic lesions.

2. Murphy FB, Steinberg HV, Shires GT III, Martin LG, Bernardino ME. 3.

The Budd-Chian syndrome: a review. AJR 1986;147:9-15 Mathieu D, Vasile N, Menu Y, Van Beers B, Lorphalin JM, Pnngot J. Budd-

Chiari syndrome: dynamic CT. Radiology 1987;165:409-413 4. Dunn GD, Hayes P, Breen KJ, Schenker S. The liver in congestive failure: a review. Am J Med Sci 1973;265:174-188

heart

5. Koslin DB, Stanley RJ, Berland LL, Shin MS, Dalton SC. Hepatic perivascular lymphedema: CT appearance.AJR 1988;150:111-113 6. Gale ME, Gerzof SG, Robbins AH. Portal architecture: a differential guide to fatty infiltration of the liver on computed tomography. Gastrointest Radio!

ACKNOWLEDGMENTS The authors thank Joel Lichtenstein helpful suggestions and Donna Propes and Ralph Shipley for their for manuscript preparation.

1983;8:231-236 7. Vogalzang AL, Anschuetz SL, Gore AM. Budd-Chian syndrome: CT observations. Radiology 1987;163:329-333 8. Solano FX, Young E, Talamo TS, Dekker A. Constrictive pencarditis mimicking Budd-Chian syndrome. Am J Med 1986;80:1 13-115