Cavernous Transformation of the Portal Vein Secondary to Cholecystolithiasis.

To the Editor: A 58-year-old man with up to a 5-year history of cholecystolithiasis presented with a 1-day history of mild abdominal pain with tenderness in the right upper quadrant before this hospital admission. He complained of similar symptoms about 5 years ago and recovered after 11 days of conservative therapy in the same hospital. The temperature was normal, and no special findings were noted on laboratory testing. Ultrasonography revealed multiple small gallstones in the lumen of the gallbladder. Unexpectedly, augmented collaboration of the portal vein was demonstrated at the Calot triangle and the bed of the gallbladder during a laparoscopic cholecystectomy (LC) [Figure 1a]. The deformed veins appeared fragile and hence were very carefully separated and ligated using clips one by one. LC was performed with completion. The previous computerized tomography (CT) of the abdomen obtained postoperatively [Figure 1b] and 5 years ago [Figure 1c] were retrospectively reviewed. The previous CT [Figure 1c] showed a normal portal vein lumen and portal vein system, with the exception of a major portal vein thrombosis and a small pyogenic liver abscess due to acute cholecystitis, while the most recent CT [Figure 1b] revealed abnormalities of the portal vein. The postoperative pathologic evaluation confirmed numerous twisted, congestive veins around the surface of the specimen [gallbladder; Figure 1d].

Figure 1

A cluster of veins located in the Calot triangle (a), which coincides with the preoperative CT findings (b), but a previous CT 5-years earlier (c) was normal, with the exception of a portal vein thrombosis and liver abscess. The postoperative pathologic evaluation (d) revealed cholecystolithiasis with deformed, congested portal veins. CT: Computed tomography.

Cavernous transformation of the portal vein (CTPV) among adults is quite rare, with an incidence of 15.6% among extrahepatic portal vein obstruction (EHPVO), including one-third of thrombotic portal veins,[1] and accordingly are thought to be secondary to EHPVO triggered by inflammation, adjacent tissue fibrosis, tumor invasion, pancreatitis, and clotting disorders.[123] CTPV is characterized by a series of tortuous collateral portal veins at the liver hilum, with portal vein occlusion at the level of the spinoportal conjunction.[2] In this case, it was more likely caused by chronic cholecystitis based on the original normal portal vein lumen. Even though LC is replete with challenges, such as the potential risk of massive hemorrhage, it is accessible and safe for skilled surgeons.[4] The patient was recovered uneventfully and discharged on postoperative day 3. At the 3-month follow-up after discharge, no surgery-related complications were noted.

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Conflicts of interest

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