Selective Arterial Embolization of Ruptured Hepatocellular Carcinoma with N-Butyl Cyanoacrylate and Lipiodol: Safety, Efficacy, and Short-Term Outcomes

Abstract

The rupture of hepatocellular carcinoma (rHCC) is uncommon but causes sudden life-threatening bleeding. Selective transarterial embolization (STAE) is an effective bleeding-control option. The optimal embolic agent is unknown, and data on the use of cyanoacrylate glue are lacking. The objective of this study was to report the outcomes of cyanoacrylate-lipiodol embolization for rHCC. We retrospectively reviewed the files of the 16 patients (14 males; mean age, 72 years) who underwent emergency cyanoacrylate-lipiodol STAE at a single center in 2012-2023 for spontaneous rHCC. All 16 patients had subcapsular HCC and abundant hemoperitoneum. The technical success rate was 94% (15/16). Day 30 mortality was 19%; the three patients who died had severe hemodynamic instability at admission; one death was due to rebleeding. Liver enzyme levels returned to baseline by day 30. No rebleeding was recorded during the median follow-up of 454 days in the 10 patients who were alive with available data after day 30. Larger prospective studies with the collection of longer-term outcomes are needed to assess our results supporting the safety and effectiveness of cyanoacrylate-lipiodol STAE for rHCC. Randomized trials comparing this mixture to other embolic agents should be performed.

Keywords: bleeding control; cyanoacrylate; embolization; glue; hepatocellular carcinoma rupture; interventional radiology.

Figure 1

Example of ruptured hepatocellular carcinoma (rHCC) in a 52-year-old male who presented with signs of active intraperitoneal bleeding. (a) Unenhanced CT scan showing abundant perihepatic hemoperitoneum (arrow). (b) Enhanced CT images at the portal phase showing features highly suggestive of rHCC: large, heterogeneous, nodular hypervascular mass in a subcapsular location in segment VI (arrow), with intratumoral blush (arrow), on healthy liver. (c) Digital subtraction angiography via the superior mesenteric artery showing occlusion of the celiac trunk by median arcuate ligament syndrome, revascularization of the hepatic artery via the pancreaticoduodenal arcades, and hypervascular tumor (arrow). (d) DSA performed after selective microcatheterization of the main feeding arterial branch via the pancreaticoduodenal arcades, showing contrast-medium blush within the tumor (arrow). (e) Visualization of the cyanoacrylate/lipiodol mixture cast after selective injection in a 1:5 ratio in the main arterial branch (arrows). (f) Final angiographic control after glue embolization demonstrating cessation of active bleeding and complete devascularization of the tumor. (g) Enhanced MR imaging control at 2 months after embolization showing complete necrosis of the tumor. Complementary wedge hepatic resection was performed within 3 months. (h) MRI scan at 5 years after surgery showing hepatic surgical scar (arrow) with no tumoral recurrence.

Figure 1

Example of ruptured hepatocellular carcinoma (rHCC) in a 52-year-old male who presented with signs of active intraperitoneal bleeding. (a) Unenhanced CT scan showing abundant perihepatic hemoperitoneum (arrow). (b) Enhanced CT images at the portal phase showing features highly suggestive of rHCC: large, heterogeneous, nodular hypervascular mass in a subcapsular location in segment VI (arrow), with intratumoral blush (arrow), on healthy liver. (c) Digital subtraction angiography via the superior mesenteric artery showing occlusion of the celiac trunk by median arcuate ligament syndrome, revascularization of the hepatic artery via the pancreaticoduodenal arcades, and hypervascular tumor (arrow). (d) DSA performed after selective microcatheterization of the main feeding arterial branch via the pancreaticoduodenal arcades, showing contrast-medium blush within the tumor (arrow). (e) Visualization of the cyanoacrylate/lipiodol mixture cast after selective injection in a 1:5 ratio in the main arterial branch (arrows). (f) Final angiographic control after glue embolization demonstrating cessation of active bleeding and complete devascularization of the tumor. (g) Enhanced MR imaging control at 2 months after embolization showing complete necrosis of the tumor. Complementary wedge hepatic resection was performed within 3 months. (h) MRI scan at 5 years after surgery showing hepatic surgical scar (arrow) with no tumoral recurrence.

Figure 1

Example of ruptured hepatocellular carcinoma (rHCC) in a 52-year-old male who presented with signs of active intraperitoneal bleeding. (a) Unenhanced CT scan showing abundant perihepatic hemoperitoneum (arrow). (b) Enhanced CT images at the portal phase showing features highly suggestive of rHCC: large, heterogeneous, nodular hypervascular mass in a subcapsular location in segment VI (arrow), with intratumoral blush (arrow), on healthy liver. (c) Digital subtraction angiography via the superior mesenteric artery showing occlusion of the celiac trunk by median arcuate ligament syndrome, revascularization of the hepatic artery via the pancreaticoduodenal arcades, and hypervascular tumor (arrow). (d) DSA performed after selective microcatheterization of the main feeding arterial branch via the pancreaticoduodenal arcades, showing contrast-medium blush within the tumor (arrow). (e) Visualization of the cyanoacrylate/lipiodol mixture cast after selective injection in a 1:5 ratio in the main arterial branch (arrows). (f) Final angiographic control after glue embolization demonstrating cessation of active bleeding and complete devascularization of the tumor. (g) Enhanced MR imaging control at 2 months after embolization showing complete necrosis of the tumor. Complementary wedge hepatic resection was performed within 3 months. (h) MRI scan at 5 years after surgery showing hepatic surgical scar (arrow) with no tumoral recurrence.

Figure 1

Example of ruptured hepatocellular carcinoma (rHCC) in a 52-year-old male who presented with signs of active intraperitoneal bleeding. (a) Unenhanced CT scan showing abundant perihepatic hemoperitoneum (arrow). (b) Enhanced CT images at the portal phase showing features highly suggestive of rHCC: large, heterogeneous, nodular hypervascular mass in a subcapsular location in segment VI (arrow), with intratumoral blush (arrow), on healthy liver. (c) Digital subtraction angiography via the superior mesenteric artery showing occlusion of the celiac trunk by median arcuate ligament syndrome, revascularization of the hepatic artery via the pancreaticoduodenal arcades, and hypervascular tumor (arrow). (d) DSA performed after selective microcatheterization of the main feeding arterial branch via the pancreaticoduodenal arcades, showing contrast-medium blush within the tumor (arrow). (e) Visualization of the cyanoacrylate/lipiodol mixture cast after selective injection in a 1:5 ratio in the main arterial branch (arrows). (f) Final angiographic control after glue embolization demonstrating cessation of active bleeding and complete devascularization of the tumor. (g) Enhanced MR imaging control at 2 months after embolization showing complete necrosis of the tumor. Complementary wedge hepatic resection was performed within 3 months. (h) MRI scan at 5 years after surgery showing hepatic surgical scar (arrow) with no tumoral recurrence.

Figure 1

Example of ruptured hepatocellular carcinoma (rHCC) in a 52-year-old male who presented with signs of active intraperitoneal bleeding. (a) Unenhanced CT scan showing abundant perihepatic hemoperitoneum (arrow). (b) Enhanced CT images at the portal phase showing features highly suggestive of rHCC: large, heterogeneous, nodular hypervascular mass in a subcapsular location in segment VI (arrow), with intratumoral blush (arrow), on healthy liver. (c) Digital subtraction angiography via the superior mesenteric artery showing occlusion of the celiac trunk by median arcuate ligament syndrome, revascularization of the hepatic artery via the pancreaticoduodenal arcades, and hypervascular tumor (arrow). (d) DSA performed after selective microcatheterization of the main feeding arterial branch via the pancreaticoduodenal arcades, showing contrast-medium blush within the tumor (arrow). (e) Visualization of the cyanoacrylate/lipiodol mixture cast after selective injection in a 1:5 ratio in the main arterial branch (arrows). (f) Final angiographic control after glue embolization demonstrating cessation of active bleeding and complete devascularization of the tumor. (g) Enhanced MR imaging control at 2 months after embolization showing complete necrosis of the tumor. Complementary wedge hepatic resection was performed within 3 months. (h) MRI scan at 5 years after surgery showing hepatic surgical scar (arrow) with no tumoral recurrence.