Limits of and Complications after Embolization of the Hepatic Artery and Portal Vein to Induce Segmental Hypertrophy of the Liver: A Large Mini-Pig Study

2016 ◽  
Vol 57 (3-4) ◽  
pp. 155-170
Author(s):  
Nils Heits ◽  
Lars Mueller ◽  
Andreas Koops ◽  
Susan Koops ◽  
Jochen Herrmann ◽  
...  
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Laboratory Data ◽  
Arterial Embolization ◽  
Technical Problems ◽  
Inflammatory Damage ◽  
Hepatic Volume ◽  
Body Weight Index ◽  
Collateral Vessels ◽  
Mini Pigs

Background: The aim of this study was to compare arterial embolization (AE) with portal vein embolization (PVE) for the induction of segmental hypertrophy regarding procedural efficacy, safety and outcome. Methods: A total of 29 mini pigs were subjected to PVE, AE or assigned to the sham (SO) group. Correspondingly, 75% of the hepatic artery or portal vein branches were embolized. Growth and atrophy of the liver lobes, calculating the liver-to-body weight index (LBWI), laboratory data, arteriography, portography, Doppler ultrasound (US) and histopathology were analyzed. Results: After PVE, 2 animals had to be excluded due to technical problems. After AE, 4 animals had to be excluded because of technical problems and early sacrifice. Postprocedural US demonstrated effective AE and PVE of the respective lobes. Four weeks after PVE, portography showed a slow refilling of the embolized lobe by collateral portal venous vessels. Four weeks after AE, arteriography revealed a slight revascularization of the embolized lobes by arterial neovascularization. Segmental AE led to extensive necrotic and inflammatory alterations in the liver and bile duct parenchyma. Significant hypertrophy of the non-embolized lobe was only noted in the PVE group (LBWI: 0.91 ± 0.28%; p = 0.001). There was no increase in the non-embolized lobe in the AE (LBWI: 0.45 ± 0.087%) and SO group (LBWI: 0.45 ± 0.13%). Conclusion: PVE is safe and effective to induce segmental hypertrophy. Portal reperfusion by collateral vessels may limit hypertrophy. AE did not increase the segmental hepatic volume but carries the risk of extensive necrotic inflammatory damage.

Portal Vein Tract Embolization After Percutaneous Transhepatic Biliary Interventions

2018 ◽  
Author(s):  
Kazim Narsinh ◽  
Steven C. Rose ◽  
Thomas Kinney
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Arterial Embolization ◽  
Bleeding Complications ◽  
Hepatic Arteriography ◽  
Portal Vein Branch ◽  
Vein Access ◽  
Suitable Target ◽  
Hepatic Artery Branch ◽  
Artery Branch

Bleeding complications during percutaneous biliary intervention result from injury to the hepatic artery, hepatic vein, or portal vein. If bleeding originating from a hepatic artery branch is suspected, hepatic arteriography should be performed with and without the drainage catheter in place over a wire, and subselective embolization can be performed if a suitable target is identified. If a bleeding hepatic artery branch is not identified, bleeding from a portal vein branch is suspected. Treatment of portal vein injuries is challenging in this situation because obtaining direct percutaneous portal vein access is ill-advised. Although injuries to the hepatic artery or vein can often be treated by tract tamponade or arterial embolization, iatrogenic communication between the portal vein and biliary system can be difficult to treat effectively. This chapter presents a method to identify portal vein-to-biliary tract communications via cholangiography, with subsequent embolization via the transhepatic tract.

Hepatic capillary pressure is estimated using triple vascular occlusion method in isolated canine liver

1996 ◽  
Vol 271 (5) ◽  
pp. R1130-R1141 ◽  
Author(s):  
T. Shibamoto ◽  
H. G. Wang ◽  
S. Tanaka ◽  
S. Koyama
Keyword(s):  
Portal Vein ◽  
Capillary Pressure ◽  
Hepatic Artery ◽  
Vascular Resistance ◽  
Gravimetric Method ◽  
Vascular Occlusion ◽  
Liver Weight ◽  
Hepatic Veins ◽  
Hepatic Hemodynamics ◽  
Hepatic Volume

We determined whether the triple vascular occlusion pressure (Pto), the equilibration pressure obtained when the hepatic artery, portal, and hepatic veins were occluded simultaneously, represented the capillary pressure (Pc) in isolated bivascularly blood-perfused canine livers. Effects of a bolus injection of histamine (0.1-60 micrograms), norepinephrine (NE; 1-600 micrograms), or acetylcholine (ACh; 0.01-10 micrograms) into the portal vein or the hepatic artery were also studied on vascular resistance distribution using Pto as a measure of Pc. The livers were perfused at constant flow via the portal vein and at constant pressure via the hepatic artery. Pto was compared with Pc measured using the traditional gravimetric method (Pc,i). Pto and Pc,i showed a strong correlation (Pto = -0.02 + 0.98 Pc,i; r = 0.83, P = 0.0018). With comparisons, the intercept was not significantly different from zero, and the slope was not different from 1.00, indicating that Pto accurately represented Pc. The resting postsinusoidal vascular resistance comprised 54% of the total hepatic vascular resistance (Rt). Portal or arterial injection of histamine increased predominantly hepatic venous resistance (Rhv) over portal resistance with liver weight gain. NE constricted both the portal vein and the hepatic artery in greater magnitude than the hepatic vein, as evidenced by a significant decrease in the Rhv/Rt ratio. This precapillary constriction was accompanied by a significant decrease in liver weight. In contrast, ACh contracted both portal and hepatic veins similarly without liver weight change. We conclude that Pto is an excellent estimate of Pc in isolated blood-perfused canine livers and that the hepatic vascular resistance sites in the resting states are located evenly in the pre- and postsinusoidal vessels. Intraportal or intra-arterial infusion of histamine, NE, and ACh produced characteristically different changes in hepatic vascular resistances and hepatic volume. The Pto technique could be applied in experimental research on hepatic hemodynamics.

Hepatic venoconstrictor effects of isoproterenol and nifedipine in anesthetized cats

1984 ◽  
Vol 62 (6) ◽  
pp. 665-672 ◽  
Author(s):  
K. L. Seaman ◽  
C. V. Greenway
Keyword(s):  
Cardiac Output ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Blood Volume ◽  
Renin Angiotensin System ◽  
Peripheral Vein ◽  
Angiotensin System ◽  
Intravenous Infusions ◽  
Hepatic Volume ◽  
Hepatic Nerves

In cats anesthetized with pentobarbital, isoproterenol infused into a peripheral vein causes a reduction in hepatic blood volume measured by plethysmography. As this response is accompanied by increases in portal and hepatic lobar venous pressures, the decrease in hepatic volume cannot be a passive emptying secondary to reduced intrahepatic pressure. We conclude that intravenous isoproterenol causes an active hepatic venoconstriction. Nifedipine produced similar responses. From this and our previous data, we conclude that in anesthetized cats, arteriolar vasodilators which increase cardiac output cause hepatic venoconstriction (hydralazine, adrenaline, dopamine, isoproterenol, and nifedipine), while those which do not increase cardiac output have no effect on the hepatic venous bed (nitroprusside and diazoxide) or cause venodilatation (nitroglycerine). The mechanism of the hepatic venoconstrictor effect of isoproterenol was investigated further. Because previous work has shown that this response does not occur when isoproterenol is infused locally into the hepatic artery or portal vein, the venoconstrictor effect of peripheral intravenous infusions must be indirectly mediated. The response was still present after hepatic denervation, adrenalectomy, nephrectomy, and after indomethacin administration indicating it is not mediated by the hepatic nerves, adrenal catecholamines, the renal renin-angiotensin system, or prostaglandins. The mechanism remains unknown.

The Glissonian Approach of the Hilum

Swiss Surgery ◽  
1999 ◽  
Vol 5 (3) ◽  
pp. 143-146 ◽  
Author(s):  
Launois ◽  
Maddern ◽  
Tay
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Posterior Approach ◽  
Hepatic Duct ◽  
Rapid Evolution ◽  
Hepatic Tissue ◽  
Detailed Knowledge ◽  
Porta Hepatis ◽  
Liver Segment ◽  
Glissonian Approach

The detailed knowledge of the segmental anatomy of the liver has led to a rapid evolution in resectional surgery based on the intrahepatic distribution of the portal trinity (the hepatic artery, hepatic duct and portal vein). The classical intrafascial or extrahepatic approach is to isolate the appropriate branch of the portal vein, hepatic artery and the hepatic duct, outside the liver substance. Another method, the extrafascial approach, is to dissect the whole sheath of the pedicle directly after division of a substantial amount of the hepatic tissue to reach the pedicle, which is surrounded by a sheath, derived from Glisson's capsule. This Glissonian sheath encloses the portal trinity. In the transfissural or intrahepatic approach, these sheaths can be approached either anteriorly (after division of the main, right or umbilical fissure) or posteriorly from behind the porta hepatis. We describe the technique for approaching the Glissonian sheath and hence the hepatic pedicle structures and their branches by the intrahepatic posterior approach that allows early delineation of the liver segment without the need for ancillary techniques. In addition, the indications for the use of this technique in the technical and oncologic settings are also discussed.

The Occurrence of a Pseudoaneurysm of the Hepatic Artery within the Thrombosed Portal Vein of a Patient with Chronic Pancreatitis: A Case Report

2008 ◽  
Vol 58 (4) ◽  
pp. 399
Author(s):  
Eun Soo Kim ◽  
Kyung Mi Jang ◽  
Min Jeong Kim ◽  
Hoi Soo Yoon ◽  
Hyun Lee ◽  
...  
Keyword(s):  
Case Report ◽  
Chronic Pancreatitis ◽  
Portal Vein ◽  
Hepatic Artery

scholarly journals Hemodynamic profile and tissular oxygenation in orthotopic liver transplantation: Influence of hepatic artery or portal vein revascularization of the graft

2006 ◽  
Vol 12 (11) ◽  
pp. 1607-1614 ◽  
Author(s):  
Carlos Moreno ◽  
Antoni Sabaté ◽  
Joan Figueras ◽  
Imma Camprubí ◽  
Antonia Dalmau ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Orthotopic Liver Transplantation ◽  
Hemodynamic Profile

scholarly journals Vascular Involvements in Cholangiocarcinoma: Tips and Tricks

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3735
Author(s):  
Roberta Angelico ◽  
Bruno Sensi ◽  
Alessandro Parente ◽  
Leandro Siragusa ◽  
Carlo Gazia ◽  
...  
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Vena Cava ◽  
High Volume ◽  
Vascular Reconstruction ◽  
Ex Situ ◽  
Vascular Involvement ◽  
Hepatic Veins ◽  
Hepatic Artery Resection ◽  
Artery Resection

Cholangiocarcinoma (CCA) is an aggressive malignancy of the biliary tract. To date, surgical treatment remains the only hope for definitive cure of CCA patients. Involvement of major vascular structures was traditionally considered a contraindication for resection. Nowadays, selected cases of CCA with vascular involvement can be successfully approached. Intrahepatic CCA often involves the major hepatic veins or the inferior vena cava and might necessitate complete vascular exclusion, in situ hypothermic perfusion, ex situ surgery and reconstruction with autologous, heterologous or synthetic grafts. Hilar CCA more frequently involves the portal vein and hepatic artery. Resection and reconstruction of the portal vein is now considered a relatively safe and beneficial technique, and it is accepted as a standard option either with direct anastomosis or jump grafts. However, hepatic artery resection remains controversial; despite accumulating positive reports, the procedure remains technically challenging with increased rates of morbidity. When arterial reconstruction is not possible, arterio-portal shunting may offer salvage, while sometimes an efficient collateral system could bypass the need for arterial reconstructions. Keys to achieve success are represented by accurate selection of patients in high-volume referral centres, adequate technical skills and eclectic knowledge of the various possibilities for vascular reconstruction.

scholarly journals Doppler ultrasound in liver cirrhosis: correlation of hepatic artery and portal vein measurements with model for end-stage liver disease score in Egypt

2020 ◽  
Vol 51 (1) ◽  
Author(s):  
Ahmed Abdelrahman Mohamed Baz ◽  
Rana Magdy Mohamed ◽  
Khaled Helmy El-kaffas
Keyword(s):  
Liver Cirrhosis ◽  
Liver Disease ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Meld Score ◽  
Hepatic Decompensation ◽  
End Stage Liver Disease ◽  
Cirrhotic Patients ◽  
Us Findings ◽  
End Stage

Abstract Background Liver cirrhosis is a multi-etiological entity that alters the hepatic functions and vascularity by varying grades. Hereby, a cross-sectional study enrolling 100 cirrhotic patients (51 males and 49 females), who were diagnosed clinically and assessed by model for end-stage liver disease (MELD) score, then correlated to the hepatic Doppler parameters and ultrasound (US) findings of hepatic decompensation like ascites and splenomegaly. Results By Doppler and US, splenomegaly was evident in 49% of patients, while ascites was present in 44% of them. Increased hepatic artery velocity (HAV) was found in70% of cases, while 59% showed reduced portal vein velocity (PVV). There was a statistically significant correlation between HAV and MELD score (ρ = 0.000), but no significant correlation with either hepatic artery resistivity index (HARI) (ρ = 0.675) or PVV (ρ =0.266). Moreover, HAV had been correlated to splenomegaly (ρ = 0.000), whereas HARI (ρ = 0.137) and PVV (ρ = 0.241) did not significantly correlate. Also, ascites had correlated significantly to MELD score and HAV (ρ = 0.000), but neither HARI (ρ = 0.607) nor PVV (ρ = 0.143) was significantly correlated. Our results showed that HAV > 145 cm/s could confidently predict a high MELD score with 62.50% and 97.62 % sensitivity and specificity. Conclusion Doppler parameters of hepatic vessels (specifically HAV) in addition to the US findings of hepatic decompensation proved to be a non-invasive and cost-effective imaging tool for severity assessment in cirrhotic patients (scored by MELD); they could be used as additional prognostic parameters for improving the available treatment options and outcomes.

scholarly journals Multidisciplinary treatment of left hepatic artery pseudoaneurysm after hepatobiliary resection for gallbladder cancer: a case report

2019 ◽  
Vol 5 (1) ◽  
Author(s):  
Ryusei Yamamoto ◽  
Teiichi Sugiura ◽  
Yukiyasu Okamura ◽  
Takaaki Ito ◽  
Yusuke Yamamoto ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Portal Vein ◽  
Liver Failure ◽  
Hepatic Artery ◽  
Remnant Liver ◽  
Left Hepatic Artery ◽  
Artery Pseudoaneurysm ◽  
Hepatobiliary Resection ◽  
Portal Vein Arterialization ◽  
Arterial Inflow

Abstract Background When a postoperative hepatic artery pseudoaneurysm develops after massive hepatectomy, both an intervention for the pseudoaneurysm and patency of hepatic artery should be considered because occlusion of the residual hepatic artery results in critical liver failure. However, the treatment strategy for a pseudoaneurysm of the hepatic artery after hepatobiliary resection is not well established. Case presentation A 65-year-old woman underwent right hepatectomy, extrahepatic duct resection, and portal vein resection, for gallbladder cancer. Although the patient had an uneventful postoperative course, computed tomography on postoperative day 6 showed a 6-mm pseudoaneurysm of the hepatic artery. Angiography revealed the pseudoaneurysm located on the bifurcation of the left hepatic artery to the segment 2 artery plus the segment 3 artery and 4 artery. Stent placement in the left hepatic artery was not feasible because the artery was too narrow, and coiling of the pseudoaneurysm was associated with a risk of occluding the left hepatic artery and inducing critical liver failure. Therefore, portal vein arterialization constructed by anastomosing the ileocecal artery and vein was performed prior to embolization of the pseudoaneurysm to maintain the oxygen level of the remnant liver, even if the left hepatic artery was accidentally occluded. The pseudoaneurysm was selectively embolized without occlusion of the left hepatic artery, and the postoperative laboratory data were within normal limits. Although uncontrollable ascites due to portal hypertension occurred, embolization of the ileocolic shunt rapidly resolved it. The patient was discharged on postoperative day 45. Conclusion Portal vein arterialization prior to embolization of the aneurysm may be a feasible therapeutic strategy for a pseudoaneurysm that develops after hepatectomy for hepatobiliary malignancy to guarantee arterial inflow to the remnant liver. Early embolization of arterioportal shunting after confirmation of arterial inflow to the liver should be performed to prevent morbidity induced by portal hypertension.

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