Breast implant during orthotopic liver transplant to avoid hepatic outflow obstruction.

Donor-recipient size mismatch in liver transplantation is a recognized but uncommon situation. It can lead to a partial or complete obstruction of the inferior vena cava with subsequent hepatic outflow obstruction. Placement of a breast implant in the right upper quadrant of the abdomen during liver transplantation is a technically easy resource and can protect the liver graft from kinking or rotation.

A comparative study of two anti-coagulation plans on the prevention of PVST after laparoscopic splenectomy and esophagogastric devascularization.

Cirrhosis and portal hypertension (PH) has a high incidence in China. Laparoscopic splenectomy and esophagogastric devascularization (LS + ED) was confirmed as an effective and safe surgical approach. But compared to open surgery (OS + ED), the rate of portal vein system thrombosis (PVST) was found to be higher after LS + ED. PVST is a common and potentially life-threatening complication after LS + ED in patients with cirrhosis and PH. Anti-coagulation therapy should be given early, but no standard plan for PSVT prophylaxis has been developed for all patients. In this study, the efficacy and safety of early use of low molecular weight heparin (LMWH) to prevent PVST were retrospectively evaluated compared with conventional anti-coagulant therapy. Of 219 patients with cirrhosis and PH undergoing LS + ED at our hospital from January 2008 to June 2013, 139 received early anti-coagulant therapy with LMWH, and 80 received conventional anti-coagulant therapy. The rates and types of PVST, perioperative coagulation function, intra-abdominal active bleeding, and esophagogastric variceal bleeding (EGVB) were compared in these two groups. Of the 139 patients in the early anti-coagulation group, 42 (30.2 %) experienced postoperative PVST, including two (1.4 %) with main trunk. Of the 80 patients in the conventional anti-coagulation group, 40 (50.0 %) experienced postoperative PVST, including 12 (15.0 %) with main trunk; three (3.8 %) experienced recurrent EGVB due to main trunk thrombosis, and one (1.3 %) underwent an immediate second laparotomy for uncontrollable active bleeding. The rates of postoperative PVST (P = 0.004), main trunk thrombosis (P = 0.000), and EGVB (P = 0.048) were significantly lower in the early than in the conventional anti-coagulant group, but all tested perioperative indices of coagulation function and rates of intraperitoneal active bleeding were similar. Early anti-coagulation with LMWH is safe and effective in patients with LS + ED for cirrhosis and PH.

Do postliver transplant patients need thromboprophylactic anticoagulation?

Postoperative thromboprophylactic anticoagulation against Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) is standard of care with current evidence-based guidelines. However, majority of liver transplant (LT) patients have thrombocytopenia and/or prolonged INR before surgery. Studies or guidelines regarding role of prophylactic anticoagulation after LT are lacking. There is a need to balance the risk of thrombosis with significant hemorrhage, implying those needing transfusion or return to OR due to bleeding. We conclude that after LT, anticoagulation is not required routinely for DVT/PE prophylaxis. Rather, it is indicated in specific circumstances, chiefly for prophylaxis of hepatic artery thrombosis or portal vein thrombosis in cases with use of grafts, pediatric cases, small size vessels, Budd Chiari syndrome, amongst others.

Review of the surgical approach to prevent small-for-size syndrome in recipients after left lobe adult LDLT.

Left lobe liver grafts increase the donor safety in adult-to-adult living-donor liver transplantation (ALDLT). However, the left lobe graft provides about 30-50 % of the required liver volume to adult recipients, which is insufficient to sustain their metabolic demands, which can lead to small-for-size syndrome (SFSS). Transient portal hypertension and microcirculatory hemodynamic derangement, apart from outflow obstruction, during the first week after reperfusion are the critical events associated with small-for-size graft transplantation. The incidence of SFSS in left lobe ALDLT can be decreased by increasing the left lobe graft volume by effective utilization of the caudate lobe with preserved vascular supply, by modulating the portal pressure with splenectomy or a porto-systemic shunt or by hepatic venous outflow reconstruction to prevent the development of venous congestion. In this review, we discuss the pathophysiology of SFSS and the various surgical strategies that can be performed to prevent SFSS in an effort to enhance the donor safety during living-donor liver transplantation.

Immunosuppressants reduce venous thrombosis relapse in Behçet's disease.

OBJECTIVE: To investigate and describe the long-term outcome of venous thrombosis in patients with Behçet's disease (BD). METHODS: In a retrospective cohort of 807 BD patients, a reported 296 patients (36.7%) (73.3% male, median age 30 years [interquartile range 24-36 years]) met the international classification criteria for BD and had venous thrombosis. We assessed factors associated with thrombosis relapse and mortality. RESULTS: There were a total of 586 venous thrombosis events, including 560 cases of deep thrombosis and 26 cases of superficial thrombosis. Deep venous thrombosis events included 323 cases of limb thrombosis (55.1%), 77 cases of cerebral venous thrombosis (13.1%), 57 cases of pulmonary embolism (9.7%), 63 cases of vena cava lesions (10.7%), 14 cases of Budd-Chiari syndrome (2.4%), and 13 cases of cervical vein thrombosis (2.2%). One hundred of 296 patients (33.8%) experienced at least 1 venous thrombosis relapse. The mortality rate was 6.4% (19 of 296 patients) after a median followup of 4.75 years (interquartile range 2-7 years). In univariate analysis, death was associated with cardiac involvement (P = 0.026) and Budd-Chiari syndrome (P = 0.004). In multivariate analysis, the use of immunosuppressive agents was found to prevent relapse of venous thrombosis (hazard ratio 0.27 [95% confidence interval 0.14-0.52], P = 0.00021), and there was a trend toward prevention of relapse with the use of glucocorticoids (hazard ratio 0.62 [95% confidence interval 0.40-0.97], P = 0.058). CONCLUSION: Immunosuppressive agents significantly reduce venous thrombosis relapse in BD.

Long-term follow-up of liver transplantation for Budd-Chiari syndrome with antithrombotic therapy based on the etiology.

BACKGROUND: Because myeloproliferative disorders (MPDs) are a frequent cause of Budd-Chiari syndrome (BCS), treatment directed toward altering platelet production and function may be more rational and effective than anticoagulation after liver transplantation. METHODS: We reviewed data on 25 patients who received liver transplantation for BCS at our institution from 1987 to 2007. Posttransplant antithrombotic treatment was based on the cause of BCS: 17 patients with MPDs received hydroxyurea/aspirin; 5 received warfarin; and 3 (2 whose hypercoagulable disorder was corrected and 1 with sarcoidosis) received no therapy. RESULTS: Both graft survival (88% at 5 years) and patient survival (92% at 5 years) were superior in the BCS group compared with the 2609 patients who received liver transplants for other indications. Vascular complications included three instances of hepatic artery stenosis (NS compared with non-BCS liver recipients), one of portal vein thrombosis (nonsignificant [NS]), and one of portal vein stenosis (NS). All 25 patients underwent multiple liver biopsies with no bleeding complications. CONCLUSIONS: Using hydroxyurea and aspirin to treat patients with BCS caused by an MPD seems to be safe and effective and avoids the risks of anticoagulation with warfarin.

Recurrent abdominal thrombosis despite heparin thromboprophylaxis in a patient with transient eosinophilia.

A 21-year-old girl with an ischemic bowel developed portal and splenic vein thrombosis 3 weeks later, despite thromboprophylaxis low-molecular-weight heparin. An extensive thrombophilia screen was negative and the only possible reason for her vascular occlusion was transient but severe eosinophilia. The role of transient eosinophilia in thrombosis is discussed in the light of other similar rare cases.

Posttransplant complex inferior venacava balloon dilatation after hepatic vein stenting.

Orthotopic and living related liver transplantation is an established mode of treatment of end-stage liver disease. One of the major causes of postoperative complications is vascular anastomotic stenosis. One such set of such complications relates to hepatic vein, inferior vena cava (IVC), or portal vein stenosis, with a reported incidence of 1-3%. The incidence of vascular complications is reported to be higher in living donor versus cadaveric liver transplants. We encountered a patient with hepatic venous outflow tract obstruction, where the hepatic vein had been previously stented, but the patient continued to have symptoms due to additional IVC obstruction. The patient required double-balloon dilatation of the IVC simultaneously from the internal jugular vein and IVC.

Isolated right hepatic vein obstruction after piggyback liver transplantation.

The "piggyback" technique for liver transplantation has gained worldwide acceptance. Still, complications such as outflow obstruction have been observed, usually attributable to technical errors such as small-caliber anastomosis of the suprahepatic vena cava, twisting, or kinking. Iatrogenic Budd-Chiari syndrome after piggyback liver transplantation has been reported as a consequence of obstruction involving the entire anastomosis (usually the 3 hepatic veins). Here we describe technical issues, clinical presentation, diagnosis, and treatment of 3 cases in which outflow obstruction affected only the right hepatic vein. In conclusion, all 3 patients developed recurrent ascites requiring angioplasty and/or stent placement across the right hepatic vein to alleviate the symptoms.

Experimental hepatic radiofrequency ablation using wet electrodes: electrode-to-vessel distance is a significant predictor for delayed portal vein thrombosis.

The aim of this study was to examine possible explanatory variables associated with acute and delayed portal vein thrombosis after hepatic radiofrequency (RF) ablation using wet electrodes. Coagulations were created within 1.5 cm of the right portal vein (RPV) branch in 12 pigs with (n = 6) or without (n = 6) Pringle manoeuvre. Sham operations with Pringle manoeuvre were performed in four animals. Rotational portal venography was performed prior to ablation, 10 min after ablation and 4 days after ablation. Vessel diameters and vessel patency was determined from the portal venograms. Distance between the ablation electrode and RPV was measured from 3-dimensional reconstructions of the portal venograms. The portal veins were examined by microscopy. Delayed portal vein thrombosis was found in two of six animals in the Pringle group and three of six animals in the control group 4 days after ablation (P = 1.0, Fisher's exact test). All five occurrences of delayed portal vein thrombosis were found in the six animals with a distance between the ablation electrode and RPV of 5 mm or less (P = 0.030), indicating that the electrode-to-vessel distance may be an independent explanatory factor for delayed portal vein thrombosis after RF ablation with wet electrodes.

Pivotal role of PAI-1 in a murine model of hepatic vein thrombosis.

Hepatic veno-occlusive disease (VOD) is a common complication of high-dose chemotherapy associated with bone marrow transplantation. While the pathogenesis of VOD is uncertain, plasminogen activator inhibitor-1 (PAI-1) has emerged as a diagnostic marker and predictor of VOD in humans. In this study, we investigated the role of PAI-1 in a murine model of VOD produced by long-term nitric oxide synthase inhibition using L-NAME. After 6 weeks, wild-type (WT) mice developed extensive fibrinoid hepatic venous thrombi and biochemical evidence of hepatic injury and dysfunction. In contrast, PAI-1-deficient mice were largely protected from the development of hepatic vein thrombosis. Furthermore, WT mice that received tiplaxtinin, an antagonist of PAI-1, were effectively protected from L-NAME-induced thrombosis. Taken together, these data indicate that NO and PAI-1 play pivotal and antagonistic roles in hepatic vein thrombosis and that PAI-1 is a potential target in the prevention and treatment of VOD in humans.

[The reason and treatment of portal vein thrombosis in patients with portal hypertension postoperation].

OBJECTIVE: To investigate reason and the management of portal vein thrombosis in patients with portal hypertension postoperatively. METHODS: 329 patients with portal hypertension in liver cirrhosis who had splenectomy was reviewed from 1992 to 2001. In whom 43 (13.1%) patients with portal vein thrombosis postoperative were analyzed. RESULTS: In these patients, except 1 died for portal vein phlebitis, all patients were recovered. There are 138 patients who underwent splenectomy or splenectomy and devascularization, 26 (18.8%) of them had thrombosis. 191 patients underwent splenectomy and portacaval or portasplenic shut, 17 (8.9%) of them had thrombosis. The data of these two groups have significant difference (chi(2) = 8.44, P < 0.01). CONCLUSIONS: Thrombocytosis postsplenectomy as well as the changes of portal hemodynamics is the main reason of portal vein thrombosis. Portal vein thrombosis is also in association with the operative ways. Operation standardization, dynamic examining platelet count, routine color ultrasonography examining and early anticoagulation therapy are the effective methods in preventing and managing portal thrombosis postoperation for portal hypertension.

[Portal anticoagulation in preventing thrombosis after porta-azygous devascularization for portal hypertension].

OBJECTIVE: To study the prevention method for thrombosis after porta-azygous devascularization for portal hypertension. METHODS: 71 patients with portal hypertension due to cirrhosis were divided into group A (36 patients) and group B (35 patients). In group A, a anticoagulation tube was inserted via splenic vein branch during shunt and anticoagulation therapy was given after operation. RESULTS: All the patients received color Doppler examination 3 months after operation. No thrombosis occurred in the group A and thrombosis occurred in 13 patients (37.14%) in the group B. CONCLUSION: Portal anticoagulation therapy is the effective in preventing portal thrombosis after porta-azygous devascularization for portal hypertension.

Long-term effects of interstitial laser coagulation in porcine liver with portal inflow occlusion: central versus peripheral lesions.

PURPOSE: Interstitial laser coagulation (ILC) is an attractive modality for local destruction of unresectable hepatic metastases. Portal inflow occlusion considerably increases its destructive capacity, resulting in lesions 5 cm in diameter; however, effects on adjoining major intrahepatic structures are unknown. Therefore, the purpose of this study was to assess the effects of ILC with portal inflow occlusion on the central portion of the liver as compared to the peripheral portions. MATERIALS AND METHODS: ILC was performed in pigs with portal inflow occlusion. Each animal received a single laser application with Nd:YAG light guided simultaneously through four interstitial fibers with 5 W per fiber during 6 minutes. Location of treatment was randomized to either central (n = 8) or peripheral (n = 8). Follow-up was for 1, 2, or 3 months with evaluation of liver functions and weight, as well as macroscopic and microscopic assessment of coagulated lesions and surrounding parenchyma. RESULTS: There was no treatment-related morbidity or mortality. No obstructive cholestasis or bile leakage was found. At every moment of evaluation, coagulated volumes in the central group were smaller than in the peripheral lesions (P = .03). Large vessels contiguous to the lesions in the central group were always intact and indications of portal hypertension or thrombosis of hepatic veins were not found. There were no significant differences between the two groups (liver functions [P > or = .15] and weight [P = .69]). CONCLUSION: ILC with portal inflow occlusion is a safe technique in the vicinity of vital structures in the liver of healthy pigs. These results justify studies to the feasibility and complication rate of portal inflow occlusion in patients with hepatic malignancies.

Water-glove balloon system: a useful option to salvage liver grafts with postreperfusion suprahepatic vena caval kinking.

BACKGROUND: Although exceedingly rare, kinking of suprahepatic vena cava after liver transplantation can lead to both graft failure and patient demise. The features of a case of suprahepatic vena caval kinking are herein reported along with the description of an original solution adopted to rescue the graft. METHODS: In order to correct vascular kinking, two surgical gloves filled with sterile saline solution were placed in appropriate positions in the subdiaphragmatic space. RESULTS: Caval obstruction was immediately relieved. Over a period of 7 days, gloves were progressively deflated and eventually removed without need for laparotomy. Vena caval kinking did not recur. CONCLUSIONS: The "water-glove balloon system" described in this report seems to be an efficient and inexpensive method to rescue liver grafts in the presence of kinking or torsion of the suprahepatic vena cava. Surgeons dedicated to the transplantation of the liver should therefore retain this option in their cultural background.

Successful pregnancy following orthotopic liver transplantation for idiopathic Budd-Chiari syndrome.

Budd-Chiari syndrome is a rare and serious thrombotic event with significant morbidity and mortality. Recommendations regarding future conception and management during pregnancy have not been defined. We present a patient with history of idiopathic Budd-Chiari Syndrome and subsequent orthotopic liver transplantation who was successfully managed during pregnancy. A 24-year-old white female, gravida 1 para 0, status postorthotopic liver transplantation 5 years previously for Budd-Chiari syndrome with post-transplant insulin-dependent diabetes mellitus presented to our clinic at 7 weeks of gestation for initial prenatal evaluation. Maintenance immunosuppressive therapy and prophylactic heparin anticoagulation was administered throughout the pregnancy, which was uneventful until 35 weeks gestation, at which time pre-eclampsia and premature preterm rupture of membranes prompted labor induction. The patient developed no evidence of acute or chronic hepatic rejection and no evidence of recurrent Budd-Chiari syndrome during the pregnancy or post-partum convalescence. Prudent use of prophylactic anticoagulation, close immunosuppressive monitoring, and periodic fetal and maternal surveillance are warranted in patients with previous orthotopic liver transplantation for idiopathic Budd-Chiari syndrome and may reduce risk of recurrence during pregnancy.