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Chemoembolization of Hepatic Neoplasms: Safety, Complications, and When to Worry

Julia Gates, MD1, George G. Hartnell, FRCR1, Keith E. Stuart, MD2 and Melvin E. Clouse, MD1

1 Departments of Radiology (J.G., G.G.H., M.E.C.)
2 Medical Oncology (K.E.S.), Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass.



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Figure 1.  Contrast material–enhanced CT scan shows rupture of the liver (open arrow) with extensive omental tumor (solid arrows). The patient was referred for chemoembolization despite a similar appearance at CT a few weeks earlier. This patient is not suitable for chemoembolization because the risk of worsening liver rupture with potential for extravasation is very high.

 


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Figure 2. Figures 2, 3. (2) Selective superior mesenteric arteriogram shows filling of a replaced right hepatic artery (arrow) that supplies an HCC in the right lobe of the liver. (3) Selective celiac arteriogram shows a left hepatic artery (solid arrow) that arises from the origin of the left gastric artery (open arrow). To ensure safe chemoembolization without embolization of the left gastric artery, it was necessary to use a microcatheter to access the aberrant left hepatic artery to selectively deliver chemoembolization material.

 


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Figure 3. Figures 2, 3. (2) Selective superior mesenteric arteriogram shows filling of a replaced right hepatic artery (arrow) that supplies an HCC in the right lobe of the liver. (3) Selective celiac arteriogram shows a left hepatic artery (solid arrow) that arises from the origin of the left gastric artery (open arrow). To ensure safe chemoembolization without embolization of the left gastric artery, it was necessary to use a microcatheter to access the aberrant left hepatic artery to selectively deliver chemoembolization material.

 


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Figure 4a.  (a) Selective proper hepatic arteriogram shows a vascular blush (*), which represents an HCC close to the dome of the liver; the HCC is supplied by a branch of the right hepatic artery. An attempt to select this vessel by using a 5-F Cobra (C2) catheter and a hydrophilic guide wire was successful but produced intense spasm. (b) Selective proper hepatic arteriogram obtained after injection of vasodilators (papaverine hydrochloride and nitroglycerin) shows persistence of the spasm (arrows). (c) Selective proper hepatic arteriogram obtained after recannulation of the vessel affected by spasm with a microcatheter and injection of vasodilators shows resolution of the spasm. (d) Angiogram obtained at the end of the procedure shows chemoembolization material well distributed throughout the tumor (*) and gelatin sponge powder in the feeding artery (arrow).

 


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Figure 4b.  (a) Selective proper hepatic arteriogram shows a vascular blush (*), which represents an HCC close to the dome of the liver; the HCC is supplied by a branch of the right hepatic artery. An attempt to select this vessel by using a 5-F Cobra (C2) catheter and a hydrophilic guide wire was successful but produced intense spasm. (b) Selective proper hepatic arteriogram obtained after injection of vasodilators (papaverine hydrochloride and nitroglycerin) shows persistence of the spasm (arrows). (c) Selective proper hepatic arteriogram obtained after recannulation of the vessel affected by spasm with a microcatheter and injection of vasodilators shows resolution of the spasm. (d) Angiogram obtained at the end of the procedure shows chemoembolization material well distributed throughout the tumor (*) and gelatin sponge powder in the feeding artery (arrow).

 


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Figure 4c.  (a) Selective proper hepatic arteriogram shows a vascular blush (*), which represents an HCC close to the dome of the liver; the HCC is supplied by a branch of the right hepatic artery. An attempt to select this vessel by using a 5-F Cobra (C2) catheter and a hydrophilic guide wire was successful but produced intense spasm. (b) Selective proper hepatic arteriogram obtained after injection of vasodilators (papaverine hydrochloride and nitroglycerin) shows persistence of the spasm (arrows). (c) Selective proper hepatic arteriogram obtained after recannulation of the vessel affected by spasm with a microcatheter and injection of vasodilators shows resolution of the spasm. (d) Angiogram obtained at the end of the procedure shows chemoembolization material well distributed throughout the tumor (*) and gelatin sponge powder in the feeding artery (arrow).

 


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Figure 4d.  (a) Selective proper hepatic arteriogram shows a vascular blush (*), which represents an HCC close to the dome of the liver; the HCC is supplied by a branch of the right hepatic artery. An attempt to select this vessel by using a 5-F Cobra (C2) catheter and a hydrophilic guide wire was successful but produced intense spasm. (b) Selective proper hepatic arteriogram obtained after injection of vasodilators (papaverine hydrochloride and nitroglycerin) shows persistence of the spasm (arrows). (c) Selective proper hepatic arteriogram obtained after recannulation of the vessel affected by spasm with a microcatheter and injection of vasodilators shows resolution of the spasm. (d) Angiogram obtained at the end of the procedure shows chemoembolization material well distributed throughout the tumor (*) and gelatin sponge powder in the feeding artery (arrow).

 


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Figure 5a.  (a) Selective renal arteriogram obtained after several chemoembolization treatments for metastases from a neuroendocrine tumor shows small parasitic arteries (arrows) arising from the right kidney and leading to hepatic artery branches in the right lobe of the liver. (b) Aortogram shows that it would be very difficult to embolize the small parasitic arteries without jeopardizing a large segment of the right kidney; hence, these arteries were not treated at this time.

 


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Figure 5b.  (a) Selective renal arteriogram obtained after several chemoembolization treatments for metastases from a neuroendocrine tumor shows small parasitic arteries (arrows) arising from the right kidney and leading to hepatic artery branches in the right lobe of the liver. (b) Aortogram shows that it would be very difficult to embolize the small parasitic arteries without jeopardizing a large segment of the right kidney; hence, these arteries were not treated at this time.

 


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Figure 6.  Nonenhanced CT scan of a patient with metastases from an islet cell tumor shows ethiodized oil (arrows) in the mesentery. The image was acquired 1 day after chemoembolization with one-third of the conventional dose of multiple parasitic arteries that arose from gastroepiploic and gastroduodenal artery branches. There were no adverse consequences of this procedure.

 


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Figure 7.  Venous-phase image from superior mesenteric arteriography in a patient with portal hypertension and HCC shows hepatofugal flow through a large pelvic portosystemic shunt (arrow).

 


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Figure 8.  Nonenhanced CT scan shows occult portal vein invasion by the tumor as the thread and streak sign (arrowheads).

 


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Figure 9.  Nonenhanced CT scan obtained 1 day after chemoembolization shows hyperattenuating ethiodized oil (arrow) in the collapsed lower lobe of the right lung. This finding caused no significant problems.

 


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Figure 10.  Nonenhanced CT scan obtained 1 day after chemoembolization shows bilateral deposition of ethiodized oil in the lung and pleura (arrows) with the most marked deposition in the left lung. There were no symptoms due to this finding.

 


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Figure 11.  Nonenhanced CT scan obtained after chemoembolization shows ethiodized oil in the stomach (straight solid arrow), duodenum (curved arrow), and pancreas (open arrow). Nonenhanced CT performed 1 month later showed that the extrahepatic ethiodized oil had almost disappeared. There were no adverse consequences of this extrahepatic embolization.

 


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Figure 12. Figures 12–14. (12) Nonenhanced CT scan shows gastric deposition of chemoembolization material with ethiodized oil (arrows) following the line of the gastric mucosa. (13) Nonenhanced CT scan shows calcification of the gastric wall (arrow). The calcification was caused by radiation therapy for renal cell carcinoma many years earlier. (14) Nonenhanced CT scan shows hyperattenuating areas in the lumen of the stomach due to ingestion of milk of magnesia (arrow).

 


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Figure 13. Figures 12–14. (12) Nonenhanced CT scan shows gastric deposition of chemoembolization material with ethiodized oil (arrows) following the line of the gastric mucosa. (13) Nonenhanced CT scan shows calcification of the gastric wall (arrow). The calcification was caused by radiation therapy for renal cell carcinoma many years earlier. (14) Nonenhanced CT scan shows hyperattenuating areas in the lumen of the stomach due to ingestion of milk of magnesia (arrow).

 


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Figure 14. Figures 12–14. (12) Nonenhanced CT scan shows gastric deposition of chemoembolization material with ethiodized oil (arrows) following the line of the gastric mucosa. (13) Nonenhanced CT scan shows calcification of the gastric wall (arrow). The calcification was caused by radiation therapy for renal cell carcinoma many years earlier. (14) Nonenhanced CT scan shows hyperattenuating areas in the lumen of the stomach due to ingestion of milk of magnesia (arrow).

 


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Figure 15. Figures 15, 16. (15) Nonenhanced CT scan shows diffuse gallbladder uptake of chemoembolization material (arrows) in a patient with HCC. There were no symptoms from the gallbladder uptake. (16) Nonenhanced CT scan shows changes due to emphysematous cholecystitis (arrows indicate gas in the wall of the gallbladder). Only a little ethiodized oil is present. The patient had no symptoms beyond those normally expected after chemoembolization. He was treated with antibiotics, recovered, and did not require cholecystectomy.

 


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Figure 16. Figures 15, 16. (15) Nonenhanced CT scan shows diffuse gallbladder uptake of chemoembolization material (arrows) in a patient with HCC. There were no symptoms from the gallbladder uptake. (16) Nonenhanced CT scan shows changes due to emphysematous cholecystitis (arrows indicate gas in the wall of the gallbladder). Only a little ethiodized oil is present. The patient had no symptoms beyond those normally expected after chemoembolization. He was treated with antibiotics, recovered, and did not require cholecystectomy.

 


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Figure 17a.  (a) Hepatic arteriogram obtained before chemoembolization shows two cystic arteries (arrows); the gallbladder is well demonstrated. A nonenhanced CT scan obtained 24 hours after chemoembolization (not shown) showed a normal gallbladder. (b) Nonenhanced CT scan obtained 3 weeks later, when the patient presented with right upper quadrant pain, fever, and general malaise, shows gas in the wall and lumen of the gallbladder (arrows). These changes of emphysematous cholecystitis were confirmed at cholecystectomy. Ethiodized oil was found at histologic analysis of the gallbladder.

 


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Figure 17b.  (a) Hepatic arteriogram obtained before chemoembolization shows two cystic arteries (arrows); the gallbladder is well demonstrated. A nonenhanced CT scan obtained 24 hours after chemoembolization (not shown) showed a normal gallbladder. (b) Nonenhanced CT scan obtained 3 weeks later, when the patient presented with right upper quadrant pain, fever, and general malaise, shows gas in the wall and lumen of the gallbladder (arrows). These changes of emphysematous cholecystitis were confirmed at cholecystectomy. Ethiodized oil was found at histologic analysis of the gallbladder.

 


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Figure 18a.  (a) Nonenhanced CT scan obtained 1 day after chemoembolization shows ethiodized oil in an anterior segment of the spleen (arrow). There were no symptoms. (b) Nonenhanced CT scan obtained more than 1 year later shows a hypoattenuating area (A) that corresponds to a splenic infarction. The patient had no symptoms related to the spleen throughout this period. Interval development of ascites and varices adjacent to the spleen is also evident.

 


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Figure 18b.  (a) Nonenhanced CT scan obtained 1 day after chemoembolization shows ethiodized oil in an anterior segment of the spleen (arrow). There were no symptoms. (b) Nonenhanced CT scan obtained more than 1 year later shows a hypoattenuating area (A) that corresponds to a splenic infarction. The patient had no symptoms related to the spleen throughout this period. Interval development of ascites and varices adjacent to the spleen is also evident.

 


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Figure 19a.  (a) Contrast-enhanced CT scan obtained immediately before chemoembolization shows multiple hypoattenuating tumors (arrows) in a smooth right lobe of the liver. (b) Nonenhanced CT scan obtained 4 months after right lobe chemoembolization and immediately after left lobe chemoembolization shows that the right lobe has an irregular surface, which represents pseudocirrhosis.

 


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Figure 19b.  (a) Contrast-enhanced CT scan obtained immediately before chemoembolization shows multiple hypoattenuating tumors (arrows) in a smooth right lobe of the liver. (b) Nonenhanced CT scan obtained 4 months after right lobe chemoembolization and immediately after left lobe chemoembolization shows that the right lobe has an irregular surface, which represents pseudocirrhosis.

 


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Figure 20.  Nonenhanced CT scan obtained immediately after chemoembolization of the right hepatic lobe shows small collections of gas (arrows) surrounded by deposits of ethiodized oil.

 


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Figure 21a.  (a) Nonenhanced CT scan obtained immediately after chemoembolization of the right hepatic lobe shows no evidence of infarction. (b) Nonenhanced CT scan obtained 1 month later shows extensive gas (arrows) in the treated tumor due to liver infarction and abscess formation.

 


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Figure 21b.  (a) Nonenhanced CT scan obtained immediately after chemoembolization of the right hepatic lobe shows no evidence of infarction. (b) Nonenhanced CT scan obtained 1 month later shows extensive gas (arrows) in the treated tumor due to liver infarction and abscess formation.

 


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Figure 22.  Nonenhanced CT scan obtained 1 day after chemoembolization of metastases from adenocarcinoma shows a huge amount of ascites (A) and contrast material in the liver and kidneys. The patient, who had moderate liver and renal dysfunction, underwent the procedure with a full understanding of the risks involved. There is no excretion of contrast material due to the severe renal failure resulting from worsening hepatorenal syndrome. Note the right renal infarction (arrow).

 


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Figure 23.  Nonenhanced CT scan obtained several days after chemoembolization for HCC shows liver rupture with liquefied liver spreading into the peritoneal space. It is unclear whether the rupture was directly due to chemoembolization because the rupture is adjacent to but not at the area treated. Note the small amount of gas in the treated tumor (arrow). The presence of this amount of gas is common and by itself should not cause concern.

 


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Figure 24a.  (a) Selective hepatic arteriogram shows extravasation of contrast material at the site of a recent liver biopsy (arrow). The extravasation was discovered only after chemoembolization. (b) Nonenhanced CT scan obtained later that day shows continuing leakage of ethiodized oil from the biopsy site (arrowheads).

 


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Figure 24b.  (a) Selective hepatic arteriogram shows extravasation of contrast material at the site of a recent liver biopsy (arrow). The extravasation was discovered only after chemoembolization. (b) Nonenhanced CT scan obtained later that day shows continuing leakage of ethiodized oil from the biopsy site (arrowheads).

 





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