Compressive stenosis of the left hepatic vein as a pathogenesis of postresectional liver failure: a case report
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Postresectional liver failure (PLF) is a devastating and fatal complication of major hepatic resection, and we do not have a full understanding of the pathogenic mechanisms involved. No reliable treatment other than liver transplantation currently exists for PLF.
A 46-year-old Japanese man experienced PLF after an extended right hepatectomy for liver malignancy. Seven months after surgery, the patient's Model for End-Stage Liver Disease (MELD) score had reached 23. Doppler ultrasound study and three-dimensional computed tomography images showed a stenosed left hepatic vein compressed by surrounding hypertrophied hepatic parenchyma. Transluminal balloon angioplasty and stent placement therapy were conducted eight months after surgery. The pressure gradient between the hepatic vein and right atrium decreased from 13 to 3 mmHg after stent placement. Thereafter, the patient recovered.
Hepatic venous compression by surrounding hypertrophied hepatic parenchyma might, at least in part, be associated with the occurrence of PLF. Surgeons should bear this possibility in mind when confronted with cases of PLF, as early diagnosis and stent placement improves patients' chances of recovery.
KeywordsHepatocyte Growth Factor Hepatic Vein Stent Placement Hepatic Venous Pressure Gradient Refractory Ascites
Model for End-Stage Liver Disease
postresectional liver failure
relative remnant liver volume.
Hepatic resection is the preferred treatment for hepatic malignancies like hepatocellular carcinoma or colorectal liver metastases. Although major hepatic resection is now accomplished with mortality rates of less than 5% in high volume centers, post-resectional liver failure (PLF) remains a potentially devastating complication and often proves fatal . The risk of PLF increases as the amount of resected liver parenchyma increases. In general, the relative remnant liver volume (RLV) ratio, defined as the percentage remaining liver volume compared with standard liver volume, is regarded as a reliable parameter in the prediction of PLF. In normal livers, an RLV ratio below 25% has been reported to be a strong predictor of serious hepatic dysfunction following liver resection [2, 3]. Unfortunately, no reliable disease-specific therapy exists for PLF, with the exception of liver transplantation in some limited cases, and PLF mortality rates are between 60 and 80% [4, 5]. Understanding the exact pathophysiology of PLF would enable us to establish effective treatments other than liver transplantation. Here we present a case of PLF that was successfully treated by hepatic venous stent placement therapy. We also discuss the possible pathogenesis of PLF.
A 46-year-old Japanese man was referred to our hospital with intrahepatic cholangiocellular carcinoma. The tumor was 3 cm in diameter and located at segment 8, between the root of the middle and right hepatic veins. Preoperative liver function tests were normal, and preoperative blood work was negative for hepatitis virus markers. The patient underwent an extended right hepatectomy without resection of the extrahepatic bile duct. The patient's middle hepatic vein was divided approximately 2 cm upstream from the root of the middle and left hepatic veins.
Parameters of liver function before and after operation
Total bilirubin (mg/dl)
Prothorombin time (%)
To further confirm the presence of hepatic venous stenosis, the pressure gradient between the left hepatic vein and right atrium was measured. Hepatic venous catheterization was performed through the jugular vein. The mean hepatic venous pressure was 15.6 mmHg, and the pressure abruptly decreased when the catheter was pulled through the assumed stenotic point into the right atrium. The pressure gradient between the left hepatic vein right atrium was 13.2 mmHg. The normal hepatic venous pressure gradient lies between 1 and 2 mmHg . Thus, we confirmed the presence of hepatic venous stenosis morphologically and functionally.
Written informed consent was obtained from the patient for endovascular treatment. As an initial treatment option, hepatic venous balloon dilation was performed eight months after surgery. A transluminal angioplasty catheter (Synergy Balloon Catheter, Boston Scientific, Tokyo) with a balloon diameter of 10 mm and a length of 40 mm was used for venous dilatation. Although the pressure gradient across the left hepatic vein and right atrium decreased from 13 to 4 mmHg immediately after intervention, the effect was temporary. Ten minutes after balloon dilatation, the pressure gradient had increased to 10 mmHg. Although serum bilirubin levels decreased unexpectedly to near the normal range, refractory ascites remained. Therefore, the patient underwent endovascular stent placement therapy seven weeks later.
Although many factors have been proposed to be associated with increased risk of PLF, including inadequate hepatic regeneration, pre-existing cirrhosis and prolonged liver ischemia during resection, the critical factor is believed to be an insufficient remnant liver mass . Despite this, the mechanisms of PLF in the majority of clinical cases are thought to be multifactorial, not due purely to small remnant liver volume.
An adequate hepatic venous drainage is a prerequisite in the recovery process of a damaged liver and its significance is magnified in the case of extended right hepatectomy or trisegmentectomy, whereby the left hepatic vein is the only conduit to drain the entire remaining liver. It seemed that in our case, the root of the left hepatic vein was compressed by hypertrophied liver parenchyma subsequent to a vigorous regenerative response. Although reports of postoperative hepatic venous stenosis are common, most of these are stenosis after liver transplantation, whereby hepatic veins are more prone to mechanical stenosis than in the case of hepatectomy. This is due to suture anastomosis and to the possibility of venous kinking associated with graft dislocation . It could be inferred that hepatic venous compression by surrounding hypertrophied liver parenchyma might have been overlooked as the pathogenesis of PLF in previous cases. The diagnosis of hepatic venous stenosis by means of ordinary CT images seemed to be much more difficult than expected, because a single axial CT image could not clearly depict the outline of the hepatic vein with caudal inclination. Meanwhile, with the spread of liver transplantation, the usefulness of Doppler ultrasound for the diagnosis of hepatic venous stenosis had been calrified. Ko et al. reported that a persistent monophasic wave pattern on Doppler ultrasound images suggested, but did not conclusively indicate, hepatic venous stenosis after liver transplantation . Therefore, when hepatic venous stenosis is suspected as a cause of PLF, a screening Doppler ultrasound study should be used to assist in making a definitive diagnosis, taking into consideration other studies such as three-dimensional CT imaging, hepatic venography and measurement of the pressure gradient across the stenosis.
Transluminal balloon angioplasty and stent placement therapy are currently the preferred mode of treatment for hepatic venous stenosis. According to the treatment results reported by Ko et al., hepatic venous stenoses after liver transplantation were treated favorably by balloon angioplasty, although repeat angioplasty was necessary against restenosis . The main cause of anastomotic stenosis after liver transplantation is thought to be a fibrosis or intimal hyperplasia around the anastomotic site. However, stenosis after partial hepatectomy seems to be attributable, at least in part, to compression by surrounding hypertrophied parenchyma. Therefore, as in the present case, the treatment effects of balloon angioplasty for compressed stenosis are temporary and limited. From our experience of the present case, we thought that stent placement would be a preferable treatment measure for stenosis caused by extrinsic compression.
Hepatic venous compression by surrounding hypertrophied hepatic parenchyma might, at least in part, be associated with the occurrence of PLF. Recognition of hepatic venous compression as one of the pathogenic mechanisms of PLF may help to establish an adequate mode of treatment, such as stent placement therapy, and improve the prognosis of patients without requiring liver transplantation.
Written informed consent was obtained from the patient's family for the publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
The technical assistance of Eiji Komatsu and Toru Maeda (Department of Radiology, Oita Prefectural Hospital) are gratefully acknowledged.
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