Replacement of the retrohepatic vena cava in segmental liver transplantation

Reduced grafts represent an important technical development in paediatric liver transplantation. The use of a left lateral segment graft has required preservation of the native inferior vena cava to "piggy-back" the graft onto it. We report four children who underwent left lateral segment transplantation with caval replacement using the donor iliac vein because the native retrohepatic inferior vena cava was small, friable or difficult to preserve. There were no caval or hepatic vein complications post-transplant and the donor iliac vein proved to be a satisfactory interpositional graft. The technique offers the advantages of a wider retrohepatic cava avoiding venous outflow or caval obstruction, provides good tissue to suture and is well suited for the triangulation technique of the left hepatic vein.     

Mammalian base excision repair and DNA polymerase beta

OBJECTIVE: To describe six dogs with congenital abnormalities involving the portal vein, caudal vena cava, or both. ANIMALS: Six client-owned dogs with congenital interruption of the portal vein or the caudal vena cava, or both. METHODS: Portal vein and caudal vena cava anatomy was evaluated by contrast radiography and visualization at surgery. Vascular casts or plastinated specimens were obtained in three animals. RESULTS: Portal blood shunted into the caudal vena cava in four dogs and the left hepatic vein in one. Two of these five dogs also had interruption of the caudal vena cava with continuation as azygous vein, as did an additional dog, in which the portal vein was normally formed. Portal vein interruption was present in 5 of 74 (6.8%) dogs with congenital portosystemic shunts evaluated at the Veterinary Teaching Hospital during the study period. CONCLUSIONS: Serious malformations of the abdominal veins were present in more than 1 in 20 dogs with single congenital portosystemic shunts. CLINICAL RELEVANCE: Veterinarians involved in diagnosis and surgery for portosystemic shunts should be aware of these potential malformations, and portal vein continuity should be evaluated in all dogs before attempting shunt attenuation.     

Vascular reconstruction using left renal vein graft in advanced hepatobiliary malignancy

BACKGROUND/AIMS: In surgical resection for advanced hepatobiliary malignancies involving the portal vein and inferior vena cava, vascular reconstruction is usually required. We utilized left renal vein grafts for vascular reconstruction in cases of these malignancies, and their clinical significance is evaluated in this study. METHODOLOGY: Left renal vein grafts were utilized for reconstruction of the portal vein in four patients and patch repair of the inferior vena cava was performed in two patients with advanced hepatobiliary malignancies. All six patients underwent hepatic resection with vascular resection and reconstruction. Postoperative renal function and graft patency were assessed. RESULTS: Transient slight renal disturbances appeared in some patients, but there was no severe renal dysfunction requiring specific therapy. Graft patency was maintained during the follow-up period in all patients. CONCLUSION: The use of left renal vein grafts as autovein grafts seems appropriate in cases involving reconstruction of the portal vein and in those involving patch repair of the inferior vena cava defect in surgical resection for advanced hepatobiliary malignancies.     

Budd-Chiari syndrome: a common complication of Beh?et's disease

OBJECTIVE: The Budd-Chiari syndrome is characterized by venous outflow obstruction of the liver, usually occurring as a consequence of thrombosis of the hepatic veins. Vasculitis is a major component of Beh?et's syndrome. The aim of this study was to determine the incidence of hepatic vein thrombosis in patients with Beh?et's disease and to estimate the effect of this entity upon the clinical features and course of Beh?et's syndrome. METHODS: During an 8-yr period from 1985 to 1994, from a total of 493 patients with Beh?et's disease seen at Hacettepe University Hospital, the incidence and effect of hepatic vein thrombosis on the clinical course of Beh?et's syndrome was investigated. The hepatic vein thrombosis in each case was documented by hepatic venography and confirmed by digital subtraction angiography, computed tomography, ultrasonography, and liver biopsy. Coagulation parameters including protein C, protein S, and anti-thrombin III levels were easured in each case. The survival of cases with Beh?et's syndrome complicated by Budd-Chiari syndrome and the effect of the Budd-Chiari syndrome on the survival of individuals with Beh?et's syndrome were determined using the Kaplan-Meier technique. RESULTS: Of the 493 cases of Beh?et's syndrome, 53 (10.8%) were found to have one or more large vessel thrombosis. Of these 53 patients, 14 (26.4%) had hepatic vein thrombosis. Of these 14 patients, 8 had an additional inferior vena cava thrombosis and 4 had portal vein as well as total inferior vena cava thrombosis. Only two patients with isolated hepatic vein thrombosis were identified. These two patients and two additional patients with hepatic vein thrombosis plus thrombosis of the hepatic portion of the inferior vena cava are currently alive. Of the 10 patients with total inferior vena cava and hepatic vein thrombosis (4 also had portal vein thrombosis), all 10 died with a mean survival of 10.3 months. During the same time period, 37 patients obtained from a total of 1494 patients with clinical evidence of either portal hypertension, hepatic venous outflow obstruction or inferior vena caval obstruction without Beh?et's syndrome were found to have a Budd-Chiari syndrome. Of these 37 patients, 19 (51%) had an identifiable underlying disorder responsible for their hepatic vein thrombosis. CONCLUSION: Based upon this experience, it appears as if Budd-Chiari syndrome is a relatively frequent complication of Beh?et's disease. When individuals with Beh?et's syndrome have BCS, concurrent thrombosis of the portal vein and inferior vena cava are often found, if the patency of these vessels is assessed. The clinical course of patients with Beh?et's syndrome complicated by Budd-Chiari syndrome is poor. The extent of the vascular thrombosis within the inferior vena cava rather than the presence of the hepatic vein thrombosis per se is the major determinant of survival.     

Total anomalous pulmonary venous return complicating portoenterostomy for biliary atresia

Cardiovascular anomalies such as absent inferior vena cava and preduodenal portal vein are reported in cases of biliary atresia and make hepatic portoenterostomy a technical challenge. The authors present the case of a severe cardiac anomaly that significantly altered the functional outcome of a Kasai procedure. Baby M., an 8-week-old boy born with total anomalous pulmonary venous return (TAPVR), underwent hepatic portoenterostomy for biliary atresia. Over the next 3 months he remained icteric and febrile, and failed to gain weight. After multiple antibiotic treatments for suspected cholangitis, he underwent reexploration of the portoenterostomy, with no improvement in his overall condition. His prognosis was considered dismal because correction of the cardiac anomaly is associated with a high mortality rate (> 90%). The cardiac surgeon agreed to attempt a cure of the TAPVR, provided liver transplantation is contemplated if the patient survived. Within 48 hours postoperatively, his hepatic function had improved drastically. He became afebrile, had an improved appetite and weight gain, and was finally discharged 203 days after admission. One year later, he is thriving and remains anicteric. The exact reason for this drastic improvement is not well understood, but the right-sided cardiac failure caused by the TAPVR had a significant effect on the functional outcome of the portoenterostomy.     

Inferolateral retraction reduces the risk of thermal injury to biliary structures

A liver transplant technique is described in a patient with a thrombosed portal vein and a functioning surgically created renal-lieno shunt. Permanent portal inflow to the graft was provided by division of the left renal vein (LRV) at its junction with the inferior vena cava and anastomosis of the LRV end-to-end with the donor portal vein. Although this results in splanchnic blood traversing a 360 degree roundabout from the superior mesenteric vein via the splenic and disconnected left renal veins to the donor portal vein, the anastomosis lay well and the procedure was successful.     

CT and MRI in detection of intrahepatic portosystemic shunts in patients with liver cirrhosis

OBJECTIVE: Our goal was to determine the prevalence and anatomic location of intrahepatic portosystemic shunts (IPSs) in patients with hepatic cirrhosis as shown by CT and MRI. MATERIALS AND METHODS: We retrospectively reviewed CT and MR scans of 33 cirrhotic patients who had IPSs. In addition, two series of 100 consecutive CT or MR were reviewed to determine the prevalence of IPSs and the percentage of intrahepatic and extrahepatic paraumbilical veins. RESULTS: Intrahepatic portosystemic shunts were divided into three groups according to the intrahepatic course: paraumbilical shunt between the left portal vein and the paraumbilical vein anterior to the liver (n = 29); inferior vena caval shunt between the posterior branch of the right portal vein and the inferior vena cava (n = 2); and miscellaneous (n = 2). Shunts of the paraumbilical type ran through the medial (n = 23), lateral (n = 3), or both medial and lateral (n = 3) segments of the left lobe of the liver. Twenty-five patients had one shunt, and four had more than one. Six cases were also associated with extrahepatic paraumbilical veins. CONCLUSION: Intrahepatic portosystemic shunts, especially the paraumbilical type, were not infrequently visualized in patients with hepatic cirrhosis.     

An improved technique for bloodless hepatic resection on in situ cold perfused liver

An improved technique for bloodless hepatic resection using in situ isolation and asanguinous hypothermic perfusion was described to deal with huge liver tumors involved in the liver hilum, the main hepatic veins and retrohepatic inferior vena cava. The original Fortner's technique was modified, including the choice of incision; semi-isolated perfusion of the liver portion preserved through the single portal vein; suprahepatic outlet of the perfusate and the shortening of the period of hepatic ischemia by reperfusion of hepatic artery prior to the repair or reconstruction of the portal vein. The initial successful experience of the technique applied to 2 pediatric cases with giant liver tumors was reported, and the indications, intraoperative and early postoperative courses were discussed.     

Heterotopic liver transplantation in rats: effect of intrahepatic islet isografts and split portal blood flow on liver integrity after auxiliary liver isotransplantation

BACKGROUND: Auxiliary heterotopic liver grafts atrophy in the absence of portal venous inflow; evidence suggests that an islet-derived hepatotrophic factor may exist in the portal drainage. Here we examine the effects of intrahepatic islet isografts in maintaining hepatocyte integrity in Wistar Furth rats with one of several types of arterialized auxiliary liver isografts. METHODS: In type 1 procedures the auxiliary liver was interposed into the recipient infrarenal vena cava and perfused through the graft portal vein with caval blood. In type 2 procedures the donor infrahepatic vena cava was anastomosed end-to-side to the recipient vena cava and the recipient portal vein was diverted to the graft portal vein. Both types of auxiliary grafts were arterialized; bile duct drainage was through the duodenum. Syngeneic islets were isolated and embolized into the portal veins of one half of the donor type 1 or native type 2 livers (1500 to 1700 islets). Finally, we performed six type 3 procedures in which a type 2 procedure was performed except that the portal blood flow was split so that the portal vein receiving the splenic, gastric, pancreatic, and duodenal drainage supplied the native liver and that the common mesenteric vein supplied the auxiliary graft with equivalent portal blood flow. Atrophy in heterotopic and native livers were compared for the three models after 3 months. RESULTS: Intrahepatic islets in type 1 auxiliary liver isografts without portal venous inflow did not prevent graft atrophy. Conversely, native livers deprived of portal venous inflow in our type 2 procedures, regardless of the presence of intrahepatic islet isografts, atrophied relative to auxiliary liver grafts in which portal venous inflow was provided by diverting the recipient's portal vein to the graft. In type 3 recipients atrophy was greater in the native livers than in the grafts. CONCLUSIONS: The results of our study suggest that islet-derived factors are not sufficient to prevent hepatocellular atrophy in auxiliary rat liver transplantation models and that a potent hepatotrophic factor may exist in the venous drainage of the bowel distal to the duodenum.     

The effects of intra-arterial and intraportal injections of vasopressin on the simultaneously perfused hepatic arterial and portal venous vascular beds of the dog

The hepatic arterial and hepatic portal venous vascular beds of the chloralose-urethane anesthetized dog were perfused simultaneously in situ. Vasopressin (10 mU = 1 unit) was injected in graded increasing doses into the hepatic artery and into the portal vein. Both intra-arterial and intraportal vasopressin elicited both hepatic arterial vasoconstriction and hepatic venous dilation; the delay in onset of both hepatic vascular effects was significantly shorter than that for any succeeding systemic effects (a rise in systemic arterial pressure and fall in heart rate), showing that they were not attributable to recirculation or to arterial baroreceptor reflexes. Injections of vasopressin into the inferior vena cava at the level of the hepatic veins consistently produced smaller hepatic vascular effects than either intra-arterial or intraportal injections of the same doses. The results are discussed in the context of the therapeutic role of vasopressin in controlling gastrointestinal bleeding and portal hypertension.     

Portal decompression using the inferior mesenteric vein

We report five patients with variceal hemorrhage, in three cases secondary to diffuse thrombosis of the portal, superior mesenteric and splenic veins. Mesenteric angiography demonstrated patency of the inferior mesenteric vein (IMV) in each, and successful portal decompression by anastomosis of the IMV to the left renal vein (n = 4) or the inferior vena cava (n = 1) was accomplished. Bleeding was permanently controlled: four patients have survived from one to eight years post-operatively. Because shunt procedures utilizing the IMV are technically straightforward, subtotally decompress the portal system and avoid the right upper quadrant, they may be advantageous in certain clinical settings.     

Hepatic outflow study after piggyback liver transplantation

BACKGROUND: Hepatic vein outflow is discussed in liver transplantation after preservation of recipient retrohepatic vena cava. The aim of this study was to compare two methods of suparahepatic caval anastomosis. METHODS: From January 1993 to January 1995, 81 patients received 88 liver transplants because of liver cirrhosis (n = 70), acute liver failure (n = 7), elective retransplantation after hepatic artery thrombosis (n = 2), giant hemangioma (n = 1), and combined liver-small bowel transplantation (n = 1). Seven patients underwent urgent retransplantation, 12 had preoperative transjugular intrahepatic portocaval stent, and 11 had portal vein thrombosis. Five patients required extracorporeal venous shunt. A total of 82 liver transplantations had preservation of RHVC, and 70 patients received temporary end-to-side portacaval shunt. Suprahepatic caval anastomosis was carried out in 52 patients (group 1) between the graft suprahepatic vena cava and the ostia of recipient left and median hepatic veins. Thirty patients (group 2) had associated 3 cm vertical cavotomy with partial clamping of RHVC. In the fourth postoperative month 20 patients from each group had pressure and gradient measurement made among the hepatic veins, right atria, and the RHVC. RESULTS: Mean pressure gradient between hepatic veins and right atria was 0.75 +/- 0.49 mm Hg in group 1 and 2.06 +/- 0.85 mm Hg in group 2. Between the RHVC and the right atria it was 0.63 +/- 0.5 mm Hg in group 1 and 2.22 +/- 1.29 mm Hg in group 2. A pressure gradient higher than 3 mm Hg was considered hemodynamically significant. This pressure gradient was found between the hepatic veins and right atria in 10% of patients in group 1 and 40% of patients in group 2 (p = 0.03) and between the RHVC and right atria in 15% of patients in group 1 and 30% of patients in group 2 (p = 0.3). CONCLUSIONS: Preservation of the recipient RHVC with recipient caval anastomosis at the ostia of the median and left hepatic veins is a reliable technique without any hepatic venous outflow alteration. Associated cavotomy is not necessary.     

The so-called spontaneous nodular panniculitis (Weber-Christian lipodystrophy)

In 24 patients without liver disease lipids and LCAT activity were determined in the inferior vena cava, the hepatic vein, the pulmonary vein and in the left ventricle. The total cholesterol, free cholesterol and cholesterol ester concentrations are identical and differences in the LCAT activity cannot be demonstrated.     

Budd-Chiari syndrome. Treatment options and the value of liver transplantation

The Budd-Chiari syndrome encompasses a group of conditions that cause partial or complete obstruction of the hepatic venous outflow tract. This leads to hepatocyte necrosis which can manifest as a devastating fulminant illness, or a more indolent condition that eventually presents with features of portal hypertension. Doppler ultrasonography of the hepatic veins and inferior vena cava has become the initial diagnostic test of choice, but most patients require venography and liver biopsy prior to definitive therapy. Multiple therapeutic modalities have been used for the Budd-Chiari syndrome, including medical, radiological, and surgical approaches. The role, indications, and outcome of liver transplantation for individuals with the Budd-Chiari syndrome are discussed.     

Modified repair of mixed anomalous pulmonary venous connection

A modified repair technique is reported for mixed total or partial anomalous pulmonary venous connection with the right superior pulmonary vein connecting to the superior vena cava, the right inferior pulmonary vein to the right atrium or left atrium, and the left pulmonary veins to the coronary sinus. The superior vena cava is transected above the highest right superior pulmonary vein, its cephalad end is anastomosed to the right atrial appendage, and a pericardial baffle is constructed between the cardiac ostium of the superior vena cava, the ostium of the right inferior pulmonary vein, and the left atrium, including the coronary sinus, which is unroofed. The reported technique may be valuable to avoid pulmonary venous obstruction in complex mixed forms of total or partial anomalous pulmonary venous connection.     

Midazolam-flumazenil topical anaesthesia for microlaryngoscopy with jet ventilation

BACKGROUND: Enhanced production of endothelin-1 (ET-1), vasoconstrictive 21 amino acids produced by endothelial cells during ischemia and after reperfusion of the liver, is known to cause sinusoidal constriction and microcirculatory disturbances, which lead to severe tissue damage. Using a 2-hour hepatic vascular exclusion model in dogs, we tested our hypothesis that neutralization of ET-1 by monoclonal anti-ET-1 and anti-ET-2 antibody (AwETN40) abates vascular dysfunction and ameliorates ischemia/reperfusion injury of the liver. STUDY DESIGN: After skeletonization, the liver was made totally ischemic by cross-clamping the portal vein, the hepatic artery, and the vena cava (above and below the liver). Veno-venous bypass was used to decompress splanchnic and inferior systemic congestion. AwETN40, 5 mg/kg, was administered intravenously 10 minutes before ischemia (treatment group, n = 5). Nontreated animals were used as controls (control group, n = 10). Animal survival, hepatic tissue blood flow, liver function tests, total bile acid, high-energy phosphate, ET-1 levels, and liver histopathology were studied. RESULTS: Treatment with AwETN40 improved 2-week animal survival from 30% to 100%. Hepatic tissue blood flow after reperfusion was significantly higher in the treatment group. The treatment significantly attenuated liver enzyme release, total bile acid, and changes in adenine nucleotides. Immunoreactive ET-1 levels in the hepatic venous blood of the control group showed a significant increase and remained high for up to 24 hours after reperfusion. Histopathologic alterations were significantly lessened in the treatment group. CONCLUSIONS: These results indicate that ET-1 is involved in ischemia/reperfusion injury of the liver, which can be ameliorated by the monoclonal anti-ET-1 and anti-ET-2 antibody AwETN40.     

Effects of vena caval banding in experimentally induced multiple portosystemic shunts in dogs

Effects of vena caval banding on portal venous and vena caval hemodynamics were examined in 6 control dogs and in 10 dogs that had undergone attenuation (banding) of the abdominal part of the caudal vena cava and had dimethylnitrosamine-induced multiple portosystemic shunts (PSS). Additionally, indocyanine green (ICG) extraction and clearance after infusion to steady state were used to calculate hepatic plasma flow in these dogs. Sixteen dogs were randomly assigned to 2 groups: control (n = 6) or diseased (n = 10). Diseased dogs were administered dimethylnitrosamine (2 mg/kg, PO, twice weekly) until multiple PSS developed, as assessed by results of clinical laboratory tests, ultrasonography, and hepatic scintigraphy. Shunts were confirmed visually at celiotomy and by contrast portography. Venous pressures (caudal vena caval, portal, and hepatic) were recorded before and after vena caval banding for up to 7 days in dogs from both groups. Peritoneal cavity pressures were recorded in all dogs after closure of the body wall. To determine ICG extraction and clearance, a bolus injection of ICG (0.5 mg/kg, i.v.) was administered, followed by steady-state infusion of 0.097 mg/min. Extractions and clearances of ICG were measured, and from these, hepatic plasma flow rates were determined immediately before and after banding and at 6 hours, 48 hours, and 7 days after banding. The gradient (caudal vena caval pressure within 1 to 2 mm of Hg of portal pressure) between caudal vena cava and portal venous pressures established at banding was maintained after the first hour in both groups. Caudal vena cava pressures established at banding were maintained throughout the study, with the exception of the first hour in diseased dogs. Extraction ratios were higher in control dogs at all times, except at 48 hours. Clearance was higher in control dogs at all times. Hepatic plasma flow did not differ between groups, except immediately after banding, when flow was greater in diseased dogs, and differences were not found over time in either group. This study indicated that vena caval banding in this model of experimentally induced multiple PSS increases and maintains caudal vena cava pressure, relative to portal venous pressure (after the first hour) for 7 days, and that calculated hepatic plasma flow is not persistently improved by vena caval banding.     

Brief report: successful extension of the transplant renal vein with a synthetic vascular graft

Unexpected intraoperative vascular complications in the graft of the recipient during organ transplantation can be most vexing and require immediate attention and careful management so as not to impair the integrity and fate of the graft. We were confronted with a diabetic recipient with total fibrosis of the left iliac vein, patent inferior vena cava, totally and circumferentially calcified aorta and left iliac artery with the exception of a small area in the distal external iliac artery. The problem was solved by anastomosing the artery low onto the external iliac, and by interposing a venous polytetrafluoroethylene vascular graft between the renal vein and the inferior vena cava. The kidney function was excellent for 2 years but the patient succumbed to unrelated liver complications. A second patient with a renal vein PTFE graft has had normal graft function for 10 years. Probably because of the high blood flow through the kidney, venous synthetic grafts can be successfully used to correct venous problems during kidney transplantation.     

Effects of tham, isoprenaline and propranolol on blood flow and vascular resistances of the liver after in- and outflow occlusion. Relation with the splanchnic shock

The responsibility of the portal and the hepatic artery circulations during shock states has been established by studying the effects of a 15-min occlusion of two of the following blood vessels on 23 dogs: inferior vena cava below the diaphragm, portal vein and hepatic artery. Intrahepatic vascular resistances were computed from blood pressure records in these vessels and transhepatic blood flow studies using the 133Xe clearance method. The animals were treated with THAM, plasmagel, isoprenaline, and propranolol. The tolerance of the occlusion is significantly improved when the animals are treated with the association of the four drugs. The portal and the systemic arterial blood pressures return to normal more promptly. Sinusoid and peribiliary resistances are remarkably stable if compared to the changes occurring in the control animals. The well-known benefit of THAM is improved by the apparently paradoxical association of isoprenaline and propranolol. In fact, at the doses which have been used, they counterbalance their mutual disadvantages. Finally, the analysis of the hepatic blood flow rates and vascular resistances suggests that the splanchnic shock has two components: hepatic and visceral.     

Hepatic venous injury; a case report of atriocaval shunt by a centrifugal pump

Injury of hepatic vein confluence and retrohepatic vena cava is serious and often fatal. We report one such case that was successfully treated by the Biopump (Medtronic Bio-Medicus, Inc., Eden Prairie, Minn). A 21-year-old man was admitted due to a steering-wheel injury in a motor vehicle accident. CT scan showed extravasated contrast material around the right hepatic lobe, and a large low density area in the right hepatic lobe adjacent to the inferior vena cava, suggesting injury of the hepatic vein confluence or the retrohepatic vena cava. The patient underwent surgical treatment. Laceration of the liver was extended to the hepatic vein confluence. Right hepatic lobectomy and repair of the middle hepatic vein was successfully performed under atriocaval shunting by the Biopump.