• Journal of Chest Surgery
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• v.5 no.2
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• pp.107-112
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• 1972

Recently we experienced a case of the portal hypertension, extrahepatlc origin in the National Medical Center, Seoul. The case was a male aged 19 who was undergone the elective splenorenal shunt with splenectomy 9 years ago and emergency ligation of the coronary vein because of recurred variceal rupture 6 years later and had recurring esophageal varices with bleeding this time.At the age of 10 he had been occasionally suffering from nasal bleeding and visited to our Pediatric department, when there was encountered for the first time the splenomegaly, esophageal varices in the lower third esophagus on the esophagogram, and stenosis and kinking of the portal vein with rich collateral circulation on the splenoportography without hepatic functional impairment.The elective splenorenal shunt with splenectomy was undergone under the diagnosis of portal hypertension due to congenital anomaly of the portal vein and postoperatlvely no troubles had been obtained until postoperative 1st attack of massive hematemesis due to esophagenl variceal rupture recurred about 6 years later which was confirmed by control esophagogram and it was resulted by stenosis of previous anastomotic site of the splenorenal shunt.Then emergency ligation of the coronary vein was only made for bleeding control and no episodes of hematemesis had been encountered thereafter until April 1972 about 3 years after the 2nd operation, when hematemesis recurred again. In this time, recurring esophageal varices were noted in the lower third esophagus on the control esophagogram and he was employed side to end mesocaval shunt as the final step of portal decompression,and following results were obtained. 1] No postoperatlve troubles as leg edema or pain: Postoperatively leg elevation and elastic bandage on the both legs were employed until discharge. 2] During operation the portal pressure was 300 mm $H_2O$ and immediately lowered to 170 mm $H_2O$ after shunt.

• Korean Journal of Radiology
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• v.23 no.1
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• pp.68-76
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• 2022

Objective: Percutaneous portal vein (PV) stent placement can be an effective treatment for symptoms associated with portal hypertension. This study aimed to evaluate the effect of PV stenting on the overall survival (OS) in patients with malignant PV stenosis. Materials and Methods: Two groups of patients with malignant PV stenosis were compared in this retrospective study involving two institutions. A total of 197 patients who underwent PV stenting between November 2016 and August 2019 were established as the stent group, whereas 29 patients with PV stenosis who were treated conservatively between July 2013 and October 2016 constituted the no-stent group. OS was compared between the two groups before and after propensity score matching (PSM). Risk factors associated with OS were evaluated using the Cox proportional hazards model. Procedure-associated adverse events were also evaluated. Results: The stent group finally included 100 patients (median age, 65 [interquartile range, 58-71] years; 64 male). The no-stent group included 22 patients (69 [61-75] years, 13 male). Stent placement was successful in 95% of attempted cases, and the 1- and 2-year stent occlusion-free survival rate was 56% (95% confidence interval, 45%-69%) and 44% (32%-60%), respectively. The median stent occlusion-free survival time was 176 (interquartile range, 70-440) days. OS was significantly longer in the stent group than in the no-stent group (median 294 vs. 87 days, p < 0.001 before PSM, p = 0.011 after PSM). The 1- and 3-year OS rates before PSM were 40% and 11%, respectively, in the stent group. The 1-year OS rate after PSM was 32% and 5% in the stent and no-stent groups, respectively. Anemia requiring transfusion (n = 2) and acute thrombosis necessitating re-stenting (n = 1) occurred in three patients in the stent group within 1 week. Conclusion: Percutaneous placement of a PV stent may be effective in improving OS in patients with malignant PV stenosis.

• Journal of Chest Surgery
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• v.27 no.8
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• pp.710-713
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• 1994

The Budd-Chiari syndrome is a rare type of portal hypertension caused by complete or incomplete obstruction of the hepatic vein or the corresponding portion of the inferior vena cava or both. In this case, the obstruction was located just beneath the diaphragm, above the right hepatic vein opening, which was confirmed by vena cavography preoperatively. Budd-Chiari syndrome with stenosis or thrombosis of the inferior vena cava may be cured by prosthetic bypass to the right atrium. This case is caused by thrombus of unknowed primary origin. Combined mesoatrial and cavoatrial shunt should be encouraged in this specific situation. Postoperatively, there were marked fall of venous pressure and symptoms and signs improved remarkably.

• Journal of Chest Surgery
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• v.18 no.4
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• pp.673-678
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• 1985

A 21 year-old male patient had a diagnosis of Budd-Chiari syndrome caused by inferior vena caval obstruction. Conservative medical therapy failed to control the symptoms of both portal hypertension and inferior vena caval stasis. Portocaval or mesocaval shunts may relive the symptoms of chronic forms of Budd-Chiari syndrome. But when inferior vena caval stenosis is severe, another procedure has to be used. Cavoatrial or portoatrial shunt has been suggested. Therefore, a long Dacron graft was placed from the inferior vena cava just below the left renal vein to the right atrium. He exhibited almost complete relief of symptoms for 1.5 year postoperatively. And there was angiographic proof of patency of the graft. This simple procedure should be encouraged in treatment of these patients.

• The Korean Journal of Pharmacology
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• v.24 no.1
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• pp.63-70
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• 1988

Alterations in splanchnic circulatory hemodynamics along with reactivities to the alpha adrenoceptor agonists were assessed in association with the preventive effects of propranolol 10 days after portal ligation. Decreases in precapillary resistance (Ra) and postcapillary resistance (Rv) along with increases in mesenteric blood flow (MBF) and capillary pressure (CP) were observed in conjunction with an increment of splenic pulp pressure (SPP). Dose-dependent increase in Rv in response to noradrenaline, increases in Ra and RV to adrenaline, and increases in superior mesenteric arterial pressure (SMAP), Ra and Rv to phenylephrine observed in sham group were significantly attenuated by portal vein stenosis. In PPL-3 group (propranolol 3 mg/kg, i.p. three times daily for 10 days), MBF was significantly decreased in association with decrease in mesenteric venous pressure (MVP) when compared with those of protal ligated (PL) group, and decreased Ra and Rv in PL group were recovered toward the values of sham group. Likewise, in PPL-1 group (propranolol 5 mg/kg, i.p. once daily for 10 days), the pressor response of Rv to adrenaline was recovered up to the level of sham group. Thus, it is suggested that decreases in Ra and Rv in association with increases in MBF and CP may have a close relevance to the increased SPP, and the changes in circulatory hemodynamics and vascular reactivities were effectively reversed by longterm propranolol treatment. Based on these results, it is concluded that these changes observed in portal hypertension are closely related with the altered functions of the adrenoceptors in the splanchnic vascular beds.