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Stenoses of vascular anastomoses after hepatic transplantation: treatment with balloon angioplasty.

Vascular complications after liver transplantation include occlusion or stenosis at the sites of anastomosis in the hepatic artery, portal vein, and vena cava. From our experience with more than 600 liver transplants, vascular stenoses have been identified in 10 patients and treated by balloon angioplasty in nine. Three patients with hepatic artery stenosis and deteriorating graft function were treated by balloon angioplasty with a coaxial technique. A specially designed catheter facilitated a successful femoral artery approach. Portal vein stenoses in three patients resulted in portal hypertension. These were treated by balloon dilatation via transhepatic catheterization of the portal vein. Stenoses of the suprahepatic caval anastomosis were dilated in three patients with severe lower limb edema. Technical success was achieved in all three cases of hepatic artery stenosis with improvement in graft function. Recurrent stenoses in two patients were successfully treated with repeated dilatations. Portal hypertension resolved in two of three patients after portal venoplasty. Dilatation of a caval stenosis resulted in the resolution of leg edema in all three cases. Repeated dilatation was required in one case. No reduction in the portal venous pressure gradient occurred after venoplasty in one case, and an ultimately fatal caval thrombosis developed in one patient with caval stenosis before venoplasty could be performed. Our experience suggests that balloon angioplasty of arterial and venous stenoses complicating hepatic transplantation carries little risk and is a useful procedure for the treatment of these problems.

Adult↗

[Toxic-shock-like-syndrome caused by beta-hemolysing group G streptococci in a multimorbid patient with erysipelas].

HISTORY AND FINDINGS: A 41-year-old, obese man with a history of incomplete paraplegia of both legs and chronic venous insufficiency with stasis dermatitis presented with acute respiratory and hyperdynamic hemodynamic failure. He was transferred from another hospital to the department of intensive care medicine for further diagnosis and treatment. A livid coloured, necrotizing-hemorrhagic swelling of the right lower leg was noted. INVESTIGATIONS: Laboratory tests revealed an inflammation probably due to bacterial infection, anemia, acute renal failure, acute hepatic dysfunction, coagulopathy and lactic acidosis, indicating multi-organ failure and septic shock. No focus of sepsis was found at abdominal sonography and exploratory laparotomy. Chest X-Ray and computed tomography revealed bilateral pneumonia. Doppler ultrasonography of both legs showed acute isolated thrombosis of the right posterior tibial vein. TREATMENT AND COURSE: In addition to a chronic venous ulcer-necrotizing hemorrhagic erysipelas had developed in the right lower leg. A swab taken at surgery and blood cultures grew Streptococcus dysgalactiae ssp. equisimilis (group G streptococci, GGS). Despite intensive care treatment and high dosage penicillin G therapy the patient died two days after admission from septic shock and multi-organ failure. CONCLUSIONS: Group G streptococci cause a variety of common and severe infections. Erysipelas is infrequently associated with GGS but, much more often, with group A streptococci (GAS). This unusual and fulminant case emphasizes the importance of considering Streptococcus dysgalactiae as a causative agent in septicemia with multiple predisposing factors and soft-tissue infections.

Adult↗

Improved patency of transjugular intrahepatic portosystemic shunts in humans: creation and revision with PTFE stent-grafts.

PURPOSE: To determine whether polytetrafluoroethylene (PTFE) stent-grafts yield longer patency for creation or revision of transjugular intrahepatic portosystemic shunts (TIPS). MATERIALS AND METHODS: Fourteen PTFE-covered Wallstents were placed in 13 patients with TIPS: seven at shunt creation and seven during revision of TIPS with one to five prior thromboses at 1 day to 1 year after initial TIPS formation. In six cases, prior to stent-graft placement persistent biliary-TIPS fistulas were demonstrated despite repeated shunt revisions with additional metallic stents. RESULTS: All but one graft-lined TIPS were widely patent at a mean duration of venographic follow-up of 19 months (median, 17 months; range, 5-32 months). The limiting percentage of stenosis within the grafted shunts was 0%-10%. One patient developed stent-graft thrombosis; the prior biliary-TIPS fistula was seen despite the graft. A second, parallel PTFE-lined transcaval shunt was created in this patient; it was widely patent at 11-month follow-up. In two asymptomatic patients, stenoses developed in the short, nongrafted portions of the outflow hepatic veins. CONCLUSION: PTFE stent-grafts can markedly prolong TIPS patency, potentially reducing the need for shunt follow-up and revision and the risk of recurrent symptoms associated with shunt stenosis or occlusion.

Adult↗

[Portal thrombosis, common bile duct varices and cholestasis].

A case of cholestasis in a young patient with portal cavernomatosis is reported. This clinical picture is very infrequent and appears as a consequence of extrinsic compression on the common bile duct due to which the derivative venous collaterals. There does not appear to be any relationship between the intensity of the morphologic alteration of the biliary tract and the level of portal hypertension and the degree of extrahepatic obstruction. Diagnosis was fundamentally achieved by arteriography and retrograde cholangiography with differential diagnosis with the previously mentioned diseases being required. Chronic cholestasis advises derivative surgery in which difficulties may be found due to the presence of thick collaterals in the hepatic pedicle as occurred in this patient.

Adult↗

Transient hepatic attenuation differences (THAD) not connected to focal lesions.

PURPOSE: To report our experience with helical CT evaluation of transient hepatic attenuation differences (THAD), and in particular of those not associated with focal lesions, in an attempt to provide an aetiopathogenetic picture that accounts for the morphology, evolution and density of THAD. MATERIALS AND METHODS: Between January 1998 and January 2001 we observed THAD in 130/988 biphasic helical CT liver examinations performed in the arterial and portal dominant phase. THAD were associated to focal hepatic lesions in 87 patients; in 43 patients there was no such association. This second group of patients, composed of 23 males and 20 females ranging in age from 17 to 80 years (average = 58.8), was enrolled in the study. THAD were associated to: Budd-Chiari syndrome (9), portal venous thrombosis (10), liver cirrhosis (7), acute inflammation of an adjacent organ (4), dilatation of the entire biliary tree (3), hepatic stasis caused by heart failure (2) and constrictive pericarditis (1), fine-needle percutaneous biopsy (2), arterioportal shunting (2), parenchymal compression by fractured ribs (2) and by a strengthened phrenic pillar (1). THAD were evaluated according to extension, morphology and density. For each case at least 10 density measurements were performed by sampling regions of interest on the parenchyma with THAD and on the contralateral parenchyma. The results (mean and standard deviation) were compared to those relative to 30 healthy patients. 22/43 patients were followed up for 6#150;24 months by at least one US and helical CT examination. During CT, the direct appreciation of vascular thrombus during the portal dominant phase was also considered. RESULTS: We detected 18 localised and 25 diffuse THAD. The localised sectoral THAD (11), wedge-shaped with clear border sign, were associated to thrombosis of a portal branch (6), fine-needle percutaneous biopsy (2), arterioportal shunting (2) and partial Budd-Chiari syndrome (1). The localised non-sectoral THAD (7), with variable morphology and without the clear border sign, were associated to acute inflammation of an adjacent organ (4) and to parenchymal compression by the ribs or diaphragm (3). Diffuse THAD associated to Budd-Chiari syndrome (8) and to heart failure (3) showed mosaic enhancement of hepatic parenchyma (patchy pattern); those linked to portal trunk thrombosis (4) and cirrhosis (7) revealed predominant enhancement of external hepatic parenchyma (central-peripheral phenomenon); finally, those concurrent with dilatation of the entire biliary tree showed parenchymal enhancement close to the dilated bile ducts (peribiliary pattern). Follow-up (22/43) demonstrated complete THAD regression after removal (5/22) and less conspicuity of THAD after partial overcome of the stoppage (1/22). In 2/22 cases of arterioportal shunting no substantial changes were seen. The remaining 14/22 cases showed a gradual, slow tendency towards THAD regression with hypotrophy of the involved parenchyma and compensatory contralateral hypertrophy even in the case of endurance of the causative agents. CONCLUSIONS: Based on our experience and the literature we suggest a classification for THAD unrelated to focal hepatic lesions. We recognise 4 causes: portal vein stoppage-obstruction, portal in-flow diversion, trauma and inflammation. When THAD is related to the first three causes pathogenesis is portal hypoperfusion. In the fourth group the mediators of the arterial phenomena are those of inflammation even though portal hypoperfusion might be involved as well. THAD identification makes the detection of vascular thrombi easier by comparison with their direct finding during the portal dominant phase. Finally, THAD are to be investigated for their potential utility in the detection and characterisation of several hepatic diseases. As a consequence, hepatic CT studies cannot ignore arterial dominant phase evaluation, even if no focal hepatic lesions are expected.

Adolescent↗

Portal vein thrombosis: prevalence, patient characteristics and lifetime risk: a population study based on 23,796 consecutive autopsies.

AIM: To assess the lifetime cumulative incidence of portal venous thrombosis (PVT) in the general population. METHODS: Between 1970 and 1982, 23,796 autopsies, representing 84% of all in-hospital deaths in the Malmö city population, were performed, using a standardised protocol including examination of the portal vein. PVT patients were characterised and the PVT prevalence at autopsy, an expression of life-time cumulative incidence, assessed in high-risk disease categories and expressed in terms of odds ratios and 95% CI. RESULTS: The population prevalence of PVT was 1.0%. Of the 254 patients with PVT 28% had cirrhosis, 23% primary and 44% secondary hepatobiliary malignancy, 10% major abdominal infectious or inflammatory disease and 3% had a myeloproliferative disorder. Patients with both cirrhosis and hepatic carcinoma had the highest PVT risk, OR 17.1 (95% CI 11.1-26.4). In 14% no cause was found; only a minority of them had developed portal-hypertension-related complications. CONCLUSION: In this population-based study, PVT was found to be more common than indicated by previous clinical series. The markedly excess risk in cirrhosis and hepatic carcinoma should warrant an increased awareness in these patients for whom prospective studies of directed intervention might be considered.

Adult↗

Contrasting haemodynamic patterns of portal hypertension in hepatosplenic schistosomiasis.

18 cases of hepatosplenic schistosomiasis taken at random were studied. The transumbilical portal pressure, the trans-splenic portal pressure, the occluded thoracic duct pressure, and thoracic duct lymph flow were measured simultaneously before and after splenectomy. The findings were correlated with the clinical data, liver pathology, and operative findings. The transumbilical portal pressure-trans-splenic portal pressure gradient was found of significant importance. It was considered positive when the transumbilical portal pressure was higher than the trans-splenic portal pressure, in such cases the primary generating factor of portal hypertension is most probably of hepatic origin (post or presinusoidal obstruction; organic or functional). The gradient was considered negative when the transumbilical portal pressure was lower than the trans-splenic portal pressure; in such cases the primary generating factor of portal hypertension is most probably of splenic origin (hyperdynamic spleen) or in the portal vein (thrombosis). A significant correlation was found between the type of this gradient, the thoracic duct lymph flow and the clinico-pathological state. The thoracic duct flow was highest in the non-bleeders. Definite contrasting haemodynamic patterns were found between bleeders and non-bleeders. The bearing of these contrasting patterns on the selection of the operative procedure in the treatment of portal hypertension is suggested.

Blood Pressure↗

[Some principal surgical techniques for living donor liver transplantation].

OBJECTIVE: To investigate some principal surgical techniques of living donor liver transplantation (LDLT). METHODS: Eleven patients of LDLT have been performed at our department from January 2001 to March 2002. The left lobe (segments II, III, IV, including the middle hepatic veins) was transplanted in 8 patients, the left lateral lobe (segments II, III) in one and the right lobe (segments V, VI, VII, VIII, not including the middle hepatic veins) in 2. The plane of liver resection was determined on the basis of donor liver volumetry using CT scan and the anatomic analysis of vascular structure of the hepatic vein, portal vein and hepatic artery using intraoperative ultrasound. The hepatic parenchyma was transected using ultrasound aspirator without blood vessel clamping or graft manipulation. The isolated graft was perfused in situ through the portal vein branch. The liver graft was transplanted into the recipients who underwent total hepatectomy with preservation of the inferior vena cava. The hepatic vein reconstruction was performed in end to end fashion or end to side to the vena cava after venoplasty. Arterial anastomoses were performed using microsurgical technique. Biliary reconstruction was made by using duct-to-duct anastomosis and placement of a T tube. RESULTS: All the 11 donors are uneventfully discharged after operation. In the 11 recipients, an 8-year-old girl needed retransplantation because of hepatic artery thrombosis, one case died of serious chronic rejection on the postoperative day 72. Ten recipients recovered and were discharged from hospital, whose liver function and cuprum oxidase had returned to normal. CONCLUSIONS: The procedure of LDLT is relatively safe for the donor. Reconstruction of vessels is a key step in the procedure. Comprehending anatomical variation of vessels pre- and intra-operatively and correct surgical management might reduce the incidence of complications.

Adolescent↗

Clinical characteristics and prognosis of hepatocellular carcinoma: analysis based on serum alpha-fetoprotein levels.

The purpose of this study was to determine whether a relation does exist between clinicopathologic features and the prognosis of hepatocellular carcinoma (HCC) with respect to serum alpha-fetoprotein (AFP) levels at diagnosis. We reviewed the clinical data of 309 pathologically proven HCC cases divided into three groups: group 1 with normal AFP (<20 IU/mL), group 2 with moderately elevated AFP (20-399 IU/mL) and group 3 with markedly elevated AFP (> or =400 IU/mL). Of these, there were 76 (24.6%), 78 (25.2%), and 155 patients (50.2%) in groups 1, 2, and 3, respectively. We found that HCC patients with high AFP tended to have greater tumor size, bilobar involvement, massive or diffuse types, and portal vein thrombosis. Nonetheless, we could not establish a correlation between increased AFP and Okuda's stages, degree of tumor differentiation, or extrahepatic metastasis. The median survival rates in groups 1 (6 months) and 2 (7 months) were significantly longer than that of group 3 (3 months). On multivariate logistic regression analysis, positive hepatitis B surface antigen (HBsAg) status and bilobar tumor involvement represented the independent factors for predicting high AFP values. We concluded that AFP is useful not only for diagnosis, but also as a prognostic indicator in patients with HCC . However, it cannot be considered a sensitive tumor marker, particularly during the early stages in HBsAg-negative patients.

Adolescent↗

Use of polytetrafluoroethylene patch for temporary wound closure after pediatric liver transplantation.

Despite numerous options for pediatric transplantation, closure of the abdominal wall after liver transplantation is occasionally difficult, resulting in increased abdominal pressure and possible vascular compromise. Since 1990, we have utilized a 2-mm thick sheet of polytetrafluoroethylene (PTFE) to overcome this situation in 21 transplants for 17 patients. The median age was 0.9 months. Ten of the 21 transplants utilized full-size grafts. The donor to recipient weight ratio was 1.7+/-1.2. Cadaveric left lateral segments were used in 8 of 21 transplants (weight ratio, 7.4+/-5.9), living donor left lateral segments were used in 3 of 21 transplants (weight ratio, 13.2+/-6.7). We were able to remove 14 of 21 patches with one additional operation, whereas 4/21 patches required two operations and 3/21 required three operations. Reoperations identified two cases of hepatic artery thrombosis not previously identified by duplex ultrasonography. There were no technical problems or adverse effects associated with the use of the PTFE patch. After patch removal, the fascia was closed with a nonabsorbable suture and the skin was allowed to close by secondary intention. There were no wound infections, portal vein thrombosis, or fluid and electrolyte abnormalities. PTFE is a safe, temporary alternative to primary wound closure in liver transplantation when the size of the graft or intestinal and graft edema does not allow conventional closure of the abdomen. Infectious, fluid/electrolyte, or ventilatory complications were not noted. The necessity of a second-look operation is useful in assessing the graft and vascular patency. The majority of patches can be removed within the first postoperative week.

Child, Preschool↗

[Prospective study of the risk factors for the development of post-thrombotic syndrome after proximal deep venous thrombosis].

BACKGROUND AND OBJECTIVE: The incidence and risk factors for the development of post-thrombotic syndrome (PTS) are not well known, so the aim of our study is to evaluate the development of PTS after proximal deep vein thrombosis (DVT) and its relationship with several clinical, laboratory and therapeutic factors. PATIENTS AND METHOD: Prospective, observational study. INCLUSION CRITERIA: consecutive patients with acute symptomatic proximal DVT in the lower extremities diagnosed between February 2000 and July 2002. EXCLUSION CRITERIA: life expectancy < 12 months, impossibility for follow-up, renal or hepatic failure, previous PTS or varicosis and recurrent thrombosis during follow up. Endpoint: PTS at 12 months. Explicative variables: clinical risk factors for DVT, D-dimer value, hypercoaguable state, anticoagulant therapy and compression stockings compliance. Multivariable analysis (logistic regression) was performed. RESULTS: One hundred and seventy two patients with DVT were evaluated for inclusion. Sixty nine were excluded and 87 patients completed follow-up. PTS appeared in 47 patients (54%). Compliance of compression stockings was adequate in 57% of patients and decreased 45% the risk for PTS (p = 0.01). No significant associations were observed between PTS and others variables. Multivariable analysis confirmed the protective effect of compression stockings (RR = 0.3; p < 0.01) and previous ipsilateral DVT appeared significatively associated with PTS development (RR = 8; p = 0.01) CONCLUSIONS: About 50% of patients with proximal DVT develop PTS within 1 year. Previous ipsilateral DVT is the strongest risk factor for PTS. Regular compression stocking use decreases the risk of PTS by 50%.

Aged↗

Intrahepatic portal vein branches after extrahepatic portal vein occlusion. Experimental study.

BACKGROUND/AIMS: Prehepatic portal hypertension caused by extrahepatic portal vein occlusion is a situation in which hepatocytes are not damaged by disease despite the fact that portal blood is unable to reach them due to portal vein occlusion. We explored the patency of intrahepatic portal vein branches after extrahepatic portal vein occlusion for the possibility of revascularization by splenoportal shunt. METHODOLOGY: Prehepatic portal hypertension was induced in 8 mini-pigs by external compression of the portal vein with a device consisting of an inflatable silicone balloon mounted on a silicone cuff and attached to a subcutaneous chamber. Another device consisting of cannula and a subcutaneous chamber was placed into the splenic vein for portal pressure monitoring and portal venograms. Both devices were placed during laparotomy with their chambers positioned subcutaneously. Portal vein compression was initiated one week later and was accomplished in two steps. Extrahepatic portal vein occlusion and the patency of intrahepatic portal vein branches were confirmed by direct portal venography. Alteration of the intrahepatic portal bed was examined at necropsy after 4 weeks, checking for the presence of occlusion or thrombosis. RESULTS: Portal vein occlusion was achieved in 5 animals, while severe stenosis was demonstrated in the remaining three. Portal venograms demonstrated patency of the lobar portal vein branches filled by hepatopetal collaterals around the occluded portal vein. All intrahepatic branches were free of thrombus at gross examination. CONCLUSIONS: In the absence of the hepatic parenchymal disease, lobar intrahepatic portal vein branches remain patent despite truncal portal vein occlusion and are supplied by rapidly developed hepatopetal collaterals.

Animals↗

Septic postpartum ovarian vein thrombosis.

This report describes the clinical findings and outcome of a patient suffering from septic postpartum ovarian vein thrombosis. Treatment modalities are well described and range from hysterectomy and thrombectomy to the use of vena cava filters in combination with anticoagulation and antibiotics. Defervescence with a combination infusion of tissue plasminogen and heparin were used. This treatment approach has been found particularly successful in cases of ilio-femoral, hepatic, renal and vena caval thromboses.

Adult↗

Portal hypertension, hepatic infarction, and liver failure complicating pancreatic islet autotransplantation.

A patient with chronic pancreatitis who underwent subtotal pancreatectomy and pancreatic islet tissue autotransplantation by portal vein embolization developed marked portal hypertension requiring surgical portal systemic decompression. The patient subsequently developed extensive hepatic infarction and died fo liver failure. Postmortem studies showed organizing thromboemboli containing pancreatic acinar and islet tissue in the intrahepatic portal venous radicles and widespread ischemic infarcts with periportal sparing. Factors contributing to hepatic infarction were thrombosis of portal venous radicles, portasystemic shunting, and systemic arterial hypotension. Marked portal hypertension, hepatic infarction, and liver failure are potential complications of pancreatic islet tissue autotransplantation.

Humans↗