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PubMed1995

Vascular complications after pediatric liver transplantation.

From February 1986 to July 1994, 81 hepatic transplantations were performed in 73 children, with an overall patient survival rate of 83%. Forty-two patients received whole-liver grafts (WLG) and 39 had reduced-size grafts (RSG). The mean patient weight was 19.7 kg, with 29 patients weighing less than 10 kg. Seventeen vascular complications (21%) occurred in 13 children: 8 (10%) had hepatic artery thrombosis (HAT), 5 (6%) had portal vein thrombosis (PVT), 1 had both HAT and PVT (1%), and 3 (4%) had aortic conduit perforation (ACP). There was no significant difference in the incidence of HAT between RSG (5%) and WLG (14%) or between children weighing less than 10 kg (10%) and those weighing more than 10 kg (10%). The site of arterial reconstruction, end-to-end to the recipient common hepatic artery or end-to-side to the infrarenal aorta, had no significant effect on the occurrence of HAT (7% v 8%), but HAT occurred in 2 of 6 cases (33%) in which an aortic conduit was used. PVT documented in 5 cases (6%) was associated with technical complications (2), preduodenal portal vein (2), and a circulating cardiolipid antibody (1), and required thrombectomy, with no graft loss. Combined HAT and PVT was found in one patient 2 years postretransplantation for HAT. Although graft function is normal, portal hypertension persists. The aortic conduit, used in six patients, led to arterial perforation (3), HAT (2), and death (2). Of the 8 cases of HAT, 1 was diagnosed during autopsy and 7 occurred within 30 days and required retransplantation (6) or thrombectomy with rearterialization (1).(ABSTRACT TRUNCATED AT 250 WORDS)

Anastomosis, Surgical↗

PubMed2001

Reversal of portal flow after acute rejection in living-donor liver transplantation.

Portal hepatofugal flow is rare after liver transplantation. We experienced a case in which hepatofugal portal flow was observed in acute rejection. A 6-year-old boy with glycogen storage disease type Ia underwent living-donor liver transplantation. On postoperative day 7, portal venous peak velocity was markedly decreased without portal thrombosis and obstruction of the hepatic vein, and hepatic arterial peak velocity increased reciprocally. Based on a diagnosis of acute rejection, made on postoperative day 8, we initiated steroid pulse therapy. Despite the employment of this therapy, continuous hepatofugal portal flow was observed in the entire liver on postoperative day 8. On day 12, as the liver disorder progressed, the Doppler waveform in the portal vein changed from continuous to pulsatile hepatofugal flow. The patient died of liver failure on day 14. The histological findings of a biopsy specimen on day 9 showed centrilobular necrosis, while total hepatocellular necrosis was seen at autopsy. Hepatofugal flow after liver transplantation is considered to be an ominous sign caused by several factors, and its appearance indicates a fatal condition.

Child↗

PubMed1994

Use of distal splenorenal shunt in children referred for liver transplant evaluation.

Variceal bleeding remains a common cause of morbidity for children with both intrahepatic and extrahepatic portal hypertension. Occasionally, patients referred for liver transplant evaluation have significant variceal bleeding, despite adequate synthetic liver function. During a 7-year period, 322 children were referred for liver transplant evaluation. Six underwent distal splenorenal shunt surgery after evaluation. There were four boys and two girls. The average age was 11 +/- 4 years, and the average weight was 39 +/- 15 kg. The etiology of variceal bleeding was intrahepatic portal hypertension in five (1 biliary atresia, 2 chronic hepatitis, 2 congenital hepatic fibrosis) and extrahepatic portal vein thrombosis in one. Two patients had no previous attempts at sclerotherapy (one because of an abnormality in platelet function, the other because of extensive gastric varices), and four had multiple previous sclerotherapy treatments. No patient had preoperative encephalopathy. Three cases were Child's class A, and three were Child's class B. Preoperative evaluation of the portasystemic system was performed with magnetic resonance (MR) imaging or splenoportography. All patients underwent a distal splenorenal shunt procedure, four of whom also had splenopancreatic disconnection. One patient required 100 mL of blood replacement, and five required no blood. The average length of hospital stay was 9.8 +/- 2.2 days. Postoperative complications were minimal. All patients are alive, without recurrent gastrointestinal bleeding or encephalopathy, and they have patent shunts, which was confirmed by MR or Doppler ultrasound at a mean of 25 +/- 20 months after shunt surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2003

Monosegmental living donor liver transplantation.

BACKGROUND: Living donor liver transplant (LDLT) program has been started from 1990 in Japan, and is still major form of liver transplantation because of the scarcity of cadaveric donor organs. In small infants, implantation of left lateral segment grafts can be a problem because of a large-for-size graft. Until November 2002, we performed 867 transplants for 828 patients (561 children and 306 adults), and 14 cases received monosegment grafts from living donors. METHODS: Fifteen patients, median age 211 days, median weights 5.95 kg, received monosegmental LDLT. The indication for using this technique was infants with an estimated graft-to-recipient weight ratio of over 4.0%. RESULTS: Graft and patient survival is 85.7%. There were no differences in donor operation time and blood loss between monosegmentectomy and left lateral segmentectomy. Segment III grafts were indicated in 13 cases. Two vascular complications were observed (one hepatic artery thrombosis and one portal vein thrombosis). CONCLUSIONS: Monosegental living donor liver transplantation is a feasible option with satisfactory graft survival in small babies with liver failure.

Body Weight↗

PubMed1998

Ultrasonography of portosystemic shunts in dogs and cats.

Ultrasonography is a rapid, accurate, noninvasive diagnostic test for primary (congenital) and secondary (acquired) portosystemic shunting in dogs and cats. Two-dimensional, gray-scale ultrasonography alone enables diagnosis of most congenital portosystemic shunts and determination of intra- versus extrahepatic location. Use of duplex- and color-flow Doppler ultrasonography aids detection of congenital and acquired extrahepatic portosystemic shunts. The underlying cause of acquired portosystemic shunting is portal hypertension; this may be documented by finding either hepatofugal or reduced velocity hepatopetal portal blood flow by duplex-Doppler. Also, ultrasonography may enable detection of lesions involved in the pathogenesis of portal hypertension, for example, hepatic arterioportal fistula, hepatic parenchymal lesions, and portal vein thrombosis.

Animals↗

PubMed2002

Anemia and the liver. Hepatobiliary manifestations of anemia.

Many types of hemolytic anemia may be associated with liver disease. Liver injury can be caused by the adherence of deformed or hemolyzed erythrocyses to hepatic vascular endothelium. Adhesion of large numbers of hemolyzed red blood cells to hepatic macrophages, or occlusion of hepatic sinusoids by fragmented red cells, can also result in injury of the liver. Thrombosis of the hepatic or portal vein is associated with some types of hemolytic anemia, and can cause severe liner injury. These are some examples of hepatic injury that can be caused by hemolytic anemias. This article discusses some aspects of liver disease that is associated with sickle cell anemia, paroxysmal nocturnal hemoglobinuria, glucose-6-phosphate dehydrogenase deficiency, hereditary spherocytosis, and HELLP syndrome.

Anemia↗

PubMed1987

Budd-Chiari syndrome: dynamic CT.

A retrospective multi-institutional study was carried out on a series of 38 patients with histologically proved Budd-Chiari syndrome: Five patients had acute disease, and 33 had subacute or chronic disease. All patients underwent dynamic CT scanning. Angiography was performed in 20 cases, inferior cavography in 22, and wedge-hepatic venography in 16. In all acute cases, CT showed global liver enlargement with diffuse hypodensity on plain scans and patchy enhancement after contrast material injection. Thrombosis of the three main hepatic veins was always demonstrated. In subacute or chronic disease, plain CT scans showed abnormalities of liver morphology and hypodensity either in atrophic areas (19 cases) or in the periphery of the liver (eight cases). With dynamic CT, patchy enhancement was present in 28 cases. Correlation with angiography in 15 cases revealed a normal portal blood flow in enhanced areas and an inversed portal blood flow in atrophic areas. Different morphologic and enhancement patterns on CT scans could be related to the direction of portal blood flow, which changes with different stages of Budd-Chiari syndrome.

Acute Disease↗

PubMed1999

Low-molecular-weight heparins in pregnancy.

We conducted a systematic review, with MEDLINE and Cochrane Library data base searches and bibliographic reviews, of English-language reports describing therapy with low-molecular-weight heparin (LMWH) in pregnancy. Altogether 40 citations, excluding abstracts, were identified. When the quality of evidence was categorized according to the method outlined by the U.S. Preventive Services Task Force, 2 articles were level I, 3 were level II-1, 3 were level II-2, 4 were level II-3, 9 were level III, and the remaining 19 were classified as other (i.e., below level III). Of the 728 pregnant women and 1 postpartum woman described in the 40 citations, 340 (47%) received dalteparin, 192 (26%) enoxaparin, 108 (15%) certoparin, 54 (7%) nadroparin, 30 (4%) other LMWH, and 6 (< 1%) unspecified. The indication for LMWH in most patients (606 pregnancies, 83%) was for thromboprophylaxis. Daily doses ranged from 2500-22,000 U for dalteparin, 20 mg (2000 U)-80 mg (8000 U) for enoxaparin, 3000 U for certoparin, and 2050-15,000 U for nadroparin. Regimens included fixed dosages, increasing dosages as pregnancy progressed, dosages based on body weight, and dosages titrated according to anti-Xa levels. Duration of therapy ranged from a single dose to 476 days. Maternal anti-Xa levels were reported for 255 pregnancies. Target anti-Xa levels ranged from 0.1-0.6 U/ml and measured values from 0.0-0.7 U/ml. Major maternal findings were 18 local and generalized skin reactions, 27 bleeding complications, 9 thromboembolic events, 8 deep vein thromboses, 1 bilateral renal vein thrombosis, 4 pulmonary emboli, 1 hepatic infarction, 4 cases of thrombophlebitis, 12 cases of preeclampsia, 1 placental abruption, and 2 osteoporotic vertebral fractures. A major fetal finding was lack of anti-Xa activity in fetal or cord blood. Published experience suggests that LMWHs are generally safe and effective when administered for thromboprophylaxis during pregnancy. Until prospective, randomized, controlled trials comparing them with unfractionated heparin are performed, their benefits in pregnancy will remain inconclusive.

Clinical Trials as Topic↗

PubMedDate not supplied

Endoscopic sclerotherapy for bleeding oesophageal varices: experience in Sudan.

INTRODUCTION: Bleeding due to oesophageal varices is the commonest cause of upper gastrointestinal tract haemorrhage in Sudan. Endoscopic injection sclerotherapy (EST) is a valuable therapeutic modality for the management of variceal bleeding. Other options for treatment such as variceal banding are either expensive or unavailable. STUDY AIMS: A retrospective study to evaluate the outcome of EST in the management of bleeding oesophageal varices due to portal hypertension in a developing country (Sudan). PATIENTS AND METHODS: A total of 1070 patients over a period of 10 years (1986-1996) were studied. Inclusion criteria was bleeding oesophageal varices consequent to portal hypertension. EST was performed using a standard technique. Ethanolamine oleate 5% was the sclerosing agent utilized. The procedure was done on a day- case basis. RESULTS: There were 904 males (84.5%) and 166 females (15.5%). The cause of portal hypertension was schistosomal periportal fibrosis (PPF) in 999 (93.3%) patients, liver cirrhosis 59 (5.5%), mixed PPF and cirrhosis 5 (0.46%), portal vein thrombosis 6 (0.64%) and congenital hepatic fibrosis was present in 1 patient. A total of 100 (9.4%) patients presented with bleeding which occurred after surgery. Full obliteration of varices required a mean of 4 sessions with a range of 2-6. 462 (43.2%) have been followed up until complete sclerosis of varices. CONCLUSION: This study provides evidence that endoscopic injection sclerotherapy is an essential component in the management of bleeding oesophageal varices caused by portal hypertension. It is a feasible and a cost-effective therapeutic strategy in developing countries.

Adolescent↗

PubMedDate not supplied

Association of the Budd-Chiari syndrome with lupus anticoagulant. Case report and critical review.

The Budd-Chiari syndrome (BCS) was diagnosed in a 30-year-old male hospitalized with hepatomegaly, abdominal collateral vessels and hepatic veins and inferior vena cava thrombosis (IVC) in 1988. The presence of circulating lupus anticoagulant (LAC) was suspected and demonstrated on this occasion in view of an earlier diagnosis of systemic lupus erythematosus (SLE) and recurrent vein thrombosis dating from 1981. There are sporadic reports of an association of BCS with SLE and other autoimmune diseases. The recent literature also describes associations with hypercoagulability due to LAC. These are reviewed together with the personal case to provide the rationale for correct diagnosis and therapy.

Adult↗

PubMed1990

[Oral contraceptive and hepatic effects].

The general use of synthetic estrogens like DC pointed out that near many skilled collateral effects, some others that are showing with a decrease of bile excretion (cholestasis), reversible with their administration interruption; with hepatic cells adenoma that are potentially premalignant and can transform into hepatocellular carcinoma; with vascular complications such as (most frequently in carcinomatousis) "hepatic peliosis" and "thrombosis" of suprahepatic veins (Budd-Chiari's syndrome). There is no overall increase in the incidence of gallbladder disease (cholelithiasis and cholecystitis).

Chemical and Drug Induced Liver Injury↗

PubMed1979

Primary pulmonary hypertension presenting as portal hypertension.

A two and a half-year old child is described who presented with signs of portal hypertension (hematemesis, hepatosplenomegaly, ascites). Her subsequent work-up revealed that the "pressure-head" originated within the pulmonary arterial bed. Indeed, severe changes of primary pulmonary hypertension were found at autopsy. What is unique about this case is the absence of cardiopulmonary symptoms prior to the development of suprahepatic portal hypertension. In addition, the pulmonary disease developed in the absence of underlying chronic hepatic disease or extrahepatic portal vein thrombosis which, reportedly, can lead to pulmonary hypertension.

Autopsy↗

PubMed1996

Radiology of pancreatic tuberculosis: a report of three cases.

We report three cases of biopsy proven pancreatic tuberculosis. The patients presented with abdominal pain and intermittent fever. Ultrasound and computed tomography revealed a diffusely enlarged pancreas with focal hypoechoic/hypodense lesions in all three patients. In addition, one patient had a large pancreatic cyst with internal echoes. Associated findings included peripancreatic and mesenteric lymph nodes, bowel wall thickening of ileocecal junction, focal hepatic or splenic lesions, splenic vein thrombosis, and ascites. Pancreatic tuberculosis should be considered in the differential diagnosis of focal pancreatic lesions, especially if associated with ancillary findings such as enlarged hypodense nodes in the peripancreatic region or in the mesentery in patients presenting with longstanding fever and abdominal pain.

Adult↗

PubMed1994

[Vascular complications of liver transplantation: surgical treatment].

Vascular complications constitute a major cause of morbidity and mortality after liver transplantation. They are dominated by arterial complications, the most frequent being hepatic artery thrombosis. Venous complications essentially consist of portal vein thrombosis. The preventive treatment of vascular complications is based on a better understanding of the risk factors. Close cooperation between surgeon, and radiologist is essential for effective surgical correction, which requires a rapid diagnosis and is designed to save not only the patient's life, but also, whenever possible, the liver transplant.

Aneurysm, False↗

PubMed2005

Twenty cases of adult-to-adult living-related liver transplantation: single-center experience in Saudi Arabia.

BACKGROUND: The deceased donor organ shortage has forced surgeons to implement innovations, including living-related liver transplantation (LRLT). OBJECTIVE: To present the first 20 cases of adult LRLT in a single center in Saudi Arabia. METHODS: From November 2000 to May 2004, we performed 20 cases of LRLT. Eighteen donors were men and 2 were women. Their median age was 27 years. Seventeen of the recipients were men and 3 were women of median age 55 years. One patient received combined liver and kidney grafts. RESULTS: All cases had liver cirrhosis. Seven had hepatitis C; six, hepatitis B and C; three, hepatitis B; one, alcoholic cirrhosis; one, Bylar disease, one hepatic schistosomiasis, and one cryptogenic cirrhosis. Three cases had associated hepatocellular carcinomas. There was no donor mortality. In the recipients, the overall patient and graft survival was 85%. While 10 donors presented uneventful postoperative courses, 8 experienced minor complications and 2, major complications: biliary stricture and portal vein thrombosis. Recipients complications included biliary complications (35%), acute rejection (20%), hepatitis C reactivation (20%), hepatic vein stenosis (10%), hepatic artery stenosis (5%), and hepatocellular carcinoma recurrence (5%). CONCLUSIONS: LRLT has become a standard option in adults with end-stage liver failure in our center.

Adult↗

PubMed1983

Mesenteric vein thrombosis and vascular plasminogen activator.

A 60-year-old woman with livedo reticularis was examined for defective release of vascular plasminogen activator by a newly described chromogenic assay. Her activator level was only 0.007 Committee on Thrombolytic Agents (CTA) units/mL, compared with a mean of 0.19 CTA units/mL for 84 female controls. Subsequently, the patient died as a result of thrombosis of the portal, splenic, hepatic and superior mesenteric veins with small-bowel infarction. The patient's family had a history of deep and superficial vein thrombosis. Her family's medical history was similar to a recently described pedigree, with low levels of releasable plasminogen activator associated with venous thrombosis. We believe that mesenteric vein thrombosis is a serious potential consequence of defective release of vascular plasminogen activator.

Female↗

PubMedDate not supplied

Doppler measurement of hepatic arterial flow in dogs: technique and preliminary findings.

The common hepatic artery in 10 healthy adult beagles, 20 healthy pups (13 Deerhounds and seven Irish Wolfhounds), and seven dogs with either a congenital or acquired hepatic disorder was examined by duplex-Doppler ultrasonography. Peak systolic velocity (Vs), resistive index (RI), pulse rate, angle of insonation, and sample volume depth were recorded. Measurements in Beagles were made after a 24 h fast and repeated 2 h after feeding. The mean Vs and RI in fasted Beagles were 1.5 m/s (range 1.1-2.3 m/s) and 0.68 (range 0.62-0.74), respectively. Postprandially, there were no significant differences in any of these variables. Mean Vs and RI were lower in pups: 1.0 m/s (range 0.8-1.3 m/s) and 0.59 (range 0.46-0.65), respectively (P < .001). Two dogs with congenital arterioportal fistula had higher mean Vs (P < .001) and lower mean RI (P < .05) than normal pups. No significant differences were detected between normal Beagles, three dogs with portal vein thrombosis, and two dogs with acquired hepatic insufficiency. Differences in measured hepatic blood flow in dogs of different age or breed will complicate diagnostic use of hepatic arterial Doppler measurements.

Animals↗

PubMed1995

Impact of magnetic resonance imaging on the diagnosis of abdominal complications of paroxysmal nocturnal hemoglobinuria.

Magnetic resonance (MR) imaging is a method of choice for assessing vascular patency and parenchymal iron overload. During the course of paroxysmal nocturnal hemoglobinuria (PNH), it is clinically relevant to differentiate abdominal vein thrombosis from hemolytic attacks. Furthermore, the study of the parenchymal MR signal intensity adds informations about the iron storage in kidneys, liver, and spleen. Twelve PNH patients had 14 MR examinations of the abdomen with spin-echo T1- and T2-weighted images and flow-sensitive gradient echo images. Vessels patency and parenchymal signal abnormalities--either focal or diffuse--were assessed. MR imaging showed acute complications including hepatic vein obstruction in five patients, portal vein thrombosis in two patients, splenic infarct in one patient. In one patient treated with androgens, hepatocellular adenomas were shown. Parenchymal iron overload was present in the renal cortex of eleven patients with previous hemolytic attacks. On the first MR study of the remaining patient with an acute abdominal pain showing PNH, no iron overload was present in the renal cortex. Follow-up MR imaging showed the onset of renal cortex iron overload related to multiple hemolytic attacks. Despite the fact that all our patients were transfused, normal signal intensity of both liver and spleen was observed in three of them. MR imaging is particularly helpful for the diagnosis of abdominal complications of PNH.

Abdominal Pain↗