PMC6614111_01
The patient's preoperative course: He had been initially treated with emergent arterial embolization of the ruptured main tumor in the segment 5. Multiple HCC lesions were treated by consecutive TACE and sorafenib administration. Although, other small HCC lesions remained controlled, the main pre-ruptured tumor in the segment 5 developed up to 6.5 cm in diameter directly involving the first and second portion of the duodenum.
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Hence, the chemotherapeutical sorafenib was selected and administered repeatedly (Fig. 1).
(a) Abdominal enhanced CT scan showed the tumor in the liver segment 5, invading the first and second portion of the duodenum (arrowheads). (b) An upper GI endoscopy revealed an ulcerative lesion on the posterior wall of the duodenal bulb.
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A pre-operative examination by CT revealed a massive HCC in segment 5 of 6.5 cm in diameter, protruding from the liver and penetrating the duodenal wall (Fig. 2a), while other small HCC lesions appeared to be controlled. A gastroendoscopy revealed an ulcerative mass lesion in the posterior wall of the duodenal bulb (Fig. 2b), which was revealed to be HCC following histology analysis of a biopsy sample.
The schemas of HPPD. (a) The dissected points are shown by heavy lines. T: tumor, GB: gall bladder. (b) The way of reconstruction is shown.
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We started the surgical treatment with the partial hepatectomy of segment 5 using the Pringle maneuver, and removed the tumor with the liver parenchyma as surgical margin (Fig. 3a). Billroth II approach as in distal gastrectomy (Fig. 3b). Blood loss amounted to two liters due to the bleeding from the fragile collateral vessels surrounding the extended tumor and from those developed in the adhesional planes that formed due to the previous TACE treatments.
(a) The resected specimen. The tumor invaded the duodenum (arrows) and developed ulceration (arrowheads). (b) Macroscopically, the tumor was soft and the cut surface was grayish and brown. (c) Microscopic image of the boxed area. Duodenal invasion by the tumor cells was also microscopically evident (inset: high power view).
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Pathological examination was compatible with the pre-operative findings and revealed poorly-to-moderately differentiated HCC cells directly invading the duodenal wall and extending inside the duodenal lumen (Fig. 4).