Author(s)

Battaglia V, Zingoni G, Brunu M, Signorini F, Bonechi C, Nardini L, Bartolozzi C

Patient

female, 72 year(s)

A 72-year-old woman affected by HCV lasting for 20 years with preserved hepatic function and normal alfa-feto protein value, came at our attention to investigate and treat a 3 cm hepatocellular carcinoma (HCC) in segment VI diagnosed in another hospital one month before.

Baseline ultrasound (US) examination performed before therapy confirmed the presence of 3 cm HCC in segment VI. Because of the size and location, radiofrequency thermal ablation (RFA) was chosen as the therapeutic approach (Fig. 1).
The patient underwent US-guided RFA of the lesion. The RFA procedure was carried out under mild sedation through a multitined hook. The device was opened at its largest dimension in order to obtain an ablation area with a diameter of 4 cm.
Contrast enhanced US examination (CEUS) performed two hours after ablation showed a complete response of the treated lesion (Fig. 2).
Computed tomography (CT) examination, performed one month after therapy, confirmed the presence of a complete response of the target lesion (Fig. 3).
Three months after therapy, a magnetic resonance (MR) examination was performed, as a scheduled imaging assessment of tumour response. The MR study included baseline T1 and T2 weighted sequences and contrast enhanced images performed after intravenous injection of Gadolinium chelate (Gd-EOB-DTPA), acquired in dynamic and hepatobiliary phases. A complete response of the treated area was diagnosed (Fig. 4).
However, caudally of the lesion, a wedge shaped large area of altered enhancement both on dynamic and hepatobiliary phases was detected (Fig. 5,6).
This area showed in fact a lack of enhancement on the arterial phase that was evident also in the following phases as well as a reduced and low enhancement on hepatobiliary phase images.

Indications of treatment for HCC are complex and depend on several factors: tumour characteristics such as number of lesions, size, location, relationship to vessels and hilar structures.
Moreover, it is necessary to consider liver function and the general patient status.
RFA represents the most applied tool and permits to destroy tumours by heating tissue to temperatures exceeding 60°C. It is nowadays considered as the treatment of choice for patients with a single HCC smaller than 2-3 cm, even when surgical resection is possible [1]. Tumour response after RFA is usually assessed with CT or MR imaging, not only to assess the outcome of the therapy but also to detect complications.
RFA complications may be classified in 3 groups: vascular (e.g., portal vein thrombosis, hepatic vein thrombosis with partial hepatic congestion, hepatic infarction, and subcapsular haematoma), biliary (e.g., bile duct stenosis and biloma, abscess, and haemobilia), and extrahepatic (e.g., injury to the gastrointestinal tract, injury to the gallbladder, pneumothorax and haemothorax, and tumour seeding) [2].
Regarding intrahepatic complications, the damage to vascular and biliary structures may frequently determine alterations in parenchymal perfusion as a consequence of the thermal damage.
In fact, RFA may cause thrombosis of small portal branches and inflammation of biliary ducts with subsequent dilatation, which causes peribiliary plexus obstruction [3].
Pathophysiological studies have demonstrated a communication between the two hepatic inflows (70% portal vein, 30% hepatic artery), mainly through the sinusoid system and peribiliary plexus. These shunts attempt to locally compensate for reduced portal inflow under the action of the autonomous nervous system and humoral mediators (primarily adenosine and prostacycline) [2].
Generally, altered perfusion is due to thrombosis of small portal branches caused by thermal damage. In our case MR showed a low/absent perfusion of the portion of the VIth segment located caudally of the treated area on all dynamic and hepatobiliary contrast enhanced images. This alteration of the perfusion, and thus of the metabolic activity of the parenchyma, must be related to a conspicuous damage of small arterial and portal branches and of the peribiliary plexus.
Moreover, this portion of the parenchyma appeared as mildly hyperintense on baseline T2 and hypointense on T1 weighted images. This peculiar signal intensity must be related to an edema of the damaged tissue and probably to an initial necrotic component.
Differential diagnosis must be poned with transient hepatic attenuation differences (THAD), at CT or transient hepatic signal intensity differences (THID), at MR.
At CT, a THAD is generally seen as an area of high attenuation on hepatic arterial phase images that shows normal attenuation on portal venous phase images, due to the increased arterial flow as compensation for compromised portal venous flow. In the same way THID appear at MR as hyperintense on arterial phase images after contrast administration [4].