A routine cancer therapy delivered through the liver’s own plumbing went unexpectedly and dramatically wrong, and the case is now forcing interventional radiologists around the world to rethink a procedure they have long considered among the safest tools in their arsenal. In a case report published in CVIR Oncology, physicians at Lausanne University Hospital in Switzerland describe how a 71-year-old man being treated for hepatocellular carcinoma developed a rare cascade of vascular injuries after transarterial radioembolization, or TARE, a treatment in which millions of microscopic radioactive spheres are threaded through the hepatic arteries to destroy tumors from within. What began as a small, catheter-induced tear in one of the liver’s feeding arteries ended, just seven days later, with radiation inflaming and weakening major vessels throughout the organ, forcing an emergency embolization to prevent potentially fatal bleeding. The patient survived, his tumor responded completely to treatment, but the biological story behind his recovery carries lessons that reach well beyond a single hospital ward.
TARE has become a mainstay of modern liver cancer care because of its unusual elegance. Rather than flooding the whole body with chemotherapy, clinicians deliver yttrium-90, a beta-emitting isotope bound to glass or resin microspheres roughly the width of a red blood cell, directly into the arteries that feed the tumor. The spheres lodge in the small vessels surrounding the malignancy and bathe it in high-dose radiation while sparing most healthy tissue. The technique works across the full spectrum of liver cancer severity, from early-stage disease where it can bridge patients to transplant, to advanced stages where it serves primarily to control tumor growth. Its safety record is genuinely impressive: serious adverse events occur in only about nine percent of patients, and vascular injury is estimated at no more than one percent of cases, typically arising when arterial anatomy is unusually complex, vessels have been weakened by prior chemotherapy, or pre-existing vascular abnormalities are present.
The Swiss case began conventionally enough. The patient, a man in his early seventies with liver fibrosis caused by chronic hepatitis C, was found on ultrasound to have a thirty-millimeter lesion in segment VIII of the liver, near the organ’s central hilum where major bile ducts and blood vessels converge. Magnetic resonance imaging and biopsy confirmed a moderately differentiated hepatocellular carcinoma, staged at an early BCLC stage with well-preserved liver function. A multidisciplinary tumor board weighed the options carefully. Percutaneous ablation, usually the first choice for small tumors, was judged too risky because of the lesion’s close proximity to a portal vein branch and the biliary tree. The team instead selected TARE, planning a curative dose of yttrium-90 glass microspheres engineered to deliver an estimated 324 gray to the perfused liver and more than a thousand gray to the tumor itself.
The workup phase went smoothly. Angiography revealed an anatomical quirk, a common hepatic artery arising from the superior mesenteric artery rather than its usual origin, but the team successfully navigated the tortuous route, advanced a microcatheter into the anterior sectoral artery supplying the tumor, and confirmed excellent targeting with technetium-99m-labeled macroaggregated albumin, the standard pre-treatment tracer. Two weeks later, during the therapeutic session, the trouble started. As the microcatheter was advanced along the same vessel, it caused a focal iatrogenic dissection, a tear in the arterial lining that separated the vessel wall into a true lumen and a false channel. Dissections of this kind are a recognized hazard of catheter work; guidelines from the Society of Interventional Radiology suggest they should prevent completion of the intended treatment in fewer than one percent of cases.
The team responded with textbook technique. They swapped the stiffer 2.7 French microcatheter for a softer, more flexible 1.98 French device paired with a fine guidewire, and successfully re-entered the true lumen. Digital subtraction angiography visualized the dissection, but selective intra-arterial CT angiography, a more detailed cross-sectional view taken from inside the vessel, showed no contrast stagnation in the false lumen, no pooling around the catheter tip, and preserved tumor enhancement that looked essentially identical to the simulation phase. Encouraged by these images, the physicians proceeded and administered 2.9 gigabecquerels of yttrium-90. Only afterward did post-treatment positron emission tomography reveal the flaw in that confidence: focal radioactive tracer uptake outside the liver tissue, in the region of the hepatic hilum, exactly where the dissection had occurred. Dosimetry calculations estimated that some 678 gray of radiation, an extraordinary dose by any standard, had pooled on the damaged arterial wall.
The critical insight, one the authors emphasize with some force, is that contrast dye is not a reliable proxy for microsphere behavior. Contrast agents and yttrium-90 spheres differ in particle size, density, and the way they move with blood flow, so a vessel that appears well perfused on angiography can still trap radioactive particles unevenly. In this patient, the dissection created abnormal flow conditions at the hepatic hilum that the intraprocedural imaging could not fully resolve. The spheres that should have been distributed throughout the tumor instead accumulated along an injured arterial wall, setting the stage for a form of collateral damage that is rarely reported and poorly understood: radiation-induced arteritis of the liver’s major vessels.
Because the patient remained symptom-free, he was discharged with daily telephone monitoring and a scheduled CT angiography seven days later, a deliberate precaution given the enormous extraparenchymal dose. That scan proved decisive. It revealed diffuse arteriopathy involving the common, right, and left hepatic arteries and their proximal branches, with multiple wall irregularities and three pseudoaneurysms, the largest measuring seven millimeters in the right hepatic artery. Pseudoaneurysms are balloon-like outpouchings formed when a weakened vessel wall balloons outward under pressure, and their rupture can trigger catastrophic intra-abdominal hemorrhage. The rapid onset of these changes, detectable within a single week, suggested a sinister synergy: mechanical injury from the catheter tearing the intima, compounded almost immediately by yttrium-90 radiation destroying the endothelial cells and muscular media of the vessel wall beneath.
The pathophysiology of radiation-induced vascular injury has been studied mostly in the context of external beam radiotherapy, where it is known to involve endothelial cell death, necrosis of the arterial media, and scarring of the adventitia that progressively narrows vessels or erodes them into aneurysms. Whether the same mechanisms unfold in the intrahepatic circulation after internal radiation has been largely uncharted territory. To the authors’ knowledge, no previous case has documented an iatrogenic arterial dissection during TARE evolving into subacute radiation-associated arteriopathy, which is precisely what makes the report valuable and unsettling. After urgent multidisciplinary consultation and shared decision-making with the patient, the team performed prophylactic coil embolization, deploying a series of detachable and pushable platinum coils through the hepatic arteries to pack shut the abnormal segments. Because the pathology was diffuse and multifocal, a covered stent, which would have preserved the vessel while sealing it, was not feasible, so the physicians accepted permanent sacrifice of the arterial tree. The patient’s preserved Child-Pugh A liver function and compensatory portal venous blood supply made the risk acceptable, though the team openly acknowledged a sobering trade-off: closing these arteries eliminated any possibility of future endovascular treatments if the cancer returned.
The outcome was, by any measure, a success story wrapped around a cautionary tale. Final angiography confirmed complete exclusion of the pseudoaneurysms and abnormal vessels, and transiently elevated liver enzymes normalized within five days. Magnetic resonance imaging at four weeks and three months showed a complete response of the original tumor by RECIST 1.1 criteria, with no biliary injury or hepatic ischemia, and preserved liver function throughout follow-up. A small new lesion in a distant segment was later treated successfully with percutaneous radiofrequency ablation. The authors distill the experience into several key lessons: anticipate vascular injury in patients with complex anatomy, reconsider microsphere delivery whenever arterial dissection occurs, maintain close post-procedural surveillance to catch vascular complications early, and weigh carefully whether definitive arterial embolization forecloses future treatment options. In asymptomatic patients, surveillance alone may suffice, since small pseudoaneurysms can stabilize or resolve, but their natural history is unpredictable and rupture can be lethal, so management must be individualized. For a procedure performed tens of thousands of times each year, this single case is a powerful reminder that even a one-percent risk deserves a protocol, and that the liver’s arteries, once injured and then irradiated, can fail in ways we are only beginning to describe.
Subject of Research: Iatrogenic arterial dissection during transarterial radioembolization leading to radiation-induced hepatic arteritis
Article Title: Iatrogenic arterial dissection leading to radiation induced arteritis following transarterial radioembolization
Article References: Adami, M., Boughdad, S., Villard, N., Schaefer, N., Rafael, D., & Tsoumakidou, G. (2026). Iatrogenic arterial dissection leading to radiation induced arteritis following transarterial radioembolization. CVIR Oncology, 2(1), Article 25. https://doi.org/10.1007/s44343-026-00061-3
Image Credits: AI Generated
DOI: 10.1007/s44343-026-00061-3
Keywords: transarterial radioembolization, hepatocellular carcinoma, yttrium-90, arterial dissection, radiation-induced arteritis, hepatic artery, pseudoaneurysm, coil embolization, interventional radiology, dosimetry, vascular complication, case report
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Tags: arterial dissectioncase reportcoil embolizationdosimetryemergency embolization in liver cancerhepatic arteryhepatic artery damage from radioembolizationhepatocellular carcinomahidden vascular risks in liver cancer therapiesinterventional radiologyinterventional radiology challenges in TAREliver cancer vascular injuryliver tumor treatment safety concernsmicroscopic radioactive sphere-induced vascular injurypseudoaneurysmradiation-induced arteritisrare arterial injury post-TAREtransarterial radioembolizationtransarterial radioembolization safety risksvascular complicationvascular inflammation after liver cancer treatmentvascular injury case report in oncologyyttrium-90yttrium-90 radioembolization complications
