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PubMedDate not supplied

MRI of Budd-Chiari syndrome.

A retrospective study was undertaken to reassess the various magnetic resonance imaging (MRI) features of Budd-Chiari syndrome (BCS). MRI examinations of 22 patients with pathologically confirmed BCS were studied. Spin-echo (SE) T1- (TR = 300-450 ms/TE = 12-15 ms), and SE T2-weighted (TR = 1600-2000 ms/TE = 30-60/90-120 ms) MRI images were obtained in all patients. Gradient-recalled-echo (GRE) images (TR = 7-60 ms/TE = 3-19 ms, flip angle = 10-40 degrees) were obtained in 14 patients. MRI showed thrombosis of three or two hepatic veins in 19 (86%) and 3 (14%) patients, respectively. Spontaneous intrahepatic anastomoses was depicted in five (23%) patients. Ascites appeared in 15 patients (68%). Thrombosis or external compression of the inferior vena cava (IVC) by an enlarged caudate lobe was depicted in six (27%) and five (23%) patients, respectively. Prominent azygos and hemiazygos veins were demonstrated in seven (32%) patients (six of whom had thrombosis of the IVC). MRI showed hepatomegaly in all patients and enlarged caudate lobe in 18 (82%) patients. SE T1- and SE T2-weighted MRI images revealed inhomogeneous signal intensity of hepatic parenchyma in 14 (64%) patients. SE T1- and SE T2-weighted MRI images showed homogeneous signal intensity of hepatic parenchyma in eight (36%) patients. Our results demonstrate that BCS displays various features on MRI images, and such information is important for diagnosis.

Adult↗

PubMed1990

[Paroxysmal nocturnal hemoglobinuria].

Paroxysmal nocturnal hemoglobinuria, first described in the late 19th century, is an acquired disorder characterized by hemoglobinemia and hemoglobinuria. The major clinical manifestation of PNH is chronic intravascular hemolysis of various severity. Patients-mostly young adults - may also present with episodes of abdominal or back pain. Common cause of death is thrombosis especially of the hepatic veins. Granulocytopenia and thrombocytopenia may be the initial manifestation of PNH, indicating that the disorder is a primary bone-marrow disease, affecting not only the erythrocytes but also other peripheral blood cells and the haematopoietic stem cell. The course of the disease is variable. Partial complete recovery was described, but also fatal thrombosis. The major phenotypic expression of PNH is an increased susceptibility of the erythrocytes to the lytic action of complement in vitro. The enhanced complement susceptibility is most probably due to membrane defects: two membrane proteins regulating the complement cascade in PNH cells were missing, the decay-accelerating factor, DAF, inhibiting the activation of the lytic complement complex and the C8 binding protein, C8bp, which interferes with the lytic process. Aside from the lack of the complement regulators also other membrane defects have been described (e.g. of acetylcholinesterase or alkaline phosphatase). The proteins as well as DAF and C8bp are linked to the cell membrane via a phosphatidylinositol (PI) anchor, leading to the speculation that the disease results from a deficiency in the post-translational PI anchoring mechanism. The diagnosis of PNH is based on the Hamtest, but will be extended to the quantitation of the above described membrane proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Complement System Proteins↗

PubMed2000

Budd-Chiari syndrome and inferior vena cava thrombosis in a nephrotic child.

We observed Budd-Chiari syndrome in a boy aged 2 years 6 months with nephrotic syndrome due to hepatic vein and inferior vena cava thrombosis, confirmed by Doppler imaging. Normal values of the routine hemostatic parameters proved that they are of little predictive value for the thrombotic state. Immediate heparin infusion was initiated. High doses of heparin up to 59 IU/kg per hour were required for efficient anticoagulation. A remission of the nephrotic syndrome was achieved with vincristine. Oral anticoagulation with a vitamin K antagonist was continued for 6 months. Doppler imaging then indicated full re-establishment of the blood flow through the affected vessels. The clinical and Doppler data in this case are compatible with acute Budd-Chiari syndrome due to incomplete outflow obstruction of the hepatic veins and inferior vena cava. The favorable outcome was due to the immediate heparin infusion and prompt remission of the nephrotic syndrome. Doppler imaging was an important tool for non-invasive diagnosis and follow-up.

Anticoagulants↗

PubMedDate not supplied

Factors influencing survival in hepatocellular carcinoma patients with macroscopic portal vein tumor thrombosis after surgery, with special reference to time dependency: a single-center experience of 381 cases.

BACKGROUND/AIMS: The prognosis ofhepatocellular carcinoma with macroscopic portal vein tumor thrombosis is extremely poor. The risk factors may differ at different postoperative intervals. This study was undertaken to clarify the surgical outcome and time dependency of factors influencing survival in these patients. METHODOLOGY: We analyzed clinicopathological variables of 381 hepatocellular carcinoma patients with macroscopic portal vein tumor thrombosis who underwent hepatic resection. Survival rates were calculated using Kaplan-Meier method. The stratified Cox models were used to identify factors independently influencing short- and long-term survival, respectively. RESULTS: The cumulative 1-, 2-, 3-, 5-, and 10-year survival rates in 381 patients were 47%, 23%, 16%, 12%, 6%, respectively. The 1-, 3-, and 5-year survival rates calculated from time of re-resection were 36%, 14% and 0% in patients undergoing re-resection for intrahepatic recurrence within 2 years after first operation, and 85%, 53% and 32% in those more than 2 years after first operation (P<0.05). Multivariate analysis showed that portal vein infusion chemotherapy, serum alpha-fetoprotein > 20 mg/L and positive surgical margin were significant prognostic factors within 2 years after operation. In contrast, alanine aminotransferase > 80 U/L was the only significant factor beyond 2 years after operation. CONCLUSIONS: The survival of hepatocellular carcinoma patients with macroscopic portal vein tumor thrombosis was poor, but the prognosis of patients who had tumor recurrence more than 2 years after operation was much better than those with tumor recurrence within 2 years. Evaluation of time-dependency of risk factors may have important clinical implication in determining the therapeutic strategy.

Adult↗

PubMed2000

Splenomegaly, hypersplenism and coagulation abnormalities in liver disease.

Splenomegaly is a frequent finding in patients with liver disease. It is usually asymptomatic but may cause hypersplenism. Thrombocytopenia is the most frequent manifestation of hypersplenism and may contribute to portal hypertension related bleeding. A number of therapies are available for treating thrombocytopenia due to hypersplenism including splenectomy, partial splenectomy, partial splenic embolization, TIPS etc. None is entirely satisfactory. Hypersplenism usually improves following liver transplantation. Therapy with cytokines such as thrombopoietin may offer hope for the future. Patients with liver disease also have abnormalities in coagulation. This is not surprising as all coagulation proteins (except for von willebrand factor vWF) and most inhibitors of coagulation are synthesized in the liver. Genetic or acquired abnormalities of coagulation may predispose to thrombosis of the hepatic or portal veins with significant clinical sequelae. An understanding of the mechanisms involved in coagulation and thrombosis is valuable in choosing from the increasing treatment options available. These include clotting factors, haemeostatic drugs and newer therapies such as recombinant factor VIIa. Splenic artery aneurysms are the most common visceral artery aneurysms in man. Rupture is frequently catastrophic. These aneurysms are being increasingly recognized in liver transplant patients and require treatment before or during transplant surgery.

Blood Coagulation Disorders↗

PubMedDate not supplied

[Peroperative echotomography in the surgery of liver tumors].

Intra-operative ultrasonography was performed in 10 patients with apparently single malignant tumours of the liver without invasion of the portal or hepatic veins. Five patients had hepatocellular carcinoma associated with cirrhosis and 5 had a secondary liver cancer. At laparotomy other tumoral lesions in 3 cases, portal vein thrombosis in 2 cases and invasion of the left hepatic vein in 1 case were detected by ultrasonography. In 2 patients deep intra-hepatic tumours less than 2 cm in diameter, which were neither visible nor palpable, were also detected by this method. As a result of the examination, subsegmental resection was carried out in 3 cases and hepatic lobectomy in 2 cases. Intra-operative ultrasonography therefore is a useful method to locate invisible tumours and vascular structures, thus preventing vascular injuries during the operation, facilitating limited tumoral resections and generally improving prognosis in patients operated upon for malignant hepatic tumours.

Adult↗

PubMed1995

Our first 100 consecutive pediatric liver transplants.

Orthotopic liver transplantation (OLT) is nowadays accepted as the best therapy for end-stage liver disease. The difficulties involved are even greater in children than in adults, and it is debatable whether exclusively pediatric programs are warranted. The aim of this paper is to analyze our experience at the Children's Hospital "La Paz", with the first consecutive 100 OLT in children, 61% of whom weighed less than 20 kg. Since 1986, 220 pediatric patients were evaluated as candidates, 100 OLT were performed in 78 patients and 13 died on the waiting list, currently maintained below 15 cases. Indications were: cholestasis (45), metabolic disease (18), fulminant hepatic failure (3), primary liver tumors (2) and cirrhosis (10). Mean age was 66 months (range = 7 to 216) with a mean weight of 21 kg (range = 6 to 60), twenty patients weighed less than 13 kilograms. OLT was performed by standard technique. Reduced or segmental grafts were necessary in 8 instances. Twenty-two patients were retransplanted and 2 received three grafts. Indications for retransplantation were: hepatic artery thrombosis (8), primary nonfunction (4), chronic rejection (7), portal thrombosis (2) and Budd-Chiari recurrence (1). Acute rejection was observed in 52 patients, and eight cases developed a chronic rejection. These episodes were treated with "bolus" of steroids, monoclonal antibodies (OKT-3) and FK-506. Surgical complications included: hepatic artery thrombosis 12%, portal vein thrombosis 3% and biliary fistula or stenosis 13%. The incidence of primary non-function was 7%. Actuarial survival rate at 5 years was 75%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1987

Hepatocellular carcinoma growing in the pulmonary arteries, complicated with venous thrombosis.

A case of hepatocellular carcinoma (HCC) complicated with vascular invasion of the portal vein, hepatic vein, and pulmonary artery, accompanied by inferior vena caval and renal vein thrombosis, is reported. The patient was a 38-year-old female, positive in serum HBsAg and anti-HBe. Because portal trunk thrombosis was pointed out at the first diagnosis, incomplete transcatheter hepatic arterial embolization was carried out three times and one-shot therapy of anti-cancer agent given once. Four months after the first therapy, the patient died of oliguria and hypotension of sudden onset. The autopsy revealed not only intrahepatic vascular invasion but also tumor growth in the bilateral pulmonary arteries and thrombosis from the inferior vena cava to both renal veins unaccompanied by right atrial growth. Because the renal vein was thrombosed and HCC was accompanied by vascular invasion, especially pulmonary arterial invasion, the patient was thought to have become oliguric and hypotensive before severe hepatic failure. The metastatic tumor had grown in the pulmonary trunk without intra-atrial expansion because of the histological tight junction between the tumor and the wall of that vessel.

Adult↗

PubMed2003

The effects of desflurane and propofol on portosystemic pressure in patients with portal hypertension.

UNLABELLED: Physicians perform hepatic venous pressure measurements to guide medical therapy aimed at reducing portal hypertension. These measurements are frequently performed during general anesthesia. Since most general anesthetic drugs reduce liver blood flow, it is likely that hepatic venous pressures will be altered. We therefore examined the effects of two frequently used anesthetic drugs on hepatic venous pressure in a prospective randomized study to determine if pressure measurements taken during general anesthesia were similar to awake values. We studied 21 patients with hepatitis C, excluding patients with hepatofugal flow and portal vein thrombosis. All patients had free and wedged hepatic venous pressures measured awake with sedation and after anesthesia with either propofol or desflurane. Desflurane significantly increased free hepatic venous pressure (11.9 +/- 4.4 to 23.5 +/- 4.1 mm Hg; P < 0.05) and decreased hepatic venous pressure gradient (21.6 +/- 7.4 to 14.7 +/- 5.2 mm Hg; P < 0.05), whereas propofol did not change these variables. We conclude that desflurane, but not propofol, alters hepatic venous pressure measurements from the awake state, significantly increasing free hepatic venous pressure and decreasing the hepatic venous pressure gradient, an indirect measure of portosystemic pressure. Changes in the hepatic venous pressure gradient must be interpreted with caution during desflurane general anesthesia. IMPLICATIONS: Desflurane reduces the blood pressure difference between the portal and systemic circulations. This can cause errors in assessment of the success of medical therapy of portal hypertension. Propofol has less effect on the difference between the portal and systemic circulation.

Adult↗

PubMed1991

The Sugiura procedure for patients with hemorrhagic portal hypertension secondary to extrahepatic portal vein thrombosis.

The Sugiura procedure (SP) was performed upon 27 patients with hemorrhagic portal hypertension secondary to extrahepatic portal vein thrombosis (EPVT) without associated hepatic disease. There were 14 female and 13 male patients. The mean age was 28 +/- 14 years. The causes of EPVT were protein C deficiency in two; antithrombin III deficiency in one patient, a history of omphalitis in two patients, a history of pancreatitis in one patient and idiopathy in 21 patients. The SP was completed in two surgical stages in 14 patients and in one stage in nine. There was one operative death. One patient had mild postoperative encephalopathy, and two patients rebled at long term follow-up study. Actuarial survival rate was 82 per cent at five and ten years. It is concluded that the SP is a good alternative for the management of hemorrhagic portal hypertension secondary to EPVT.

Actuarial Analysis↗

PubMed1997

Liver transplantation for extra hepatic biliary atresia.

Kasai portoenterostomy has transformed the prognosis for children with Extra Hepatic Biliary Atresia (EHBA). However, for children developing end stage liver disease following portoenterostomy, liver transplantation (OLT) is the treatment of choice. Between February 1989 and March 1996, 64 children with EHBA underwent 79 transplants (26 males, 38 females; median age 2.2 years, range 5 months-17 years; median weight 11.4 kg, range 5-65 kg). Of these, 58 (85%) had undergone previous portoenterostomy. Nineteen patients (30%) had gastrointestinal bleeding prior to OLT assessment. Mean serum bilirubin was 229 mumol/liter (range 11-801 muml/liter). Four children had associated polysplenia syndrome. Of the 79 transplants, 30 received whole and 41 reduced-size cadaveric grafts and 9 living related grafts. Eleven patients (17%) died, nine within one month of surgery. Thirteen patients were retransplanted once and one twice. There were 16 vascular complications (10 hepatic artery thrombosis, 3 portal vein thrombosis, 3 venous outflow obstruction) and 10 biliary complications (4 anastomotic leaks, 6 strictures). Ten patients (16%) had bowel perforation following the transplant. The 5 year actuarial patient and graft survival for this group is 84% and 69% respectively with normal physical and mental development in the majority. OLT provides satisfactory treatment for children with EHBA with end stage liver disease with long term survival in the majority.

Adolescent↗

PubMed2000

Focal nodular hyperplasia of the liver: direct evidence of circulatory disturbances.

Focal nodular hyperplasia of the liver is a lesion characterized by a well-circumscribed region of hyperplastic liver parenchyma and contains a stellate fibrous scar. The lesion is thought to be because of liver-cell hyperplasia that is caused by focal circulatory disturbances. We describe here a pediatric case of this lesion that provided direct histopathologic evidence of circulatory disturbances. We identified arterial and portal thrombi, as well as recanalization of arteries in the nodule. Hepatic necrosis was also seen in the lesion. We speculate that thrombosis of the hepatic artery and/or portal vein was the cause of hepatic necrosis and that reperfusion following hepatic arterial recanalization resulted in nodule formation. Although there was no stellate scar present in our case, the presence of bile ductular proliferation at the periphery of the nodule was helpful in distinguishing this lesion from adenoma and hepatocellular carcinoma. The early stage of nodular formation may explain the lack of a stellate scar in our case. The patient was treated earlier with actinomycin D and vincristine following surgical excision of Wilms' tumor. It is possible that such chemotherapy contributed to thrombosis in our case.

Antineoplastic Agents↗

PubMed2006

[A case of infiltrative hepatocellular carcinoma with main portal vein tumor thrombosis successfully treated by transarterial chemoembolization].

A 63-year-old HBsAg-positive male patient was admitted for the evaluation of a liver mass that was detected on ultrasonography. Spiral computed tomography (CT) revealed infiltrative hepatocellular carcinoma (HCC) in the right hepatic lobe with main portal vein tumor thrombosis. His liver function was Child-Pugh class A and the serum alpha fetoprotein level was 7,400 ng/mL. Transarterial chemoembolization (TACE) via the right hepatic artery was performed. Following 3 sessions of TACE every 2 months, spiral CT revealed no evidence of viable tumor. The thrombi within the main portal vein disappeared with performing localized hepatic infarction at the site of the previous tumor. He is still alive 15 months after the third TACE without evidence of recurred tumor and his liver function remains well preserved. This case suggests that TACE might be effective and safe even in the patients with infiltrative HCC with main portal vein tumor thrombosis, if the extent of the tumor is limited and the liver function and portal flow via the collaterals are preserved.

Carcinoma, Hepatocellular↗

PubMed1999

Living related liver transplantation for acute liver failure in children.

The mortality rate among children with acute liver failure (ALF) on the waiting list for liver transplantation is high. We present our experience with living related donor liver transplantation (LRD-LT) in children who required urgent transplantation for ALF. Between December 1995 and July 1997, 6 children underwent LRD-LT for ALF. Cause of liver failure, recipient and donor demographics, clinical and laboratory data, surgical details, complications, and 6-month and 2-year graft and patient survival were recorded. Five boys and 1 girl received left lateral segment grafts from their parents. The mean age was 4 +/- 2.8 years (range, 1 to 9 years). ALF was caused by Wilson's disease in 1 patient and sickle cell intrahepatic cholestasis syndrome in 1 patient; in 4 patients, the cause was unknown. All patients had mental status changes; 2 were on life support. Mean pretransplantation liver function test values were: alanine aminotransferase, 972 +/- 565 U/L (normal, 1 to 53 U/L), total bilirubin, 31.3 +/- 12.4 mg/dL (normal, 0.1 to 1.2 mg/dL), prothrombin time, 34.3 +/- 12.4 seconds (normal, 10.8 to 13.3 seconds), international normalized ratio, 8.46 +/- 5.4 (normal < 2), and fibrinogen, 109 +/- 23.9 mg/dL (normal, 175 to 400 mg/dL). The donors were 5 mothers and 1 father. The mean donor age was 32.5 +/- 7.6 years (range, 19 to 40 years). No donor required blood transfusion, and no donor had any early or late postoperative complications. The donors' mean hospital length of stay was 5 days. In five cases, grafts were blood group-compatible; 1 child received a blood group-incompatible graft. All grafts functioned immediately. No patient had hepatic artery or portal vein thrombosis or biliary complications. The child who received a mismatched graft died of infection of the brain caused by Aspergillus spp at 22 days posttransplantation with a functioning graft. The child with ALF caused by sickle cell intrahepatic cholestasis syndrome developed outflow obstruction 3 months posttransplantation and required retransplantation; he eventually died of vascular complications related to his primary disease. Four children are alive at a mean follow-up of 27 months (range, 14 to 36 months). LRD-LT for children with ALF facilitates timely transplantation without drawing on cadaveric donor resources. The established safety record of LRD-LT made this option appealing to both physicians and parental donors.

Adult↗

PubMed1992

Polycythemia vera.

Polycythemia vera (PV) is one of the myeloproliferative diseases, and, as such, is an example of clonal hematopoiesis. The progeny of a single, abnormal, hematopoietic stem cell gain a growth advantage over their normal counterparts resulting in overproduction of red cells generally accompanied by overproduction of granulocytes and platelets as well. There are a variety of nonspecific symptoms at onset related to the increased red cell mass and hematocrit accompanied by the more specific manifestations of pruritus, erythromelalgia, and hepatic, portal, and mesenteric vein thrombosis. Splenomegaly and hypertension are common. The laboratory hallmark is an increased red cell mass. There is also often an increase in white cell count, platelet count, and leukocyte alkaline phosphatase along with other findings reflecting the increased rate of turnover of hematopoietic cells. The bone marrow biopsy generally displays hypercellularity involving all three cell lines and absent iron stores. The diagnosis of PV depends on excluding spurious polycythemia in which there is a high hematocrit but a normal red cell mass and secondary polycythemia in which there is an increased red cell mass in response to tissue hypoxia or the inappropriate production of erythropoietin, generally by a tumor. In addition, one should try to establish the diagnosis in a positive fashion by a combination of studies of the blood and bone marrow. Phlebotomy and occasionally plateletpheresis should be used as acute therapy. Chronic therapy is guided by the knowledge that patients treated with phlebotomy alone have an increased rate of thrombotic complications particularly in older patients and those with previous thrombotic disease. Myelosuppressive therapy can reduce the incidence of these complications, but is commonly associated with an increased incidence of second malignancies, particularly acute leukemia. At present, hydroxyurea is the myelosuppressive agent of choice. Antiplatelet agents have a limited role except in the palliation of the syndrome of erythromelalgia. Median survival is approximately 10 years. As implied above, the causes of morbidity and mortality vary with the mode of chronic therapy which has been employed, leukemia being more common after myelosuppressive therapy and thrombotic complications being more common after therapy with phlebotomy alone. Ten percent to 50% of patients move into a spent phase followed by postpolycythemic myeloid metaplasia, irrespective of previous therapy employed. Eventually, the major problems may be cytopenias and massive splenomegaly.

Humans↗

PubMed2006

Diagnosis and management of allograft failure.

The article focuses on diagnosis and management of allograft failure in four main categories: (1) ischemic-reperfusion injury (primary nonfunction), (2) technical complications (hepatic artery and portal vein thrombosis), (3) chronic rejection, and (4) recurrent disease. It also discusses the complex problems involved in retransplantation for allograft failure.

Graft Rejection↗

PubMed2003

Outcome of pediatric live-donor liver transplantation-the Toronto experience.

BACKGROUND/PURPOSE: Live-donor liver transplantation (LDLT) has developed to address the critical shortage of cadaveric organs that accounts for 20% of children who die while awaiting for a liver transplant in Ontario each year. This report reviews the outcome of the pediatric recipients of LDLT at the authors' center. METHODS: The charts of all children who received a LDLT between June 1996 and March 2002 were reviewed retrospectively. RESULTS: Thirteen children (mean age, 3.6 years) underwent LDLT. All donors were parents except for one cousin. Ten grafts were left-lateral segments, 2 were right lobes, and 1 was a left lobe. Three patients required a SILASTIC((R)) (Dow Corning, Midland, MI) patch for delayed abdominal wall closure. Patient and graft survival rate was 100% with a median follow-up of 376 days. Major postoperative complications included biliary leaks (n = 2), biliary strictures (n = 1), portal vein thrombosis (n = 1), and hepatic venous complications (n = 1). There were no cases of hepatic artery thrombosis. Ten of 12 children became Positive for Epstein-Barr virus (EBV), and 3 of these patients had readily treatable post-transplant lymphoproliferative disorder. CONCLUSIONS: LDLT is an acceptable alternative to cadaveric transplantation for children with end-stage liver disease.

Adolescent↗

PubMed1996

Management of esophageal varices in children by endoscopic variceal ligation.

Endoscopic variceal sclerotherapy (EVS) has been considered the mainstay of therapy for bleeding esophageal varices in adults. However, recent data have shown that endoscopic variceal ligation (EVL) is just as efficacious and has fewer complications than EVS. Although there are many reports concerning EVL in adults, only a few studies have been done in children. This report describes experience with EVL in 22 children with esophageal variceal hemorrhage. Eighty-seven EVL procedures were performed during a 9-year period in 22 children. The causes of portal hypertension were biliary atresia (10), portal vein thrombosis (8), chronic active hepatitis (1), cirrhosis secondary to cystic fibrosis (2), and primary sclerosing cholangitis (1). The age range at the onset of variceal bleeding was 8 months to 19 years. Twelve patients had EVS before EVL treatment was begun. Distal esophageal varices (one to four per session) were mechanically ligated using an elastic band ligature device attached to a flexible endoscope. The aim of therapy was obliteration of distal esophageal varices by EVL, every 2 to 4 weeks, until eradication. Subsequent EVL was dictated by the status of the varices. Outcome was assessed with respect to survival, rebleeding, status of varices, and complications. The patients underwent a mean of four sessions of EVL (range, one to eight). Four patients subsequently underwent liver transplantation. Of the 18 patients remaining (average follow-up period, 5.3 years), 12 had their varices eradicated (average of four EVL sessions), four are still in treatment, one has not been evaluated in the past 4 years, and one died of liver failure. Complications included bleeding between sessions (6 patients), cervical esophageal perforation (1 patient), and transient fever (2 patients). No child has experienced symptoms of esophageal stenosis or gastroesophageal reflux. Two patients died of liver disease, unrelated to bleeding from portal hypertension. EVL is effective in controlling variceal hemorrhage in children with portal hypertension, regardless of etiology. The complication rate is low, and EVL is an acceptable and perhaps preferable alternative to EVS in children with esophageal varices.

Adolescent↗