Recovery of liver perfusion after focal outflow obstruction and liver resection

BACKGROUND: Live liver donation requires extended liver resection in the donor with transection of the middle hepatic vein. This leads to focal outflow obstruction in the remnant liver or the partial graft. This study was designed to characterize the pathophysiological correlate of focal outflow obstruction in a small-for-size liver and its course of recovery in a rat model. METHODS: Ligation of the right median hepatic vein was combined with 50% hepatectomy. Microcirculation was visualized by orthogonal polarization spectroscopy after each operative step and before killing on days 1, 2, and 7. Histologic evaluation included morphological assessment, immunohistochemical determination of proliferation using BrdU, and laminin and von Willebrand factor expression, which both indicate vascularization of sinusoids. RESULTS: After ligation of the right median hepatic vein, congestion was visible and no sinusoidal blood flow was detected in the obstruction zone. By day 1 confluent centrilobular necrosis developed. Sinusoidal perfusion in the obstruction zone recovered partially. Many dilated vascularized sinusoidal canals connecting the obstruction zone with the normal zone were visible. Proliferative activity in the obstruction zone was markedly reduced compared with the normal zone. By day 7, liver parenchyma in the obstruction zone looked normal as did sinusoidal perfusion. In the border zone, few dilated vascular canals were apparent. CONCLUSION: Confluent centrilobular necrosis in the early postoperative phase, resulting from focal outflow obstruction, may be crucial for the development of a small-for-size syndrome. The exclusion of the outflow-obstructed zone from the functional liver mass during preoperative radiological risk assessment seems to be the logical consequence. Recovery of focal outflow obstruction occurs spontaneously by means of dilated sinusoids in the border zone, forming vascularized sinusoidal canals, which could serve as intrahepatic anastomosis.     

儿童肝移植术后肝静脉流出道梗阻的血管腔内治疗进展

流出道梗阻是儿童肝移植术后的血管并发症。血管腔内介入治疗已成为治疗术后流出道梗阻的首选治疗方法。本文对近年来儿童肝移植术后流出道梗阻血管腔内治疗进展进行综述。     

Hepatic venous outflow reconstruction in adult living donor liver transplants without portal hypertension

Graft congestion is one of the causes of poor graft function in segmental liver transplantation. Three factors are implicated in segmental graft congestion: graft size, hepatic venous outflow and portal inflow. The graft size must be matched to the body weight, which is conventionally done by using graft to body weight ratio. Hepatic blood outflow must be optimized by hepatic vein reconstruction, which can be complicated. High portal blood flow has been shown to be detrimental to small-for-size grafts. These factors are strictly connected to each other. They can all contribute to graft congestion and poor function, while one factor can compensate for the others and decrease congestion. Ideally, all the accessory veins should be reconstructed, if possible, to maximize the outflow. In the absence of portal hypertension and with an adequate sized graft, complex venous reconstruction may not be necessary. We present a case report of an adult living donor liver transplant with the favorable conditions of normal portal pressure and a large sized graft, but complicated by the presence of several accessory hepatic veins. A simple hepatic vein anastomosis was sufficient for adequate outflow and prompt graft function.     

Hepatic venous outflow obstruction after right lateral sector living-donor liver transplantation, treated by insertion of an expandable metallic stent

Hepatic venous outflow obstruction is a relatively uncommon but important and devastating complication occurring after liver transplantation. Recently, right lateral sector liver grafts have sometimes been used in living-donor liver transplantation (LDLT), but, to our knowledge, early hepatic venous outflow obstruction has never been reported in right lateral sector LDLT. A 58-year-old woman was diagnosed with liver cirrhosis and hepatocellular carcinoma and underwent right lateral sector LDLT. Postoperatively, she developed liver dysfunction. Doppler ultrasound examination revealed flat waveforms and low-flow velocity in the right hepatic vein (RHV). A computed tomography (CT) scan revealed a ventrally distorted RHV due to hypertrophy of the liver graft. Hepatic venous obstruction was suspected and a hepatic venogram was performed. The venogram revealed stenosis of the RHV due to the distortion of the vein. We performed percutaneous transfemoral balloon dilatation, but this was not effective. We then inserted an expandable metallic stent (EMS) into the RHV. After the EMS placement, the condition of the patient improved. Venogram and CT data suggested that the obstruction of the RHV developed because of distortion of the RHV to the ventral side during liver regeneration.     

Direct visualization of nitric oxide release by liver cells after the arrest of metastatic tumor cells in the hepatic microvasculature

BACKGROUND: Our previous studies have shown that the injection of B16F1 melanoma cells into the mesenteric vein can induce the rapid local release of nitric oxide (NO) in the liver, causing apoptosis of the melanoma cells in the liver sinusoids and inhibiting the subsequent formation of hepatic metastases. In this study, we have investigated the distribution and cellular source of NO in this model. MATERIALS AND METHODS: In situ liver perfusion was established in both wild-type (wt) and endothelial nitric oxide synthase knockout (eNOS KO) C57BL/6 mice. A specific fluorescent NO probe, 4,5-diaminofluorescein diacetate (DAF-2 DA) (5 micromol/L), was perfused into the portal venous system to label the liver tissue. Then, a MitoTracker Orange labeled B16F1 melanoma cell suspension (2 x 10(6) cells/ml) was injected through a portal vein catheter by a peristaltic pump. Images of the liver tissue were taken by confocal microscopy from a selected area to determine the cellular source of NO. For quantification, the fluorescence intensity of this area was measured over time by Fluoview software. RESULTS: Diaminotriazolofluorescein (DAF-2T) fluorescence (indicating NO generation) was detected in hepatic parenchymal cells located in the periportal region in both wt C57BL/6 and eNOS KO C57BL/6 mice and was intensified by increased flow rate in the portal venous system. The B16F1 cells arrested in the periportal sinusoids, corresponding to zone 1 of the hepatic acinus. DAF-2T fluorescence was expressed by both sinusoidal lining cells and hepatocytes at the site of tumor cell arrest. The fluorescence intensity of these cells increased approximately 2-fold over a time of 500 s. In contrast, there was no increase in the fluorescence intensity of the sinusoidal lining cells and hepatocytes in mice perfused with buffer or in eNOS KO mice perfused with B16F1 cells. CONCLUSION: This study demonstrates that NO is produced by hepatic parenchymal cells mainly located in the periportal zones and that the arrest of the B16F1 melanoma cells causes an eNOS-dependent local burst of NO by the sinusoidal lining cells and hepatocytes in the periportal areas.     

Complex outflow anatomy in left lateral lobe graft and modified venous reconstruction in pediatric living donor liver transplantation

Hepatic venous outflow reconstruction is of critical significance in pediatric patients undergoing living donor liver transplantation. Accurate knowledge of the anatomical variations is important to obtain appropriate size segmental grafts. The diameter of the hepatic veins and the potential risk of complications at the level of the anastomosis require an adequate primary vascular reconstruction. We describe a venous outflow reconstruction technique, in a living related left lateral lobe graft, with unfavorable hepatic venous anatomy.     

Hepatic venoplasty in living-donor liver transplantation using right lobe graft with middle hepatic vein

Inclusion of the middle hepatic vein in a right lobe graft from a living-donor may improve venous drainage and avoid graft dysfunction, but reconstruction of the middle hepatic vein is technically difficult. We developed a hepatic venoplasty technique, which was applied in eight consecutive right lobe liver transplantations. The right and middle hepatic veins of the graft were joined together to form a triangular cuff for a single anastomosis to the recipient's inferior vena cava. Hepatic venoplasty was successful in all cases, and no interposition graft was required. Venovenous bypass was not used. All grafts showed immediate function, and no hepatic venous outflow obstruction was observed. There was no reoperation and the graft survival rate was 100%. This hepatic venoplasty technique can be applied systemically as a standard one in right lobe liver graft with the middle hepatic vein to simplify the recipient hepatectomy and to obviate venous outflow obstruction.     

成人活体肝移植术后肝静脉狭窄的诊断与介入治疗:2例报道并文献复习

肝静脉狭窄是肝移植术后的一种严重并发症,在活体肝移植术后发生率较高。本文通过回顾性分析2例成人活体肝移植术后肝静脉狭窄患者的相关资料,结合国内外相关文献,探讨肝移植术后肝静脉狭窄的诊断方法及介入治疗效果。经皮肝静脉造影术可确诊肝静脉流出道梗阻,经皮经肝球囊、支架成形术是治疗活体肝移植术后早期肝静脉狭窄的一种安全、简便、有效的方法。     

Hepatic Venous Outflow Reconstruction in Right Lobe Living-Donor Liver Graft Using Recipient''s Superficial Femoral Vein

Venous congestion of a liver graft from a life donor is a disastrous complication with a high risk of graft failure. For safety reasons, the middle hepatic vein (MHV) is currently unanimously left with the donor. As this vessel provides major venous draining of the right anterior sector, reconstruction of significant MHV tributaries is controversial. We describe here successful venous outflow reconstruction in adult-to-adult right lobe living-donor liver transplantation (RL-LDLT) using the recipient's superficial femoral vein (SFV). Six months after transplantation, graft function and perfusion are excellent, and the patient is free of venous morbidity related to the harvest of the SFV.     

肝切除术中涉及肝静脉并发症的处理与预防

目的　对肝切除术中涉及肝静脉并发症的原因 ,处理方法及预防措施进行总结 ,减少并发症发生率。方法　对 17例涉及肝静脉并发症的病例进行分析 ,将其分成两类 ,一类为肝静脉破裂导致出血或空气栓塞 ,另一类为肝静脉狭窄导致肝脏血液回流受阻。对其发生的原因、处理经过及预防措施进行总结。结果　 12例肝静脉破裂出血或空气栓塞的病人术中均抢救成功。 5例肝静脉狭窄的病人有 3例术中及时处理狭窄得到解除 ,另 2例术后经内科及介入治疗获得缓解。结论　仔细辨认 ,妥善处理肝静脉 ,是防止其破裂的关键。肝脏创面张力较大时应避免将其强行对拢缝合 ,以免压迫肝静脉。     

Hepatic portal venous gas: Report of a case

Hepatic portal venous gas is easily diagnosed radiographically by the appearance of tubular lucencies branching horizontally from the porta hepatis and extending to within 2 cm of the liver capsule. Associated conditions vary from benign to potentially lethal diseases which require emergency operations. A case of hepatic portal venous gas secondary to small bowel obstruction is presented and a review of the literature is also provided. Received: March 31, 1999 / Accepted: January 7, 2000     

Arterialized venous perfusion of composite tissue

The results of our experiment prove that arterialized venous perfusion is a viable means of nourishing complex composite tissue without using the arterial tree. Previous laboratory findings, coupled with the results of this experiment, demonstrate that as long as proximal arterial inflow is ensured, both the arterial and venous trees need not be intact to keep tissue alive. Rather, it seems that the prerequisites for tissue survival are that at least one of the two systems be intact and that there be sufficient inflow and outflow channels available. Whether these channels are arteries or veins is probably not important. The use of properly placed efferent or afferent arteriovenous fistulas allows one system to provide both physiologic functions. Whether the efferent arterial anastomosis stays open over the long term appears to be inconsequential. Survival is ensured by either direct perfusion with oxygen delivery through the venous tree or through the eventual ingrowth of recipient vessels into the flap by way of the delay phenomena. This perfusion technique is ideally suited for tissue with an inadequate arterial tree but with an intact venous system devoid of venous valves (most veins less than 1.5 mm in diameter). A well-vascularized recipient bed capable of providing vessel ingrowth into transferred tissue may be important in the case of delayed arteriovenous fistula occlusion secondary to intimal hyperplasia; therefore, further experimental study of these flaps must be undertaken before arterialized venous flaps can be recommended for placement in recipient sites compromised due to radiation, ischemia, diabetes, or other causes of small vessel disease in the recipient bed. Although efferent arteriovenous fistulas are currently used to provide arterialized venous perfusion in selected cases of end stage arterial occlusive and vasospastic disease, perhaps their greatest role is in the management of tissue transfer with an inadequate arterial tree. Much knowledge must be gained to understand the physiologic principles and requirements for optimal perfusion. Many questions are left unanswered. For example, in those arteriovenous fistulas that narrow or occlude secondary to neointimal hyperplasia or other causes, which channels (veins or arteries?) are used for perfusion during recipient vessel growth? Can intimal hyperplasia be reversed or prevented by drug therapy and would this be advantageous? Can venous valves be made incompetent so that this technique can be used for larger vessels?(ABSTRACT TRUNCATED AT 400 WORDS)     

Simplified hepatic resection utilizing absorbable polyglycolic acid-based tape and other ligature apparatus

Hepatic resection has been increasing in frequency in the management of metastatic or primary neoplasms of the liver. Although mortality for this procedure has steadily decreased, the associated morbidity remains high. Morbidity is mainly associated with operative time and blood loss, especially in jaundiced and cirrhotic patients. During hepatic resection, control of bleeding from various sources is the most important problem faced by surgeons. During conventional lobectomy, despite prior control of hepatic artery and portal vein to that lobe, bleeding still occurs from the opposite lobe or back flow from hepatic veins. We usually apply Pringle's maneuver for hemostasis, but consequently there is postoperative hepatic dysfunction. We have previously investigated methods for vascular occlusion at the site of liver resection. We developed a new absorbable polyglycolic acid-based tape (breadth, 3 mm; length, 70 cm) for use in hepatic mass ligation, as well as two types of ligature apparatus. Hemostasis was achieved with these devices, and all lobar, segmental, and non-anatomic resections were performed without prior control of the portal venous system, hepatic arterial inflow, and hepatic venous outflow before parenchymal resection. This significantly shortened the operative time, as well as decreasing the blood loss during hepatic resection, with consequent reduction of postoperative morbidity. The use of this absorbable tape may reduce the incidence of local infection, abscess formation, and septicemia. Received for publication on March 26, 1997; accepted on Jan. 28, 1998     

活体肝移植肝静脉流出道狭窄的诊断与治疗

肝静脉流出道狭窄是肝移植术后较为罕见的并发症,在活体肝移植中发生率为2％～4％。2006年6月至2010年5月,解放军总医院2例接受右肝活体肝移植的患者术后出现肝静脉流出道狭窄,接受保守治疗或介入球囊扩张成形术治疗。术后疗效显示：保守治疗肝静脉流出道狭窄具有一定的风险性;而介入肝静脉造影、球囊扩张以及金属支架置入能有效诊断和治疗肝静脉流出道狭窄。     

Hepatic portal venous gas associated with cholangitis following pancreaticoduodenectomy: Report of a case

A 63-year-old man developmented fever and shock 2 weeks after undergoing a pancreaticoduodenectomy for carcinoma of the gallbladder with duodenal involvement. Computed tomography (CT) of the abdomen showed transient hepatic portal venous gas in the right lobe of the liver, which had probably been induced by obstruction of the bilioenteric anastomosis by the biliary drain. The gas and bacteria, both of which are commonly observed in cases of bilioenteric anastomosis, may have been diffused through the sinusoid into the portal venous system. Thus, hepatic portal venous gas could be a serious sign when it develops in patients with cholangitis following bilioenteric anastomosis.     

Impairment of hepatosplanchnic oxygenation and increase of serum hyaluronate during normothermic and mild hypothermic cardiopulmonary bypass

Hepatic sinusoidal endothelial cells (SECs) are more vulnerable to hypoxia or hypothermia than hepatocytes. To test the hypothesis that hepatic venous desaturation during cardiopulmonary bypass (CPB) leads to impairment of SEC function, we studied the plasma kinetics of endogenous hyaluronate (HA), a sensitive indicator of SEC function, and hepatosplanchnic oxygenation during and after CPB. Twenty-five consecutive patients scheduled for elective coronary artery bypass graft surgery, who underwent normothermic (>35 degrees C; n = 15) or mild hypothermic (32 degrees C; n = 10) CPB participated in this study. A hepatic venous catheter was inserted into each patient to monitor hepatosplanchnic oxygenation and serum levels of HA concentration. Hepatic venous oxygen saturation decreased essentially to a similar degree during normothermic and mild hypothermic CPB. Hepatosplanchnic oxygen consumption and extraction increased during normothermic (P < 0.05), but not mild hypothermic, CPB. Both arterial and hepatic venous HA concentrations showed threefold increases during and after CPB in both groups. A positive correlation was found between hepatosplanchnic oxygen consumption and arterial HA concentrations during CPB, suggesting a role of changes in hepatosplanchnic oxygen metabolism in the mechanisms of increases in serum HA concentrations. The failure of the liver to increase HA extraction to a great degree suggests that a functional impairment of the SEC may contribute to the observed increase of serum HA. IMPLICATIONS: Hepatic sinusoidal endothelial cells (SECs) are pivotal in the regulation of sinusoidal blood flow. This study showed that SEC function might be impaired during and after cardiopulmonary bypass, irrespective of the temperature management.     

Hepatic portal venous gas

STUDY OBJECTIVE: Hepatic portal venous gas is a radiological symptom associated with a poor prognosis (75% to 90% mortality). The aim of this retrospective study was to report 7 cases observed over a 2-year period. PATIENTS AND METHOD: From June 1997 to November 1999, hepatic portal venous gas was diagnosed in 6 patients by CT scan and in one patient by echosonography. It was not detected in any case by plain abdominal X-rays. Three patients had small bowel obstruction with necrosis, three had extensive superior mesenteric infarction and one had preperforative necrosis of the colon. RESULTS: One patient with extensive intestinal infarction and a metastatic head and neck cancer was not operated. Two patients were operated, but the extensive mesenteric infarction was not amenable to surgical management. Three of the 7 patients died, while the other four patients survived after resection of the necrotic small intestine (n = 3) and left colectomy extended to the transverse colon (n = 1). CONCLUSION: Hepatic portal venous gas was associated with intestinal necrosis in the seven cases of this series. The severity of portal venous gas is only correlated with the severity of the disease causing portal venous gas.     

Hepatic portal venous gas

BACKGROUND: Hepatic portal venous gas is an unusual entity associated with a variety of abdominal catastrophes. There is usually a grave prognosis when hepatic portal venous gas is associated with ischemic bowel disease. We reported a 57-year-old man with hepatic portal venous gas associated with extensive infarction of the jejunum and a concomitant perforation at a site in the terminal ileum leading to two operations performed 24 hours apart. Progressive ischemia and infarction after the initial laparotomy resulted in massive resection of the small bowel. METHODS: A follow-up abdominal radiography showed progressive dilatation of the small intestine and thickening of the bowel wall. Computed tomography of the abdomen showed pneumatosis intestinalis and gas collection within the intrahepatic and extrahepatic portal vein and superior mesenteric vein and free gas in the peritoneal cavity. RESULTS: At surgery, a long segment of ischemic change of the jejunum with focal necrosis and one perforation in the terminal ileum with no relation to the ischemic area was discovered. These two areas were resected respectively, and anastomosis was performed. Extensive necrosis of the residual bowel was found on the second-look operation performed 24 hours later, and subsequent resection of involved bowel was performed, resulting in a short-bowel condition. CONCLUSIONS: When hepatic portal venous gas associated with ischemic bowel disease is encountered, coexistence of other abdominal condition with no relation to ischemic segment should be considered.     

Acute hepatic vein thrombosis after liver transplantation in a child with biliary atresia and absent inferior vena cava

Stenosis of the hepatic venous outflow anastomosis is rare after liver transplantation. Hepatic venous outflow obstruction affects 5.1% to 7% of transplanted patients. Clinical findings among children include massive ascites and abdominal pain and laboratory findings demonstrate altered liver function tests and coagulopathy. In this article, we report a case of hepatic venous thrombosis occurring 22 days after living-related liver transplantation. The patient was treated with hepatic venoplasty and stent implantation.