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PubMed2004

Diagnosis of small-bowel varices by capsule endoscopy.

BACKGROUND: Capsule endoscopy is being used increasingly to investigate GI bleeding of obscure origin and disorders of the small bowel. METHODS: Four cases of small-bowel varices of various etiologies diagnosed by capsule endoscopy are described: a bleeding small-bowel varix because of hepatic portal hypertension, oozing small-bowel anastomotic or adhesion-related varices, small-bowel varices secondary to mesenteric vein thrombosis, and "idiopathic intestinal varices." OBSERVATIONS: Over a 12-month period, small-bowel varices were found in 4 of 46 patients (8.7%) who underwent capsule endoscopy for GI bleeding. Fresh blood adjacent to the varices was documented in 3 patients. The small-bowel varices had serpiginous or nodular shapes, with or without a bluish coloration. The variceal mucosa appeared mosaic-like, shining, or normal compared with surrounding mucosa. CONCLUSIONS: Capsule endoscopy is invaluable for the diagnosis of small-bowel varices. It is highly sensitive for detection of fresh blood in the small bowel. Clinical suspicion, capsule endoscopy image recognition, and alertness during capsule endoscopy interpretation are keys to diagnosis.

Adult↗
PubMed1982

[Liver hemangioma--an angiographic contribution to the differential diagnosis of sonographic lesions (author's transl)].

Small liver hemangiomas are displayed as echogenic as well as sonolucent patterns on ultrasonic scans. Differentiation from malignomas is difficult and responsible, hepatomas and solitary metastases being possible. By partial liver resection the malignant diseases can be treated successfully. Therefore an accurate diagnosis is to be aimed at. Of all the methods only angiography can ensure a certain amount of clarity. This is possible under the following circumstances: The cavernomas must be of a certain size. They must not withdraw from evidence due to large avascular areas which can result from thrombosis, fibrosis or necrosis. Moreover a superselective filling of the hepatic artery is claimed but not always possible. If the portal vein is opacified it conceals the radiologically typical image of the cavernoma. Under these circumstances only few moments of the late arterial and the hepatovenous phases remain to detect the hemangioma in the seriogram.

Adult↗
PubMedDate not supplied

Membranous obstruction of inferior vena cava in Taiwan.

Membranous obstruction of the inferior vena cava (MOVC) is a rare cause of Budd-Chiari syndrome. When compared to the West, the incidence of MOVC was reported to be higher in the Orient, India and South Africa. From 1979 to 1993, 16 consecutive Chinese patients (mean age 50 years) with MOVC were retrospectively evaluated. The diagnosis in these MOVC patients was usually delayed with a mean lag time of 111 months. Most of the cases were detected by a delicate ultrasonographic examination of the abdomen. Segmental narrowing of the inferior vena cava in 11 patients was the predominant type of MOVC, while five experienced a membranous obstructive type. Only one of five surgery-treated patients had a post-operation survival > 5 years, while five out of the nine patients who received conservative treatment still survived after a 6-15 year follow up. Two patients received percutaneous angioplasty (PTA). One survived 4 years and the other expired 5 years after the PTA. Two patients (12%) developed a hepatocellular carcinoma in their disease course, and the incidence was lower than in previous reports from Japan and South Africa. The incidence of hepatitis B surface antigen in MOVC did not increase in our patients compared with the general population. In conclusion, the inferior vena cava should be carefully evaluated in an ultrasonographic examination of the abdomen to increase the diagnosis rate of MOVC. Surgical intervention should be carefully justified according to the patient's symptoms and signs, the types of obstructive lesions and the expertise of the surgeons.

Adult↗
PubMed1992

Membranous obstruction of the inferior vena cava: comparison of findings at sonography, CT, and venography.

OBJECTIVE: Membranous or segmental obstruction of the inferior vena cava is one of the common causes of chronic Budd-Chiari syndrome. In this study, the venographic findings are compared with the results of sonography and CT in order to ascertain their role in the management of these cases. MATERIALS AND METHODS: Fifteen patients with membranous (n = 8) or segmental (n = 7) obstruction of the inferior vena cava who had been examined with sonography and CT were studied retrospectively. Diagnosis was made at surgery (n = 3) or by venacavography (n = 12). Sonographic findings were analyzed on the basis of the initial report, and CT findings were reviewed retrospectively with knowledge of the sonographic findings. RESULTS: Sonography showed membranous obstruction (n = 5), segmental cordlike obstruction (n = 3), and unspecified obstruction (n = 5) of the inferior vena cava, while CT showed a flap of the membrane (n = 1) and segmental narrowing or obstruction of the inferior vena cava (n = 7). In the remaining cases, the inferior vena cava either appeared normal (n = 6) or was not visualized (n = 1) on CT or was not described in the sonographic report (n = 2). In nine cases, CT showed one or several tiny calcific foci in the inferior vena cava. Sonography showed obliteration of at least one hepatic vein (n = 8) and of intrahepatic collateral vessels (n = 12), whereas CT was less sensitive in evaluating obliteration of intrahepatic veins (n = 4) and collateral vessels (n = 7). Sonography and CT both showed hepatic masses (n = 6), evidence of liver cirrhosis and portal hypertension (n = 14), hepatomegaly (n = 14), enlargement of the caudate lobe (n = 9), and intraabdominal (n = 11) and abdominal wall (n = 15) collateral vessels. CONCLUSION: Sonography was superior to CT in delineating pathologic venous anatomy of the inferior vena cava and hepatic veins whereas CT was better in evaluating hepatic cirrhosis and tumor. We believe that these techniques are useful complements to venography in the diagnosis and management of these cases.

Adolescent↗
PubMed2001

Clinical characteristics and outcome of a cohort of 101 patients with hepatocellular carcinoma.

AIM: To conduct a cohort study of 101 patients with hepatocellular carcinoma (HCC) presenting to a tertiary care medical referral center in Germany between 1997 and 1999. METHODS AND RESULTS: Data were retrospectively analyzed by chart review. In 95 cases (72 males and 23 females) sufficient data were available for analysis. Twenty five (29%) of 85 patients were HBsAg or anti HBc positive, 21/85 (25%) were anti HCV positive, and 6/85 (7%) were positive for both HBV and HCV-markers. Age was significantly lower in HBV positive patients than in the other two groups. Thirty one (34%) of 90 patients had histories of alcohol abuse. In 79/94 (84%) patients, cirrhosis was diagnosed. Of these cirrhotic patients, 29/79 (37%) belonged to Child Pugh's group (CHILD) A, 32/79 (40%) to CHILD B, and 18/79 (23%) to CHILD C. AFP was elevated in 61/91 (67%) patients. A single tumor nodule was found in 38/94 (40%), more than one nodule in 31/94 (34%), and 25/94 (26%) had a diffusely infiltrating tumor, i.e. the tumor margins could not be seen on imaging procedures. Portal vein thrombosis was present in 19/94 (20%). Imaging data consistent with lymph node metastases were found in 10/92 (11%), while distant metastases were found in 8/93 (9%). According to Okuda 28/94 (30%) were grouped to stage I, 53/94 (56%) were grouped to stage II, and 13/94 (14%) were grouped to stage II. Survival data were available for 83 patients. The Kaplan-Meier estimate for median survival was 8 4 months. Factors influencing survival were the Okuda score, the presence of portal vein thrombosis, and the presence of ascites. The presence of non complicated liver cirrhosis by itself, distant metastases, or infection with hepatitis viruses did not influence survival. AFP positivity by itself did not influence survival, though patients with an AFP value greater than 100 microg/L did experience shortened survival. Treatment besides tamoxifen or supportive care was associated with prolonged survival. The influence of therapy on survival was most pronounced in Okuda stage II patients. There was longer survival in those Okuda stage II patients who were treated with percutaneous ethanol injection. CONCLUSION: Even in a low incidence area such as Germany, the majority of HCC is caused by viral hepatitis and therefore potentially preventable. Reflecting the high proportion of advanced stage tumors in our patients, the median survival was poor. Patients who received active therapy had a longer survival.

Adult↗
PubMed1982

[Sonographic assessment of the portal system in portal hypertension].

Three hundred and thirty-seven patients with portal hypertension and recurrent bleeding from oesophageal varices were examined by sonography. The situation was correctly elucidated in 17 out of 21 patients (81%) with pre-hepatic blocks, in 275 out of 313 cases (88%) with intra-hepatic blocks and in two out of three cases with post-hepatic blocks. The relevant findings consisted of stenoses and occlusions of the portal venous system and collaterals in pre-hepatic blocks, dilatation of the portal venous system and hepato-fugal collaterals in intra-hepatic blocks and occlusion of the hepatic veins in post-hepatic blocks. Sonography is recommended in cases of portal hypertension because of its non-invasive nature and high accuracy as the primary form of investigation. Spleno-portography should be used only if surgery is indicated.

Esophageal and Gastric Varices↗
PubMed1984

Portal vein obstruction in patients requiring hepatic resection or transplantation.

Four patients with chronic portal vein occlusion (or near occlusion) who required major hepatic resection or transplantation are described. In each case, portal vein patency was restored, and objective evidence of long-term patency is presented in three patients. These patients demonstrate the feasibility of restoring and indefinitely maintaining portal venous flow coincident to major hepatic surgery.

Adult↗
PubMedDate not supplied

[Portal vein thrombosis in children: clinical and laboratory study of 26 cases].

Portal vein thrombosis represents one of the most frequent causes of portal hypertension in childhood. The aim of the present study was to describe the clinical and laboratorial characteristics of portal vein thrombosis in pediatric patient. We studied 26 children with diagnosis of portal vein thrombosis through splenoportography (two patients) and ultrasound scan (24 patients) which ages varied from 2 months to 11 years and 4 months (median-5 years and 3 months). Data of the patient history, physical and laboratories examination were used to a retrospective study which was done through medical record analysis. The main complaint of the examination was hematemesis, which was found in 57.6%. In 26.9% a possible risk factor for portal vein thrombosis was found [catheterization of the umbilical vein (four), sepsis (two), omphalitis (one)]. Splenomegaly was present in all cases and the associated illness to portal vein thrombosis were: hepatoportal sclerosis (three), cytomegalovirus infection (two), blastomycosis (two), virus C (two), virus B (one) and virus A (one). The time between the first bleeding and the examination at University of Campinas Hospital, in Campinas, SP, Brazil, varied from 0.23 months to 54 months with a median of 12 months. Only 11.5% of patients underwent the endoscopy with sclerotherapy before going to University of Campinas Hospital. Aminotransferases' activities were considered normal in 20 patients. We could conclude that: 1. The most frequent initial symptom was hematemesis. 2. The known risk factors for portal vein thrombosis were present in about 1/3 of the cases. 3. Laboratorial exams usually indicated absence of hepatocitic lesions. 4. The efforts towards sending the patient to a reference center were late with a delayed diagnostic and with delayed effective therapeutic conduct. 5. In about 50% of the cases there was PVT associated with other hepatic diseases.

Child↗
PubMed2005

Update on the classification, assessment of prognosis and therapy of Budd-Chiari syndrome.

Budd-Chiari syndrome (BCS) occurs as a result of obstruction of hepatic venous outflow at any level from the small hepatic veins to the junction of the inferior vena cava with the right atrium. Diagnosis can be difficult because of the wide spectrum of presentation of the disease and the varying severity of liver damage. The traditional classification of BCS--as fulminant, acute or chronic--is not prognostically useful. This makes assessing the benefit of therapy difficult, especially as there is no evidence from randomized studies. This article highlights advances in the prognosis and therapy of BCS. Identification of the site of venous obstruction has a major effect on prognosis. Portal-vein thrombosis occurs in 20-30% of cases, and acute presentation of BCS reflects an acute or chronic syndrome in 60% of BCS cases. BCS can be diagnosed and treated on a single occasion in the setting of the radiology department, with hepatic venography, transjugular liver biopsy, retrograde CO2 portography and inferior vena cava pressure measurements performed simultaneously with therapies such as dilation or stenting of webs in the inferior vena cava or hepatic veins, and placement of transjugular intrahepatic portosystemic shunts. Disruption of a portal vein thrombus can also be done during the same session. Surgical shunts have been superseded by the use of transjugular intrahepatic portosystemic shunts. Liver transplantation is reserved for fulminant and progressive chronic forms of BCS. Anticoagulation therapy must be used routinely, before and after specific therapy, regardless of whether a thrombophilic disorder is diagnosed.

Anticoagulants↗
PubMedDate not supplied

Portal vein obstruction complicating intra-arterial chemo-infusion for hepatic metastases.

In three patients with colon cancer and liver metastases who had received intra-arterial chemo-infusion of fluorouracil (5FU) and mitomycin C and/or cis-diamminedichloroplatinum (CDDP), intrahepatic portal vein thrombosis (PVT) was incidentally demonstrated by computerized tomography (CT) 6, 1 and 7 months respectively after the cessation of administration of anti-cancer agents. One patient developed complete PVT in the whole liver as shown by follow-up CT 6 months after a diagnosis of pre-existing sclerosing cholangitis, and died from rupture of oesophageal varices. In the remaining two patients, PVT was found incidentally by follow-up CT in the right portal vein (Case 2) and the right anterior portal vein (Case 3) respectively; it spontaneously recanalized in Case 2 and was still present in Case 3 2 months later. PVT seems to be one of the complications of hepatic arterial chemo-infusion and its possibility must be borne in mind in such patients, even though the exact interval between the arterial chemo-infusion and occurrence of PVT could not be determined.

Adult↗
PubMed1992

Transcatheter embolization of a high-flow congenital intrahepatic arterial-portal venous malformation in an infant.

An intrahepatic arterial-portal venous malformation (APVM) was diagnosed in a 4 1/2-month-old infant with portal hypertension. Visceral angiography showed a large saccular vascular space in the left hepatic lobe with a multiplicity of feeding arteries and drainage into the left portal vein. The lesion was successfully treated by transcatheter embolization following two unsuccessful surgical procedures. Two years later portal vein thrombosis with cavernous transformation was diagnosed, possibly a consequence of the high-flow arterial-portal shunt and its subsequent occlusion. Knowledge of the anatomic differences between this rare congenital APVM and the more commonly occurring arterial-portal fistula is crucial in planning effective transcatheter embolotherapy or surgery for these lesions.

Arteriovenous Fistula↗
PubMed1980

CT demonstration of portal and superior mesenteric vein thrombosis in hepatocellular carcinoma.

Three cases of hepatocellular carcinoma in which computed tomography (CT) demonstrated thrombosis of the portal vein are reported. In one patient, extension of the thrombus into the superior mesenteric vein was identified as well. The outstanding CT features of portal vein thrombosis were: (a) enlargement of the vein, (b) intraluminal low density area, and (c) hyperdense peripheral ring due to the enhancement of the venous wall. These findings may be useful in differentiating hepatocellular carcinoma from hepatic metastases.

Aged↗
PubMed1985

Sonographic features of portal vein thrombosis.

The ability of real-time sonography to demonstrate the liver venous network is well documented. Sonographic features of 21 cases of unsuspected portal vein thrombosis, detected by a screening sonography of the upper abdomen and subsequently confirmed by computed tomography, angiography, or surgery, are discussed. Sonographic features of portal vein thrombosis were an echogenic thrombus within the lumen of the vein (67%), demonstration of portal vein collateral circulation (48%), enlargement of the thrombosed segment of the vein (38%), and the so-called cavernomatous transformation of the portal vein (19%). Echogenic endoluminal thrombi were observed with the same incidences in malignant and benign disease. Sonography, unlike angiography, was unable to characterize neoplastic thrombi; only the combination of an echogenic thrombus and an adjacent hepatic mass was strongly suggestive of malignancy, especially hepatoma. The extensive use of sonography as a screening test in upper abdomen pathology will probably improve the detection of portal vein thrombosis, a diagnosis until now considered rare.

Adult↗
PubMed2006

Pathophysiologic observations and histopathologic recognition of the portal hyperperfusion or small-for-size syndrome.

In an attempt to more completely define the histopathologic features of the portal vein hyperperfusion or small-for-size syndrome (PHP/SFSS), we strictly identified 5 PHP/SFSS cases among 39 (5/39; 13%) adult living donor liver transplants (ALDLT) completed between 11/01 and 09/03. Living donor segments consisting of 3 right lobes, 1 left lobe, and 1 left lateral segment, with a mean allograft-to-recipient weight ratio (GRWR) of 1.0 +/- 0.3 (range 0.6 to 1.4), were transplanted without complications, initially, into 6 relatively healthy 25 to 63-year-old recipients. However, all recipients developed otherwise unexplained jaundice, coagulopathy, and ascites within 5 days after transplantation. Examination of sequential posttransplant biopsies and 3 failed allografts with clinicopathologic correlation was used in an attempt to reconstruct the sequence of events. Early findings included: (1) portal hyperperfusion resulting in portal vein and periportal sinusoidal endothelial denudation and focal hemorrhage into the portal tract connective tissue, which dissected into the periportal hepatic parenchyma when severe; and (2) poor hepatic arterial flow and vasospasm, which in severe cases, led to functional dearterialization, ischemic cholangitis, and parenchymal infarcts. Late sequelae in grafts surviving the initial events included small portal vein branch thrombosis with occasional luminal obliteration or recanalization, nodular regenerative hyperplasia, and biliary strictures. These findings suggest that portal hyperperfusion, venous pathology, and the arterial buffer response importantly contribute to early and late clinical and histopathologic manifestations of the small-for-size syndrome.

Adult↗
PubMedDate not supplied

Histopathology of portal tracts in livers after transcatheter arterial chemo-embolization therapy for hepatocellular carcinoma.

To study the influence of transcatheter arterial embolization therapy (TAE) on the portal tracts, 32 cases of hepatocellular carcinoma (HCC) with a history of TAE were examined. Portal tract elements are said to be mainly supplied by hepatic arterial blood, as is HCC. The following changes were found: peribile duct fibrosis; biliary epithelial injuries; bile duct necrosis; fibrous thickening of the intima and adventitia of arteries; thrombosis or stenosis of portal vein branches; and fibrosis of portal tract itself. We failed to correlate these histopathologic changes with the frequency of TAE or the interval between TAE therapy and surgery or autopsy. Semi-quantitative assessment disclosed that vessels of the peribiliary vascular plexus (PVP) which are known to be derived from hepatic arterial branches, were considerably decreased. There was little correlation between the degree of reduction of PVP and the observed histopathologic changes of portal tracts. It is suggested that TAE causes adverse effects on the elements of portal tracts and a reduction in the PVP in the vicinity of HCC, but the relationship between them is unclear.

Adult↗
PubMed2006

Inferior mesentericocaval shunt--an efficient therapeutical alternative in Budd Chiari syndrome associated with portal and splenic vein thrombosis in a teenager.

The authors present the case of a 17 year old girl admitted to hospital for poor general state, mild scleral jaundice, deficient nutritional state, oliguria and massive ascites. She was diagnosed with Budd-Chiari syndrome: thrombosis of the left suprahepatic vein and nonocclusive thrombosis of the inferior vena cava at the level of the 12th thoracal and the lumbar vertebrae. The specific feature of the case was the association of portal and splenic vein thrombosis. A mesentericocaval shunt with external jugular grefon was performed. The evolution at 20 months after surgery has been favorable. She has no ascites, the nutritional state has normalized and hepatic laboratory findings have returned to normal values. There still persists a high consistency splenomegaly, but without hematological hypersplenism. Even though the mesentericocaval shunt is not without complications, it represents an efficient alternative for the treatment of Budd-Chiari syndrome, when endovascular techniques are not available.

Adolescent↗
PubMed1995

[Effect of anastomosis reconstruction on vascular complications after liver transplantation].

AIM: Besides primary non function (PNF), vascular complications are responsible for the majority of early surgical and interventional therapy following liver transplantation. The purpose of this study was to evaluate the influence of the variety of arterial anastomosis on postoperative morbidity and mortality. METHOD USED: In 179 liver transplantations, vascular (arterial and portal) complications within the first 3 months were analyzed with respect to the type of reconstruction. The arterial anastomoses were divided into 3 groups according to the recipient artery used [Group (I): common hepatic artery (CHA), (II): hepatic artery (HA), (III): aorta]. For statistical analysis comparison of two proportions and the logrank test were used. RESULTS: The reconstruction was done primarily to the recipient CHA (69%, n = 124), less often to the HA (15%, n = 26) or directly to the aorta (16%, n = 29). The portal anastomosis-with the exception of two cases (dacron graft and internal iliac vein interposition)-was always end to end and resulted in four reinterventions (2.2%, kinking: n = 1, thrombosis: n = 3). Arterial complications (11.7%) like thrombosis, stenosis and dissection (n = 17), bleeding (n = 2) and steal phenomenon (n = 2) occurred more frequently. The difference in one year survival between patients with (n = 12/25, 47%) and without (n = 42/53, 79%) vascular complications was significant (chi 2 = 4.72, FG 1, logrank test p < 0.05). CONCLUSION: The rate of complications causing surgical or interventional therapy is independent of the choice of arterial reconstruction. The one year survival rate in patients with vascular complications is significantly decreased.

Adolescent↗