(Radiology. 2001;220:357-364.)
© RSNA, 2001
Altered Hepatic Hemodynamics Caused by Temporary Occlusion of the Right Hepatic Vein: Evaluation with Doppler US in 14 Patients1
Takao Hiraki, MD,
Susumu Kanazawa, MD,
Hidefumi Mimura, MD,
Kotaro Yasui, MD,
Akio Tanaka, MD,
Shuichi Dendo, MD,
Koichi Yoshimura, MD and
Yoshio Hiraki, MD
1 From the Department of the Radiology, Okayama University Medical School, 2-5-1 Shikatacho, Okayama 700-8558, Japan. Received October 2, 2000; revision requested November 15; revision received January 30, 2001; accepted February 26. Address correspondence to T.H. (e-mail: radiol@cc.okayama-u.ac.jp).
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ABSTRACT
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PURPOSE: To evaluate with Doppler ultrasonography (US) the altered hepatic hemodynamics caused by temporary occlusion of the right hepatic vein.
MATERIALS AND METHODS: The study group consisted of 14 patients being considered for hepatic arterial infusion or transarterial embolization. In all patients, maximum peak velocity of the blood flow in the right portal vein was measured with Doppler US before and during the occlusion of the right hepatic vein. In 13 patients, color Doppler US was performed to evaluate Doppler signal in the portal venous branch in the occluded area before and during occlusion. Average peak velocity in the right hepatic artery in eight patients was measured by using a transducer-tipped guide wire before and during occlusion.
RESULTS: Maximum peak velocity of the right portal vein significantly decreased with occlusion (P < .01). Hepatic venous occlusion changed the Doppler signal in the portal venous branch in the occluded area from hepatopetal to no signal in 10 patients; to weakened hepatopetal in two; and to hepatofugal in one. Average peak velocity of the right hepatic artery showed a decrease or plateau for 15–30 seconds after the start of occlusion and then a rapid increase to reach a plateau at around 75–90 seconds, with 1.5–2 times as much velocity as that before occlusion.
CONCLUSION: Increase in hepatic arterial velocity is accompanied by a decrease in the portal velocity with temporary occlusion of the right hepatic vein; the expected increased drainage through the portal vein was almost undetectable.
Index terms: Hepatic arteries, US, 952.12984, 952.12989 • Hepatic veins, stenosis or obstruction, 95.7214 • Liver, blood supply, 761.91 • Portal vein, US, 957.12983 • Ultrasound (US), Doppler studies, 95.12983
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INTRODUCTION
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Authors of recent studies (1–4) of angiography and computed tomographic (CT) arteriography performed during temporary occlusion of the hepatic vein have disclosed interesting angiographic findings. In the occluded area, they showed prolonged intensity at hepatography, which was usually followed by hepatofugal portal opacification. The hepatic hemodynamic changes providing these angiographic findings can be explained as follows: Hepatic venous occlusion induces elevation of sinusoidal pressure and reverses the pressure gradient between the sinusoid and the portal vein. As a result, the portal vein becomes the draining vein in the occluded area. Stoppage of the hepatopetal portal flow induces a compensatory increase in hepatic arterial flow (4–7).
However, these altered hemodynamics may not be fully proved with angiography or CT arteriography. Such findings as prolonged intensity at hepatography and hepatofugal portal opacification have possibly been enhanced with cessation of the hepatopetal portal flow, which might normally be expected to dilute arterial contrast material, and with injection pressure of the contrast material itself (1). For these reasons, we believe it was necessary to perform evaluation without the use of contrast material. At the time of the writing of this article, Doppler ultrasonography (US) appears to be the ideal method.
The purpose of our study was to evaluate with Doppler US the altered hepatic hemodynamics caused by temporary occlusion of the right hepatic vein, since altered hemodynamics have implications for treatment of malignant hepatic tumors.
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MATERIALS AND METHODS
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Patients and Angiography
Between January 1996 and April 2000, 18 patients who had malignant hepatic tumors were considered for possible hepatic arterial infusion or transcatheter arterial embolization during temporary occlusion of the right hepatic vein. In these patients, angiography was performed as follows: a 7-F catheter with a 20-mm occlusion balloon at the tip (Selecon MP; Clinical Supply, Tokyo, Japan) was advanced into the right hepatic vein through the common femoral vein. After the right hepatic vein was occluded by means of a balloon filled with 1.5–2.5 mL of carbon dioxide, occlusion venography was performed. Thereafter, the balloon was deflated, and then celiac, hepatic, and superior mesenteric arteriography were performed with a 4- or 5-F polyurethane catheter (Selecon PA; Clinical Supply) by using a transfemoral approach. Subsequently, celiac, hepatic, and superior mesenteric arteriography were performed, in that order, during temporary occlusion of the right hepatic vein. The balloon was deflated immediately after each angiographic examination.
Occluded venography of the right hepatic vein showed no or minimal venovenous anastomosis in 14 patients (Fig 1a). Hepatic arteriography performed during temporary occlusion of the hepatic vein showed typical findings in all 14 patients: Prolonged intensity at hepatography followed by hepatofugal portal opacification in the occluded area (Fig 1b). Also, superior mesenteric arterial portography performed during venous occlusion showed a perfusion defect and less opacification of the portal vein in the occluded area (Fig 1c). In these patients, we evaluated the hemodynamic changes caused by temporary occlusion of the right hepatic vein by means of Doppler US. Four of the 18 patients were excluded from our study because occlusion venography revealed marked venovenous anastomoses, which tend to compromise typical findings at hepatic arteriography and superior mesenteric arterial portography during hepatic venous occlusion.
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Figure 1a. Patient 14. Anteroposterior angiography performed in a 67-year-old man with metastatic hepatic tumor. (a) Occlusion venogram of the right hepatic vein shows complete occlusion (arrow), with no visible venovenous anastomosis. (b) Common hepatic arteriogram (parenchymal phase) obtained during occlusion of the right hepatic vein shows prolonged intensity at hepatography (black arrows) with hepatofugal portal opacification in the occluded area, a venous catheter (white arrow), and an arterial catheter (arrowhead). (c) Superior mesenteric arterial portogram obtained during occlusion of the right hepatic vein shows perfusion defect (thick arrows) and less portal opacification in the occluded area, a venous catheter (thin arrow), and an arterial catheter (arrowhead).
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Figure 1b. Patient 14. Anteroposterior angiography performed in a 67-year-old man with metastatic hepatic tumor. (a) Occlusion venogram of the right hepatic vein shows complete occlusion (arrow), with no visible venovenous anastomosis. (b) Common hepatic arteriogram (parenchymal phase) obtained during occlusion of the right hepatic vein shows prolonged intensity at hepatography (black arrows) with hepatofugal portal opacification in the occluded area, a venous catheter (white arrow), and an arterial catheter (arrowhead). (c) Superior mesenteric arterial portogram obtained during occlusion of the right hepatic vein shows perfusion defect (thick arrows) and less portal opacification in the occluded area, a venous catheter (thin arrow), and an arterial catheter (arrowhead).
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Figure 1c. Patient 14. Anteroposterior angiography performed in a 67-year-old man with metastatic hepatic tumor. (a) Occlusion venogram of the right hepatic vein shows complete occlusion (arrow), with no visible venovenous anastomosis. (b) Common hepatic arteriogram (parenchymal phase) obtained during occlusion of the right hepatic vein shows prolonged intensity at hepatography (black arrows) with hepatofugal portal opacification in the occluded area, a venous catheter (white arrow), and an arterial catheter (arrowhead). (c) Superior mesenteric arterial portogram obtained during occlusion of the right hepatic vein shows perfusion defect (thick arrows) and less portal opacification in the occluded area, a venous catheter (thin arrow), and an arterial catheter (arrowhead).
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There were 14 patients (10 men, four women; age range, 53–75 years; mean age, 66.1 years). Seven patients had metastatic hepatic tumor from colorectal carcinoma, six had hepatocellular carcinoma, and one had cholangiocellular carcinoma. All six patients who had hepatocellular carcinoma had cirrhotic liver, while the others had noncirrhotic liver. The size of each hepatic tumor in the occluded area was less than 3 cm in diameter.
Doppler US Evaluation
Altered hemodynamics of the portal vein.— Portal venous hemodynamics were evaluated with color Doppler US and pulsed Doppler US with a curvilinear 3.5-MHz transducer (SSD-2000 or SSD-5000; Aloka, Tokyo, Japan). Patients were examined during breath hold with intercostal manipulation.
Maximum peak velocity (MPV) of the right portal vein was obtained by means of a Doppler US measurement, with a 3-mm sample volume obtained before and during occlusion of the right hepatic vein in all patients. Comparison between the mean value of MPV obtained before and that obtained during occlusion was tested with the paired t test, and a P value less than .01 was considered to indicate a statistically significant difference.
Color Doppler US images of the portal venous branch in the occluded area were obtained before and during occlusion of the right hepatic vein in 13 of 14 patients. We could not obtain them clearly in patient 7 because of his inability to hold his breath properly. Furthermore, in four patients, color Doppler US images were obtained during occlusion and manual injection of saline at a rate of 2–3 mL/sec through the catheter (Clinical Supply) that was placed in the common hepatic artery.
Altered hemodynamics of the hepatic artery.—For the evaluation of hepatic arterial hemodynamics, we used a transducer-tipped guide wire (FloWire; Cardiometrics, Mountain View, Calif). A 3-F microcatheter (Rapidtransit; Cordis, Miami, Fla) was advanced into the target hepatic artery through the 4- or 5-F polyurethane catheter (Clinical Supply) that was placed in the celiac or common hepatic artery. The 175-cm-long, 0.018-inch, transducer-tipped guide wire was then passed through the microcatheter, and its tip was projected from the microcatheter within the target hepatic artery. The proximal end of the guide wire was connected to the velocimeter (FloMap; Cardiometrics) by means of an integrated spring-loaded connector. The free-standing velocimeter unit contained a computer processor, a video screen to display spectral wave form and numeric data, a VHS recorder, a paper printer, and a detachable hand-held control. The velocimeter processed the US signal in real time to display the blood-flow velocity profile in both spectral and numeric forms on the screen, in addition to an auditory Doppler signal.
In November 1997, the transducer-tipped guide wire became available in our institution. Between November 1997 and December 1998, Doppler US of the right hepatic artery was performed for 30 seconds after the start of occlusion of the right hepatic vein in three patients. Initial results seemed inconsistent with those reported in the literature (see Discussion). Thus, from January 1999, in five patients, Doppler US of the right hepatic artery and its branch in the occluded area was extended to 120 seconds and then for a further 60 seconds after balloon-deflation release of occlusion.
We documented the video-screen display of velocimeter on the VHS recorder. We also printed out the video-screen display before occlusion and at 0, 15, and 30 seconds after the start of occlusion in the first three patients. In the latter five patients, we captured it before occlusion at 15-second intervals for 120 seconds after the start of occlusion and then up to 60 seconds after the release of occlusion. All measurements were performed in the same part of the vascular system. We evaluated hemodynamic changes in the hepatic artery with average peak velocity (APV).
Doppler US of the portal vein in all 14 patients and of the hepatic artery in all eight patients was performed by two of our authors (T.H., S.K.).
To perform these procedures, we obtained approval of the institutional review board and informed consent from all patients. The Table summarizes the procedures.
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RESULTS
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Altered Hemodynamics of the Portal Vein
MPV of the right portal vein decreased in all 14 patients. The mean MPV was 20.8 cm/sec ± 7.6 (SD) before occlusion of the right hepatic vein but 15.3 cm/sec ± 4.5 during occlusion (Fig 2). Decrease in the value of MPV by means of occlusion was significant (P < .01).
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Figure 2. Graph shows altered right portal venous hemodynamics caused by the occlusion (occl.) of the right hepatic vein in 14 patients. MPV of the right portal vein decreased with occlusion in all patients. The mean MPV was 20.8 cm/sec ± 7.6 before occlusion and 15.3 cm/sec ± 4.5 during occlusion. The difference in these values was statistically significant (P < .01).
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In 10 of 13 patients, color Doppler signal in the portal venous branch in the occluded area changed from hepatopetal to no signal with occlusion of the right hepatic vein (Fig 3). In two patients, the signal remained hepatopetal but was weakened with occlusion (Fig 4). It changed from hepatopetal to hepatofugal with occlusion in one patient (Fig 5). Also, in all four patients in whom saline was injected manually through the arterial catheter during occlusion, hepatofugal flow appeared in the portal venous branch (Fig 4c).
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Figure 3a. Patient 3. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 58-year-old man with hepatocellular carcinoma. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal. Conversely, Doppler signal in the right hepatic vein (arrowhead) is hepatofugal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area changes to no signal during occlusion. Also, Doppler signal in the right hepatic vein (arrowhead) changes to no signal during occlusion.
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Figure 3b. Patient 3. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 58-year-old man with hepatocellular carcinoma. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal. Conversely, Doppler signal in the right hepatic vein (arrowhead) is hepatofugal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area changes to no signal during occlusion. Also, Doppler signal in the right hepatic vein (arrowhead) changes to no signal during occlusion.
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Figure 4a. Patient 8. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 71-year-old man with hepatocellular carcinoma. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area is still hepatopetal but weakened during occlusion. (c) Hepatofugal flow appears in the portal venous branch (arrow) in the occluded area, with manual injection of saline at a rate of 2-3 mL/sec through a catheter placed in the common hepatic artery.
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Figure 4b. Patient 8. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 71-year-old man with hepatocellular carcinoma. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area is still hepatopetal but weakened during occlusion. (c) Hepatofugal flow appears in the portal venous branch (arrow) in the occluded area, with manual injection of saline at a rate of 2-3 mL/sec through a catheter placed in the common hepatic artery.
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Figure 4c. Patient 8. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 71-year-old man with hepatocellular carcinoma. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area is still hepatopetal but weakened during occlusion. (c) Hepatofugal flow appears in the portal venous branch (arrow) in the occluded area, with manual injection of saline at a rate of 2-3 mL/sec through a catheter placed in the common hepatic artery.
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Figure 5a. Patient 14. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 67-year-old man with metastatic hepatic tumor. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal, while Doppler signal in the right hepatic vein (arrowhead) is hepatofugal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area changes to hepatofugal during occlusion, whereas Doppler signal in the right hepatic vein (arrowhead) changes to no signal during occlusion.
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Figure 5b. Patient 14. Oblique intercostal color Doppler US images of the portal venous branch in the occluded area in a 67-year-old man with metastatic hepatic tumor. (a) Doppler signal in the portal venous branch (arrow) in the occluded area before occlusion of the right hepatic vein is hepatopetal, while Doppler signal in the right hepatic vein (arrowhead) is hepatofugal. (b) Doppler signal in the portal venous branch (arrow) in the occluded area changes to hepatofugal during occlusion, whereas Doppler signal in the right hepatic vein (arrowhead) changes to no signal during occlusion.
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Altered Hemodynamics of the Hepatic Artery
In three patients in whom Doppler US was performed for 30 seconds after the start of occlusion of the right hepatic vein, APV of the right hepatic artery had a tendency toward a slight decrease for 15–30 seconds after the start of occlusion (Figs 6, 7). In all five patients in whom the occlusion time was 120 seconds, APV showed a decrease or plateau for 15–30 seconds after the start of occlusion. After that, APV increased rapidly to reach a plateau at around 75–90 seconds, with 1.5–2 times as much velocity as that before occlusion (Figs 6, 7). As soon as the balloon was deflated, APV began to decrease (Fig 7). APV of the hepatic arterial branch in the occluded area showed a pattern similar to that of the right hepatic artery.
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Figure 6a. Patient 12. Doppler US image of the hepatic artery in a 53-year-old man with metastatic hepatic tumor shows (a) the transducer-tipped guide wire in the examined artery. The transducer-tipped guide wire is passed through the microcatheter, and its tip (arrow) is projected from the microcatheter. The inflated balloon catheter (arrowhead) is placed in the right hepatic vein. (b) Printout of the video-screen display from Doppler US performed in the right hepatic artery before occlusion of the right hepatic vein. The velocimeter displays the blood flow velocity profile in spectral and numeric forms, including APV and MPV. ACC = acceleration index, CPI = cardiometrics pulsatility index, and RI = resistance index. APV is 33 cm/sec. (c) Printout of the video-screen display from Doppler US performed in the right hepatic artery at 90 seconds after the start of occlusion of the right hepatic vein. APV is 49 cm/sec, which is about 1 times greater than that before occlusion.
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Figure 6b. Patient 12. Doppler US image of the hepatic artery in a 53-year-old man with metastatic hepatic tumor shows (a) the transducer-tipped guide wire in the examined artery. The transducer-tipped guide wire is passed through the microcatheter, and its tip (arrow) is projected from the microcatheter. The inflated balloon catheter (arrowhead) is placed in the right hepatic vein. (b) Printout of the video-screen display from Doppler US performed in the right hepatic artery before occlusion of the right hepatic vein. The velocimeter displays the blood flow velocity profile in spectral and numeric forms, including APV and MPV. ACC = acceleration index, CPI = cardiometrics pulsatility index, and RI = resistance index. APV is 33 cm/sec. (c) Printout of the video-screen display from Doppler US performed in the right hepatic artery at 90 seconds after the start of occlusion of the right hepatic vein. APV is 49 cm/sec, which is about 1 times greater than that before occlusion.
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Figure 6c. Patient 12. Doppler US image of the hepatic artery in a 53-year-old man with metastatic hepatic tumor shows (a) the transducer-tipped guide wire in the examined artery. The transducer-tipped guide wire is passed through the microcatheter, and its tip (arrow) is projected from the microcatheter. The inflated balloon catheter (arrowhead) is placed in the right hepatic vein. (b) Printout of the video-screen display from Doppler US performed in the right hepatic artery before occlusion of the right hepatic vein. The velocimeter displays the blood flow velocity profile in spectral and numeric forms, including APV and MPV. ACC = acceleration index, CPI = cardiometrics pulsatility index, and RI = resistance index. APV is 33 cm/sec. (c) Printout of the video-screen display from Doppler US performed in the right hepatic artery at 90 seconds after the start of occlusion of the right hepatic vein. APV is 49 cm/sec, which is about 1 times greater than that before occlusion.
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Figure 7. Graph shows altered hemodynamics of the right hepatic artery caused by occlusion (occl.) of the right hepatic vein in eight patients. In the first three patients ( ,  ,  ), APV of the right hepatic artery had a tendency toward a slight decrease for 15-30 seconds after the start of occlusion. In the last five patients ( ,  ,  ,  ,  ), APV of the right hepatic artery showed a decrease or plateau for 15-30 seconds. After that, APV increased rapidly to reach a plateau at around 75-90 seconds, having 1.5-2 times as much velocity as that before occlusion. As soon as occlusion was removed, APV began to decrease. rel. = release of occlusion.
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DISCUSSION
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Approximately 30 years ago, hepatic arteriographic findings in patients with Budd-Chiari syndrome revealed crowding of arterial branches and intensity at hepatography, sometimes followed by retrograde portal opacification in the obstructed area (5,8–10). While virtually no particular notice was given to this phenomenon during the next 2 decades, Kanazawa et al (1) found in 1993 that the same phenomenon was induced with temporary balloon occlusion of the hepatic vein. After their experimental report, interventional therapy for malignant hepatic tumors was attempted during temporary occlusion of the hepatic vein (2,11,12). The effectiveness of such therapy depends on the idea that during hepatic venous occlusion, the portal vein becomes a draining vein, and the occluded area is supplied with hepatic arterial flow alone, which can compensatorily increase. However, this idea was derived mainly from studies (1–4) in which angiography and CT arteriography were performed by using contrast material.
For reasons of study uniformity and technical feasibility, we selected the right hepatic vein as the vein to be occluded in all patients. While extracorporeal Doppler US of the portal vein was possible with a 3.5-MHz transducer from the beginning of our study, precise extracorporeal evaluation of the intrahepatic artery was difficult. The transducer-tipped guide wire became available in our institution in November 1997. Whereas it was initially developed for the evaluation of coronary arterial flow (13,14), we suspected that its small caliber and flexibility might be suitable for monitoring hemodynamics of the right hepatic artery and the even thinner peripheral branches in the occluded area. For this reason, we were able to evaluate hemodynamic changes in the hepatic artery in the most recent eight of the 14 patients in our study.
In previous studies (1–4), hepatofugal portal opacification in the occluded area was often observed at angiography and CT arteriography during temporary occlusion of the hepatic vein. Therefore, the portal vein was thought to be the draining vein. However, in our study with Doppler US, we could not see any hepatofugal portal flow in the occluded area, except in one patient, and Doppler signal in the portal venous branch in the occluded area varied individually: No signal in 10 patients, weakened hepatopetal in two, and hepatofugal in one. We surmised that such variation can probably be explained by the differences in the degree of development of small venovenous anastomosis, which is another possible draining route and often exists in the liver.
To explain the frequent appearance of no signal, it is possible that the present Doppler US was not sensitive enough to capture slow hepatofugal portal flow. Manual injection of saline through the arterial catheter caused hepatofugal portal flow in all four examined patients. This may suggest that hepatofugal portal opacification at angiography and CT arteriography performed during temporary occlusion of the hepatic vein is related to the injection pressure of contrast material.
MPV of the right portal vein decreased substantially with temporary occlusion of the right hepatic vein in our study. The right hepatic lobe has not only the area occluded by the right hepatic vein but also a nonoccluded area (3). Substantial decrease in velocity of the right portal vein might reflect absence or marked decrease in hepatopetal portal flow in the occluded area.
In a scintigraphic study in pigs, in which technetium 99m-macroaggregated albumin was infused through the hepatic artery for more than 60 minutes during hepatic venous occlusion, there was a substantial increase in the amount of radioactivity measured in the occluded area and a substantial decrease in that of the nonoccluded area (1). However, the scintigraphic findings could neither demonstrate real-time hemodynamic change nor quantify flow of the hepatic artery.
Real-time and flow information, however, were obtainable in our study by using the transducer-tipped guide wire. When we began our study, we expected that marked hemodynamic change in the hepatic artery might occur as soon as hepatic venous occlusion started. We suspected, therefore, that Doppler US performed for 30 seconds after the start of occlusion would be sufficient to examine hemodynamic change in the hepatic artery.
APV of the right hepatic artery showed a surprising tendency toward a slight decrease for 15–30 seconds after the start of occlusion in the first three patients. Such a result was definitely inconsistent with those of previous scintigraphic study reports. We thought that the discrepancy between our results and the previous scintigraphic results could be explained with the different durations of hepatic venous occlusion; duration was 30 seconds in our study, while it was more than 60 minutes in the scintigraphic study. Thus, for the latter five patients, we extended the occlusion time from 30 to 120 seconds. We obtained a similar pattern in all five patients: rapid increase in APV beyond 15–30 seconds.
This slight decrease in APV of the right hepatic artery for 15–30 seconds after the start of occlusion can be explained by an elevation in peripheral vascular resistance, which is accompanied by an increase in sinusoidal pressure due to acute congestion. Increase in APV beyond 15–30 seconds indicates the start-up of intrinsic autoregulation, which overcomes elevation of peripheral vascular resistance. Hepatic arterial buffer response can be one explanation for such intrinsic autoregulation (15–17).
In the occluded area, altered hemodynamics caused by temporary occlusion of the hepatic vein, which we clarify in the present study, is thought to be beneficial in interventional therapy for malignant hepatic tumors. During hepatic arterial infusion, the concentration of the delivered agent in the occluded area through the hepatic artery may increase, as arterial flow increases, and remain at a high level due to congestion; dilution may slow down owing to absence of or decrease in hepatopetal portal flow (18–20). Transcatheter arterial embolization performed during hepatic venous occlusion should be more effective because of simultaneous embolization of the hepatic artery, sinusoid, and portal venous branch in the occluded area (11). In microwave coagulation therapy, absence of or decrease in hepatopetal portal flow during hepatic venous occlusion may lead to more extensive coagulation because of subsequent decrease in the cooling effect of the portal flow (21).
Our study had four limitations. First, although our study group included patients with and those without cirrhosis, we could not evaluate changes in hepatic arterial flow with Doppler US in patients with cirrhosis. This was due to the limited number of patients and study duration. However, we surmise that hepatic arterial flow may increase in patients with cirrhosis, because hepatic arteriography performed in patients with cirrhosis showed similar hepatographic findings in the occluded area compared with that in patients without cirrhosis. Second, with Doppler US, we could not clearly demonstrate draining of the increased arterial flow. We hypothesize that increased arterial flow (a) stagnates in the sinusoids and central veins; (b) drains into the nonoccluded area through small venovenous anastomoses, including invisible and visible ones at occlusion venography; and (c) simultaneously drains into the portal vein with slow hepatofugal flow, which is rarely depicted with extracorporeal Doppler US. Further studies will be necessary to confirm this hypothesis. Third, there is a potential influence of the intraarterial catheter on the Doppler measurements performed in the hepatic artery. This is a potential for diminished increase in the hepatic arterial flow compensation because of luminal narrowing by the catheter. Fourth, our experiment simulated acute hepatic venous occlusion. Therefore, our results may not be applicable to the more common chronic hepatic venous occlusion seen clinically.
In conclusion, with Doppler US, we could clarify altered hemodynamics caused by temporary occlusion of the hepatic vein. In the occluded area, arterial velocity began to increase from 15 to 30 seconds beyond the start of occlusion and reached a plateau at 75–90 seconds, with approximately 1.5–2 times as much velocity as that before occlusion, while prominent drainage by the portal vein was rarely observed. We believe that these altered hemodynamics caused by temporary occlusion of the hepatic vein may increase the effectiveness of interventional therapy for malignant hepatic tumors.
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FOOTNOTES
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Abbreviations: APV = average peak velocity,
MPV = maximum peak velocity
Author contributions: Guarantor of integrity of entire study, S.K.; study concepts and design, all authors; literature research, T.H., S.K.; clinical studies, T.H., S.K., H.M., K.Y.; data acquisition, T.H., S.K., H.M., K.Y.; data analysis/interpretation, all authors; statistical analysis, T.H., S.K.; manuscript preparation and definition of intellectual content, all authors; manuscript editing, T.H., S.K., Y.H.; manuscript revision/review and final version approval, all authors.
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Y. Itai, T. Hiraki, and S. Kanazawa
Drainage Vein under Acute Occlusion of a Hepatic Vein * Drs Hiraki and Kanazawa respond:
Radiology,
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224(2):
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