Transarterial Chemoembolisation
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Direct answer
Transarterial chemoembolisation (TACE) treats unresectable hepatocellular carcinoma by exploiting the tumour's almost exclusive dependence on hepatic arterial blood: a catheter is threaded from the femoral or radial artery into the tumour-feeding branch, a chemotherapy emulsion — commonly doxorubicin or cisplatin mixed with Lipiodol — is delivered, and the feeder is embolised so the drug is trapped while the supply is cut. It is the standard for intermediate-stage (BCLC B) disease in a Child-Pugh A or B liver, it is palliative rather than curative, and response is assessed by mRECIST, which measures viable enhancing tissue rather than total lesion size. Contraindications centre on decompensation — Child-Pugh C, jaundice, clinical encephalopathy — and on complete portal vein thrombosis in most protocols.
What you must remember
- Where TACE sits in the BCLC algorithm: very early/early (0-A) disease is for ablation, resection or transplant; intermediate (B) multinodular disease is for TACE; advanced (C) with vascular invasion or metastases is for systemic therapy; terminal (D) is supportive. TACE is for B.
- Procedure skeleton: femoral or radial access, celiac and superior mesenteric angiography, microcatheter superselection of the segmental tumour feeder, chemotherapy-Lipiodol emulsion, then particles (PVA or gelatin sponge) until stasis.
- Two variants: conventional TACE with Lipiodol emulsion, and DEB-TACE with drug-eluting beads releasing doxorubicin slowly — the latter gives more predictable pharmacokinetics, with broadly comparable outcomes.
- Post-embolisation syndrome: fever, right upper quadrant pain, nausea and transient transaminase rise for a few days — expected and managed expectantly; a source of infection must still be excluded when fever persists.
- Contraindications: Child-Pugh C or decompensation, bilirubin generally above about 2-3 mg/dL, complete portal vein thrombosis, extensive bilobar disease with poor liver reserve, and poor performance status.
- Response assessment: mRECIST — viable tumour is enhancing tissue in the arterial phase; complete response means no enhancing focus, and assessment is with contrast CT or MRI at 4-8 weeks, then surveillance.
- Curative set for comparison: resection for single tumours with preserved liver function, thermal ablation for lesions up to about 3 cm, and transplantation within the Milan criteria — one lesion up to 5 cm or up to three lesions each up to 3 cm, without vascular invasion or spread.
One session, start to follow-up
A 62-year-old with hepatitis B cirrhosis, Child-Pugh A, has two tumours of 3 cm and 2.5 cm in the right lobe and a patent portal vein. He is BCLC B and unsuitable for resection because of multinodularity. After right radial access, a microcatheter is parked in the segment VII feeder, a doxorubicin-Lipiodol emulsion is injected until the tumour blush saturates, and particles are delivered to stasis. He develops fever and pain that evening — post-embolisation syndrome — and settles with analgesia over 48 hours. Contrast CT at six weeks shows both lesions densely opacified with Lipiodol and no arterial enhancement: complete response by mRECIST. Surveillance continues, and a new enhancing nodule at one year triggers a further session or ablation, because TACE controls rather than cures.
The scenario the exam tests against is the same patient arriving with bilirubin of 4 mg/dL and ascites: TACE now risks liver failure, and the correct answer moves to systemic or best supportive therapy — the procedure is judged by what it does to the remaining liver, not to the tumour.
Where students slip
The recurring slip is treating TACE as curative or as first-line for everything hepatic. It is palliative, repeated on demand, and outranked by ablation and surgery in early disease. The second is the portal vein physiology: arterial embolisation is survivable only if the portal vein is patent — hence portal vein thrombosis as the classical contraindication. Third is response assessment: candidates quote lesion shrinkage, but Lipiodol retention and necrosis keep lesions the same size while they are dead — which is precisely why mRECIST measures enhancement. In the Indian context, HCC arises mostly on hepatitis B and increasingly on non-alcoholic fatty liver disease cirrhosis, living-donor transplantation is the transplant reality, and TACE serves as the bridge to transplantation in listed patients — a viva answer that shows systems thinking rather than a procedure list.
Frequently asked questions
Which stage of hepatocellular carcinoma is treated with TACE?
Intermediate-stage BCLC B disease — multifocal tumours without vascular invasion, metastases or decompensation — in a Child-Pugh A or B liver, as palliative therapy.
How does TACE exploit hepatic blood supply?
HCC is almost exclusively artery-supplied while the normal liver receives most inflow from the portal vein, so selective arterial chemotherapy and embolisation starve the tumour yet spare the parenchyma.
What is post-embolisation syndrome?
Self-limiting fever, abdominal pain, nausea and transaminase elevation for a few days after TACE, managed supportively while persistent fever prompts a search for infection or abscess.
Which liver-related findings contraindicate TACE?
Decompensated Child-Pugh C disease, significantly raised bilirubin, encephalopathy or refractory ascites, and complete portal vein thrombosis in most protocols.
How is response to TACE assessed?
By mRECIST on contrast CT or MRI, scoring only viable arterial-enhancing tissue, with complete response defined as disappearance of all enhancing foci regardless of residual lesion size.