Imaging and Diagnosis of Hepatocellular Carcinoma

No. Dr. George has operated on perihilar cholangiocarcinoma patients with bilirubin as high as 30 to 35. Surgical practice has also evolved: where extended resections once left only the left lateral section or right posterior sector achievable, his unit now more often does a left- or right-with-caudate resection with extended bile duct resection, preserving more liver parenchyma. Preoperative biliary drainage, usually percutaneous (PTBD) rather than endoscopic nasobiliary drainage, is reserved for patients with cholangitis or those planned for portal vein embolisation.

Alpha-fetoprotein is the marker primarily elevated in hepatocellular carcinoma. CA19-9 comes primarily from the biliary system and can rise somewhat in cirrhotic patients, but not to a high degree, so it remains the more specific marker for cholangiocarcinoma.

After HCC resection on a normal liver, patients are generally placed on lenvatinib long-term. After transplant, there is no separate adjuvant chemotherapy; instead, immunosuppression is adjusted to tacrolimus plus everolimus rather than the standard tacrolimus and mycophenolate, since everolimus is associated with a lower recurrence risk. For cholangiocarcinoma with nodal or vascular invasion, patients are referred to medical oncology for cisplatin or gemcitabine-based adjuvant therapy, usually once they have recovered, six to twelve weeks later, from preoperative jaundice and cholangitis.

No, this is not typical of the Pringle manoeuvre itself. Needing a stent afterwards points to bile duct involvement: a narrowed biliary confluence after a right hepatectomy, a bile leak that progressed to a stricture after a hepaticojejunostomy, or compromised duct vascularity following preoperative radiotherapy. The Pringle manoeuvre alone may raise liver enzymes, but it should not cause obstructive jaundice.

For HCC after resection or an interventional procedure, MRI is favoured over repeated CT scans, both to limit cumulative radiation and contrast exposure and because MRI catches smaller lesions earlier, while they are still resectable or eligible for salvage transplant. Cholangiocarcinoma follow-up similarly relies on CT or MRI rather than ultrasound, alongside tumour markers, AFP and PIVKA-II for HCC, CA19-9 for cholangiocarcinoma.

A triphasic CT scan captures an arterial phase, a portal venous phase, a hepatic venous phase and a delayed phase, sometimes acquired 5 to 10 minutes after contrast injection to capture washout. A simple contrast-enhanced CT scan lacks this phased detail and is not sufficient to diagnose HCC reliably.

The classical finding is arterial phase hyperenhancement, where the tumour appears brighter than the surrounding liver, followed by washout in later phases, where it appears darker. This happens because early HCC is fed mainly by the hepatic artery rather than the portal vein, so it lights up early and then loses that enhancement while the rest of the liver continues to fill from the portal vein.

MRI is more sensitive than CT and can detect smaller lesions earlier, but its longer acquisition time can be a problem for sick patients who struggle to hold their breath through the sequence. In practice, MRI is reserved for cases where CT findings are inconclusive.

Only around 5 percent of HCC patients require a biopsy, generally those who already have metastatic disease, those too unwell for curative treatment, or those being planned for neoadjuvant therapy. For the rest, an arterially enhancing lesion with venous washout on a properly phased scan is treated as diagnostic without biopsy.