Causes of APF include trauma, iatrogenic causes (e.g., biliary drainage, percutaneous biopsy, and radiofrequency ablation), congenital disease, malignant tumors, and splanchnic artery aneurysm rupture [1,2,3,4, 6,7,8]. Some APFs appear to be cryptogenic. Surgery-related APFs are rare, although cases of APF after gastrectomy and laparoscopic cholecystectomy have been reported [17, 18]. To the best of our knowledge, however, only one case of APF after hepatectomy has been documented, and this previous case occurred in a 3-month-old infant after right trisegmentectomy . The infant had been successfully treated by super-selective embolization using titanium coils. His artery, portal vein, and bile duct were ligated, respectively. This approach was distinct from our approach, FSTG.
A simple question arose in the present case: Is FSTG dangerous during hepatectomy? FSTG is currently a safe and reproducible hepatectomy technique because of its simplicity, and this technique has therefore become a standard method during major hepatectomy [9, 10]. In our institution, we also employ perihilar FSTG during major hepatectomy for hepatocellular carcinoma, metastatic tumors, and benign diseases. In the present case, we understood that it is difficult to discuss the mechanism of APF development. We considered that our case was an agnogenic APF and that a relation between perihilar FSTG and resultant APF was also unclear. Our procedures of perihilar FSTG involved a transfixation suture, and we here speculated that perihilar FSTG might have been a possible cause of the APF. We also speculated that other possible causes (e.g., technical error) were observed, and recognized that a responsible cause of our APF was still obscure. We had not experienced similar cases of APF after hepatectomy accompanied by FSTG, although we found no reports of FSTG-related APF.
Although our patient was asymptomatic, CT detected a small amount of ascites. APFs, especially those on the proximal side (e.g., intrahepatic or perihilar Glissonean pedicle), often result in refractory symptoms of portal hypertension (such as gastrointestinal bleeding, ascites, and diarrhea) . In the present case, a definitive diagnosis of APF was made only 3 months after hepatectomy, and we considered that the reason why the patient had no symptoms was the prompt diagnosis of APF followed by adequate IVR. If prompt diagnosis followed by adequate therapy had failed, his portal hypertension would likely produce intractable symptoms over time. A simple question arose in the present case: Why symptoms of portal hypertension did not appear in this case? We speculated one possible reason was that APF was developed not at the main trunk level but at the stump of anterior Glissonean pedicle which was located at relatively peripheral lesion compared with main trunk.
Therapeutic strategies for APFs include surgery (e.g., partial hepatectomy and ligation of the related hepatic artery) and IVR (e.g., transarterial embolization). Our patient had an adequate length between the stump of the anterior hepatic artery and the bifurcation of the right hepatic artery, and it was considered suitable for transarterial embolization. We suggest that angiography should be considered as the first-choice imaging technique to elucidate the details of APFs and subsequently determine the optimal therapy .
Glissonean pedicle transection (i.e., FSTG) is now routinely employed during hepatectomy worldwide. We consider this maneuver to be very useful during major hepatectomy. The occurrence of APF after surgery is considered to be low [16,17,18]. However, once an APF has developed, the patient will experience a poor clinical course accompanied by severe portal hypertension, and this intractable complication requires surgical or interventional treatment.
APF after hepatectomy is very rare, and some APFs appear to be cryptogenic. Our thought-provoking case may be informative in terms of providing a possible explanation of the causes of APF after hepatectomy.