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Original Report |
1
Department of Radiology, University of Pittsburgh Medical Center, 200 Lothrop
St., Pittsburgh, PA 15213-2582.
2
Department of Pathology, University of Pittsburgh Medical Center, Pittsburgh,
PA 15213-2582.
Received January 6, 2000;
accepted after revision March 16, 2000.
Address correspondence to R. L. Baron.
Abstract
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CONCLUSION. Infarcted regenerative nodules exhibit a spectrum of imaging appearances in the cirrhotic liver and can resemble hypovascular hepatocellular carcinoma or other neoplasms on CT and MR imaging. Although uncommon, this abnormality must be included in the differential diagnosis of focal liver lesions in patients with cirrhosis, particularly in patients with a history of substantial gastrointestinal bleeding. Serial imaging may help differentiate these lesions from malignant tumors.
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Because these lesions are rarely found in stable patients, little information about infarcted regenerative nodules has been published in the imaging literature. However, in our experience, infarcted regenerative nodules can cause focal abnormalities in stable patients on CT and MR imaging that can be confused with neoplasms in cirrhotic patients. We reviewed the CT scans and MR images of five patients pathologically diagnosed with infarcted regenerative nodules. Then we correlated the pathologic findings with the imaging findings to better understand the spectrum of imaging findings in patients with these lesions.
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All five patients underwent CT of the liver for preoperative examination 3-90 days (mean, 44 days) before transplantation. All CT examinations were performed with and without contrast enhancement using 150 mL of iothalamate meglumine (Conray-60; Mallinckrodt Medical, St. Louis, MO) injected at a rate of 2.5-5.0 mL/sec. Unenhanced and helical biphasic (arterial and portal venous phases) contrast-enhanced imaging was performed in four patients using a 7-mm collimation, a 1:1 pitch, and scanning delays of 28 sec (arterial venous phase) and 60-70 sec (portal venous phase) after the infusion of contrast material. In one patient, unenhanced and contrast-enhanced CT scans were incrementally obtained at 7-mm intervals, with a 5-mm collimation and a 60-sec delay in imaging after the infusion of contrast material.
Two patients underwent MR imaging of the liver to exclude the possibility of malignancy; these examinations were performed 6 and 13 days before liver transplantation. MR examinations were performed on a 1.5-T scanner (Signa; General Electric Medical Systems, Milwaukee, WI). Unenhanced T1-weighted spin-echo (TR/TE, 533/12), T2-weighted spin-echo (2900/70) or fast spin-echo (4000/120; echo train length, 12), dynamic contrast-enhanced gradient-echo, and contrast-enhanced T1-weighted spin-echo images were obtained in the axial plane. Dynamic contrast-enhanced gradient-echo imaging was performed with a fast fractional-echo spoiled gradient-echo sequence (9.9/2.5; flip angle, 30°) with multisection sequential acquisition before and after IV injection of 0.1 mmol/kg of gadopentetate dimeglumine (Magnevist; Berlex Laboratories, Wayne, NJ) or gadoteridol (Prohance; Squibb Diagnostics, Princeton, NJ). Dynamic images were obtained through the liver every 20 sec until 180 sec after the injection of contrast material. After dynamic imaging, delayed contrast-enhanced T1-weighted spin-echo images were obtained at approximately 5 min.
After liver transplantation, all livers were sectioned in the axial plane at approximately 1-cm intervals to correlate imaging findings with underlying abnormalities and to determine where to obtain histologic specimens. Macroscopic and microscopic findings were recorded and compared with imaging findings. All CT and MR images were reviewed by all authors, and a consensus determination of the description of lesion characteristics was made.
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Histologic evaluation revealed infarcted nodules to be commonly characterized by a central core of amorphous eosinophilic material that represented the remnants of necrotic hepatocytes and other cellular elements. Cells with foamy cytoplasm, likely representing macrophages, variably surrounded the necrotic core. Early fibroplasia could be seen peripheral to the macrophages. In some patients, an element of vascular ingrowth was also identified at the peripheries of the lesions. Infarcted nodules were seen in both single and multiple forms. In some patients, multiple infarcted nodules coalesced to form a single necrotic area, whereas in other patients, several necrotic nodules were seen in close proximity to each other. This latter form could exist in a fibrous background, suggesting that prior necrosis and the collapse of nodules had occurred, with ultimate replacement by fibrovascular tissue. These composite structures could reach macroscopic dimensions.
Imaging Findings
CT scans revealed lesions proven to be infarcted regenerative nodules in
three patients and did not reveal infarcted nodules in two patients. Six
infarcted regenerative nodules were identified on CT in three patients. The
lesions not depicted on CT were smaller than 6 mm in diameter at pathologic
analysis. On CT, the focal lesions of infarcted regenerative nodules were
depicted as single oval nodular lesions measuring 1.5 or 2.0 cm in maximum
diameter in two patients. The third patient had multiple lesions consisting of
a large mass measuring 6 cm in diameter and three other nodular lesions
measuring 0.5-1.5 cm in diameter. Unenhanced CT revealed four lesions of
infarcted regenerative nodules that were larger than 1 cm in diameter as
hypoattenuation compared with liver parenchyma (Figs.
1A,1B,1C,1D,1E,1F,1G,1H,1I,2A,2B,2C,3A,3B,3C)
(two lesions of 0.5 cm in diameter were not visible). The large lesion
measuring 6 cm in diameter showed a bulging liver contour suggestive of mass
effect (Fig.
3A,3B,3C).
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The appearance of lesions on contrast-enhanced CT was variable. The central portion of one lesion revealed enhancement that was isoattenuating compared with surrounding liver parenchyma, whereas its peripheral portion appeared hypoattenuating on both arterial and portal venous phase helical contrast-enhanced CT scans (Fig. 1A,1B,1C,1D,1E,1F,1G,1H,1I). One lesion was homogeneously hypoattenuating on arterial phase helical CT, and although this pattern persisted in the center of the lesion during portal venous phase imaging, the periphery of the lesion showed enhancement similar to surrounding liver parenchyma (Fig. 2A,2B,2C). Two lesions showed heterogeneous patchy enhancement, consisting of iso- and hypoattenuating regions compared with surrounding liver parenchyma (Fig. 3A,3B,3C). Two small lesions measuring 0.5 cm in diameter that were not depicted on unenhanced CT were seen as homogeneously hypoattenuating nodular lesions on conventional contrast-enhanced CT.
Lesions that were isoenhancing compared with surrounding liver parenchyma on portal venous phase CT or conventional contrast-enhanced CT scans were histologically consistent with retained viable tissues or fibrotic tissues with revascularization. Conversely, the components that were hypoattenuating on CT were in regions of necrotic tissues, hemorrhage, or fibrous tissues with no or minimum revascularization on histologic analysis (Fig. 1A,1B,1C,1D,1E,1F,1G,1H,1I).
MR imaging in two patients depicted only one lesion (Fig. 1A,1B,1C,1D,1E,1F,1G,1H,1I), with one lesion measuring less than 6 mm in size not visible. The visible lesion revealed moderate hyperintensity compared with liver parenchyma on T2-weighted images, corresponding to the single lesion seen on CT and found at pathologic analysis (Fig. 1A,1B,1C,1D,1E,1F,1G,1H,1I). The lesion was not depicted on T1-weighted MR images, appearing isointense compared with the surrounding liver parenchyma. Dynamic gradient-echo MR images depicted the lesion as hypointense to liver parenchyma during arterial and portal venous phases. Delayed contrast-enhanced T1-weighted spin-echo MR images showed enhancement of the central portion of the lesion to the same degree as the surrounding liver parenchyma (the same was shown on CT), findings that correlate with the central retained viable tissues and revascularization seen histologically (Fig. 1A,1B,1C,1D,1E,1F,1G,1H,1I).
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On unenhanced CT, typical regenerative nodules in cirrhosis are either not visible or appear with higher attenuation than adjacent parenchyma when containing iron [5]. Such nodules are usually not visible on contrast-enhanced CT scans and appear isoattenuating to enhanced surrounding liver parenchyma. Similarly, it is only the siderotic regenerative nodules that are visible as hypointense lesions on T2-weighted MR images [6, 7]. In our study, the lesions of infarcted regenerative nodules were depicted as different-appearing nodular lesions of low attenuation on unenhanced CT and as heterogeneous enhancement with regions of iso- and hypoattenuation relative to the surrounding liver on contrast-enhanced CT scans. The MR imaging appearance of one lesion was different from that of regenerating nodules, showing high signal intensity on T2-weighted spin-echo MR images. Thus, these lesions can have different findings in cirrhotic livers and can be mistaken for malignancy.
On histologic analysis, infarcted regenerative nodules showed coagulation necrosis with a variable degree of autolysis, retaining ghostlike features of the components of regenerative nodules. These findings are frequently associated with variable reactive changes such as hemorrhage, congestion, inflammatory changes, or immature granulation tissue [2]. By comparing the pathologic findings with the imaging findings in our patients, we found that the variable imaging appearances of infarcted regenerative nodules closely correlated with histologic changes. The hypoattenuating zones within the nodules on imaging corresponded to the zones of necrotic tissue and old hemorrhage on histologic analysis. Although fibrosis can appear hypoattenuating on arterial phase imaging, it often can retain contrast material on delayed images. Furthermore, small blood vessel formation within zones of fibrosis can lead to enhancement on imaging (Fig. 1H). Central portions of tissue that have escaped necrosis can remain viable and show zones of enhancement (Figs. 1B, 1C, and 1F). Although none of our patients underwent temporal imaging, these correlations of imaging and pathology suggest that imaging appearances of infarcted regenerative nodules change as histologic findings evolve.
The single case report by Fukui et al. [4] referred to imaging findings of infarcted regenerative nodules as being potentially similar to those of hepatocellular carcinoma. The findings in that study confirm that infarcted regenerative nodules can simulate a variety of tumors. Although on arterial phase CT many hepatocellular carcinomas are hypervascular and show dense enhancement, a substantial number of them will be hypovascular and appear iso- or hypoattenuating on arterial phase imaging [8, 9]. Similarly, on portal venous phase CT, hepatocellular carcinoma often appears either iso- or hypoattenuating compared with the liver [8, 9], duplicating the findings revealed in our study. Moreover, multiple focal lesions of infarcted regenerative nodules can occur in a liver as shown in one of our patients (Fig. 3A,3B,3C), and these multiple lesions can resemble multifocal hepatocellular carcinoma or diffuse metastatic disease. MR imaging is not helpful for differentiating malignancies from infarcted regenerative nodules as shown by Fukui et al. [4] and by one of our patients in whom infarcted regenerative nodules were depicted as nodular lesions of hyperintensity on T2-weighted MR images (Fig. 1A,1B,1C,1D,1E,1F,1G,1H,1I). It is imperative when considering treatment options for patients with cirrhosis that benign conditions that can simulate malignancy be considered before denying a patient a treatment option such as transplantation. An awareness of the entity of infarcted regenerating nodules becomes important in such scenarios.
In summary, infarcted regenerative nodules represent an uncommon but important abnormality. These lesions have a spectrum of imaging appearances that correlates with underlying pathologic changes. Although it may be impossible to differentiate these lesions from malignancy on the basis of imaging findings alone, radiologists must be familiar with these lesions as alternative diagnoses to malignancy in the appropriate clinical setting.
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