Imaging in Oncology

Imaging in Oncology (Answer)

Answer:

4. passive venous congestion of the liver

Both the precontrasted and postcontrasted CT scans demonstrate diffuse heterogeneity of the liver. While some of the other listed diagnostic options may provide similar findings, the diagnosis of passive venous congestion was supported by the postintravenous contrasted scans through the lower thorax. These views demonstrated delayed transit of the contrast through the right heart as well as a thickened pericardium secondary to infiltration by the mesothelioma (Fig 2). Investigation into the patient's clinical history further supported the final impression. These findings included jugular venous distention without audible precordial gallops, rubs, or clicks. Swan-Ganz catheter measures included right ventricular systolic pressure of 50-52 mmHg, right ventricular end-diastolic blood pressure of 20-25 mmHg, pulmonary arterial pressure of 50/25 mmHg, and a pulmonary wedge pressure of 22-25 mmHg. Echocardiogram showed a thickened pericardium, a distended inferior vena cava (IVC), and findings consistent with an estimated right atrial pressure of 20 mmHg. These findings indicate a constrictive physiology of the heart, and the patient was referred for pericardial stripping.

Liver function tests were normal except for elevated total bilirubin, lactate dehydrogenase, creatine kinase, and prothrombin time/partial thromboplastin time. The serum albumen was low. Similar laboratory values have been described in previously reported cases of passive venous congestion..¹ Overall, these values point away from diffuse hepatoma as well as metastatic disease, which would tend to elevate the other liver enzymes as well. Also, mesothelioma tends to spread contiguously with the pericardium and sometimes the peritoneum so that the likelihood of metastatic lesions in the liver would be low.²

The cause of passive venous congestion of the liver is usually from congestive heart failure or pericardial disease.^1,3,4 The IVC and hepatic veins distend, and the hepatic sinusoids become congested. Compression, atrophy, and necrosis of the centrilobular hepatocytes occur and fatty infiltration may ensue. In chronic cases, fibrosis may develop in the centrilobular regions resulting in cardiac cirrhosis, which has the classic nutmeg appearance on gross examination.³

In passive venous congestion, CT will depict the enlarged IVC and hepatic veins since the failing right atrium cannot accommodate the returning blood. Actually, intravenous contrast administered in the upper body may reflux into the IVC and hepatic veins. As in this case, the liver parenchyma will show an inhomogeneous, mottled, reticulated, or mosaic pattern of enhancement. Linear and curvilinear regions of poor enhancement may be due to delayed enhancement in regions of small- and medium-sized hepatic veins. Larger patchy areas of poor or delayed enhancement near the periphery are probably a manifestation of nearly stagnant blood flow. This appearance may mask small underlying neoplastic lesions and biopsy may be necessary. If the underlying cause is corrected, CT abnormalities may resolve.^1,3

Although cirrhosis can appear with diffuse heterogeneity as well, other findings will most likely be present. Cirrhotic livers will also show either generalized hepatomegaly or specific hypertrophy of the caudate lobe with regression of the right liver lobe. A nodular contour of the liver may also be seen. Focal inhomogeneities of the cirrhotic liver other than hepatomas may include fatty infiltration or areas of sparing or regenerating nodules. Associated findings of subsequent portal venous hypertension (eg, an enlarged portal vein, varices, splenomegaly, and ascites) also may be seen.

Fatty infiltration of the liver can also appear resulting from triglyceride deposition within the hepatocytes. Underlying causes include obesity, corticosteroids, diabetes, malnutrition, total parenteral nutrition, alcohol abuse, chemotherapy, and toxin exposure such as carbon tetrachloride. It appears as focal, geographic, or diffuse areas of hypoattenuation. Liver parenchyma commonly spared from fatty infiltration is found around the portal vein and bifurcation, around the gallbladder fossa, near the falciform ligament, and in the quadrate lobe. Fatty infiltration does not disrupt the path of the normal liver vasculature that traverse through these areas of heterogeneity.

The Budd-Chiari syndrome also demonstrates diffuse heterogeneity similar to passive venous congestion. However, disproportionate enlargement and enhancement of the caudate lobe are common features. Furthermore, the retrohepatic IVC is commonly narrowed secondary to the caudate lobe hypertrophy. In the Budd-Chiari syndrome, hepatic veins are not usually visualized or are seen to contain discrete thrombi on IV enhancement.^1,3

References

1. Holley HC, Koslin DB, Berland LL, et al. Inhomogeneous enhancement of liver parenchyma secondary to passive congestion: contrast-enhanced CT. Radiology. 1989;170:795-800.
2. Antman KH. Natural history and epidemiology of malignant mesothelioma. Chest. 1993;103(suppl 4):373S-376S.
3. Moulton JS, Miller BL, Dodd GD 3d, et al. Passive hepatic congestion in heart failure: CT abnormalities. AJR Am J Roentgenol. 1988;151:939-942.
4. Gore RM, Mathieu DG, White EM, et al. Passive hepatic congestion: cross-sectional imaging features. AJR Am J Roentgenol. 1994;162:71-75.

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