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1/18. Massive esophageal variceal hemorrhage triggered by complicated endotracheal intubation.

    Esophageal variceal hemorrhage is frequently a catastrophic event. The specific events that trigger variceal rupture are not well understood. Acute elevations in systemic blood pressure and increased splanchnic blood flow, however, may lead to increased intravariceal pressure followed by variceal rupture and hemorrhage. This report describes a strong temporal association between complicated endotracheal intubation and abrupt onset of life-threatening variceal hemorrhage. A 52-year-old man with a history of portal hypertension was intubated emergently for airway protection because of respiratory insufficiency due to sepsis. intubation was complicated by initial inadvertent esophageal intubation and by a peak mean arterial blood pressure of 155 mmHg. At the conclusion of the procedure, the patient sustained large volume hematemesis due to esophageal variceal rupture. This case suggests a risk of triggering variceal hemorrhage as a result of intubation-induced increase in blood pressure. A number of agents, including fentanyl, have been shown to be effective in attenuating the cardiovascular response to intubation. This case report provides strong evidence in support of administering fentanyl, or a suitable alternative adjunctive medication, before intubation of patients with documented portal hypertension and a history of esophageal variceal hemorrhage.
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2/18. Severe fatty change of the graft liver caused by a portosystemic shunt of mesenteric varices.

    Portosystemic shunt is a common complication in patients with portal hypertension. Mesenteric varix is one of the collaterals that can cause post-transplant liver dysfunction. In this case report, a 45-year-old woman underwent living relative donor liver transplantation for alcoholic cirrhosis. Although the early postoperative course was uneventful, she was readmitted for treatment of liver hypofunction. Fatty change in the graft liver was confirmed by histopathology of the biopsy specimen. The venous phase of a superior mesenteric angiogram revealed large-caliber mesenteric varices comprising portosystemic venous shunts. Surgery was performed to ligate the shunts. The intraoperative color Doppler ultrasonography showed hepatofugal portal blood flow, which was corrected to hepatopetal blood flow by clamping the shunt vessels. The portal pressure was moderately elevated from 13.6 cm to 21.8 cm H(2)O. Two shunt vessels were ligated and divided. Her liver function returned to nearly normal thereafter. We recommend that descending collaterals be divided during liver transplantation.
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3/18. Mesoatrial shunt: a new treatment for the budd-chiari syndrome.

    A patient is presented with the budd-chiari syndrome. Because of a thrombosed inferior vena cava, none of the standard portal-systemic shunts could be utilized for decompression of the engorged liver. A new shunt constructed by interposing a Dacron graft between the superior mesenteric vein and the right atrium was performed. portal pressure was reduced by the shunt from 30 cm of H2O to 10 cm of H2O. Patency has been confirmed post-operatively by catheterization and with angiography. The patient is asymptomatic with normal liver function tests nine months following the procedure. A surgical approach is outlined for symptomatic patients with the Budd-Chairi Syndrom.
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4/18. Combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration for complicated gastroesophageal varices.

    The treatment of complicated gastroesophageal varices with a gastrorenal shunt and portal hypertensive gastropathy has not yet been established. We were able to control a case of complicated large gastroesophageal varices with gastrorenal shunt and portal hypertensive gastropathy using a combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration. We first applied partial splenic embolization to reduce the hyperdynamic cycle of portal hypertension and to treat thrombocytopenia. We secondarily applied endoscopic embolization for the esophageal varices. Transjugular retrograde obliteration was performed for the gastric varices 14 days after endoscopic embolization. The wedged hepatic venous pressure had not changed after transjugular retrograde obliteration. After the combination treatment, the gastroesophageal varices were successfully obliterated, but portal hypertensive gastropathy did not worsen. The platelets count, arterial ketone body ratio and ICGR15 were improved. Partial splenic embolization was useful to protect side effects of endoscopic embolization and transjugular retrograde obliteration. We conclude that the combination treatment of partial splenic embolization, endoscopic embolization and transjugular retrograde obliteration is a rational, effective and safe treatment for complicated gastroesophageal varices with gastrorenal shunt and portal hypertensive gastropathy.
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5/18. Transjugular intrahepatic portacaval stent shunt as a rescue treatment for life-threatening variceal bleeding in a cirrhotic patient with severe liver failure.

    Variceal bleeding in cirrhotic patients with severe liver failure that is not controllable by endoscopic sclerotherapy is a life-threatening situation. We report the case of a patient with decompensated cirrhosis (Pugh class C) who bled repeatedly from gastric varices despite multiple sessions of sclerotherapy. The portal vein was catheterized by a transjugular approach. A tract between a hepatic vein and the portal vein was created after balloon dilatation, and this opening was stented with an expandable stainless steel Palmaz stent. The portal vein pressure decreased from 35 mm Hg to 19 mm Hg after shunting. Gastric varices also were embolized. Two months later, bleeding had not recurred; the shunt remained opened and the marked decrease in portal pressure still persisted. endoscopy showed the disappearance of gastric varices. This procedures could become a life-saving therapeutic option for such critically ill cirrhotic patients.
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6/18. Use of a mixed endothelin receptor antagonist in portopulmonary hypertension: a safe and effective therapy?

    BACKGROUND & AIMS: Portopulmonary hypertension (PPHTN), a severe complication of portal hypertension is observed in 3%-6% of patients evaluated for liver transplantation. endothelin-1, a potent vasoconstrictor, is likely to play a role in the pathogenesis of primary pulmonary hypertension, and, in 2 recent trials, the dual endothelin receptor antagonist bosentan has shown beneficial effects in this disease. A role for endothelins in the development of both pulmonary hypertension and cirrhosis has been suggested. We therefore hypothesized that endothelin receptor blockade may be beneficial in the treatment of PPHTN. methods: We report a case of a 42-year-old patient with PPHTN and alcoholic cirrhosis treated with the mixed endothelin receptor antagonist bosentan. RESULTS: The patient rapidly improved from NYHA IV to stage II, experienced a remarkable improvement of 6-minute walking distance from 0 to 590 m within 6 months, and resumed working full-time as a locksmith after 7 months of treatment. Improvement of cardiovascular parameters included a reduction of pulmonary vascular resistance by 60%, a decrease of mean pulmonary artery pressure (mPAP) from 55 to 44 mm Hg at 9 months, and a decline of plasma B-type natriuretic peptide (BNP) from 339 pg/mL to 19 pg/mL after 1 year. There were no adverse events except for a transient decrease in systemic blood pressure. CONCLUSIONS: To our knowledge, this is the first report of a patient with PPHTN treated with an endothelin receptor antagonist. The marked and sustained improvement supports the undertaking of controlled studies of the safety and efficacy of bosentan in PPHTN.
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7/18. The role of continued drinking in loss of portal perfusion after distal splenorenal shunt.

    Fifty percent of patients with alcoholic cirrhosis who undergo distal splenorenal shunting for variceal bleeding lose portal perfusion within 1 year. Although it was previously considered that this loss of portal flow was irrevocable, the present study shows that with resolution of alcoholic hepatitis, portal perfusion can be restored. A 34-year-old patient with alcoholic liver disease and a distal splenorenal shunt lost portal perfusion 1 year after the operation. He had continued to drink alcohol and had high sinusoidal pressure. Following forced abstinence over the next 2 years, his sinusoidal pressure fell, liver volume decreased, results of liver biopsy improved, and portal perfusion was restored. Shunt patency was documented, and the same collaterals from the portal vein to the shunt could still be visualized as had been seen when portal flow was absent. Restoration of portal perfusion was attributed to decreased intrahepatic resistance secondary to abstinence from alcohol. A return to drinking in the next 9 months led to alcoholic hepatitis and once again loss of portal perfusion. This study places emphasis on increased intrahepatic resistance rather than the development of portal-to-shunt collaterals as important in the loss of portal flow in such patients.
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8/18. Excess vitamin a injures the liver.

    Chronic vitamin a intoxication in a 56-year-old female is reported. Some abnormal blood chemistries included elevated transaminase and alkaline phosphatase, increased cerebrospinal fluid and portal pressure, and elevated vitamin a in blood and liver. A liver biopsy indicated histologic evidence of perisinusoidal collagen deposition and noncoalescent fat droplets in Ito cells. Caution against the misdiagnosis of alcoholic cirrhosis for vitamin a intoxication is recommended.
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9/18. Massive colonic variceal bleeding secondary to abnormal splenocolic collaterals: report of a case.

    Even in the absence of demonstrable esophagogastric varices in the cirrhotic patient, a diagnosis of variceal bleeding from unusual sites should be entertained in the differential diagnosis of massive lower gastrointestinal hemorrhage. The varices may reflect the increased pressure in the superior or inferior mesenteric systems or in the splenic system through abnormal splenocolic anastomoses. This case has the unique feature of bleeding from varices interposed between the splenic and inferior mesenteric venous systems, as opposed to the previously described cases of varices draining directly into a portosystemic conduit.
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10/18. Mesoatrial shunting for portal decompression in alcoholic cirrhosis.

    A 36-year-old Chinese man with alcoholic cirrhosis presented to hospital with exsanguinating variceal hemorrhage. Conventional porta-systemic decompressive operations could not be done because of dense vascular adhesions from two previous operations and a sub-hepatic abcess. A mesenteric-to-right-atrial shunt was done with successful control of hemorrhage and reduction of portal pressure. Long-term follow-up reveals no further bleeding and a return to full-time employment. We conclude that mesoatrial shunting is a useful alternative procedure for portasystemic decompression in alcoholic cirrhosis, although one which will be needed only in unusual circumstances.
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