Cases reported "Hepatic Encephalopathy"

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1/26. hepatic encephalopathy--a physostigmine-reactive central anticholinergic syndrome?

    This report describes an association between hepatic encephalopathy and central anticholinergic syndrome (CAS). A 60-year-old anaemic woman was admitted unconscious and with a delayed reaction to pain but with no focal neurological deficits. She had signs of portal hypertension and a history of non-alcoholic liver cirrhosis grade child B. Suspecting upper gastro-intestinal bleeding, she was intubated for gastro-duodenoscopy and a fibrin-covered ulcer was revealed. Raised intra-abdominal pressure resulting from ascites caused cardiopulmonary failure, which required mechanical ventilation for 24 h, but extubation was possible after drainage of the ascites and blood volume replacement therapy. However, her neurological state remained unchanged despite normal blood ammonia concentration and no sedation. CAS was considered and physostigmine injected with immediate effect. The patient opened her eyes immediately and was fully orientated to personal and medical history. We suggest that hepatic encephalopathy may trigger CAS, although the significance of physostigmine in the treatment of hepatic encephalopathy remains to be addressed by controlled investigations.
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2/26. Resection of spleno-renal shunt resulting in enhanced liver volume in a patient with congenital portosystemic shunt concomitant with early gastric cancer. review of Japanese cases.

    A 73-year-old man recurring hepatic encephalopathy due to a congenital splenorenal shunt concomitant with early gastric cancer was successfully treated by surgical intervention. The portal pressures before and after the shunt resection were 13.5 and 18 cm H2O, respectively. The liver was slightly atrophic and the histological specimen showed slight fibrosis and mild infiltration of lymphocytes in the portal area. After the operation, the encephalopathy was improved and the several factors of liver function also recovered. Interestingly, the liver volume estimated by abdominal CT clearly increased 1 month after the shunt resection. The encephalopathy in congenital portosystemic shunt might result from chronic liver ischemia and atrophy. Moreover, the shunt resection may enlarge the functional liver volume by increasing the portal blood flow.
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3/26. Surgical closure of the gastrorenal shunt with distal splenorenal shunt operation for portosystemic encephalopathy.

    A 67-year-old woman was admitted to our institution for hepatic encephalopathy. Careful examination revealed a large gastrorenal shunt. On an occlusion test of the gastrorenal shunt using a balloon catheter, portal vein pressure increased to as high as 26 cm H2O from the pretest value of 17.5 cm H2O. From the significant increase of portal vein pressure, it was thought that simple closure of the shunt could cause postoperative formation of an esophageal varix and its rupture. We thus performed shunt closure with distal splenorenal shunt with splenopancreatic and gastric disconnection to prevent the hazard. In treating the encephalopathy caused by a spontaneous shunt, it is one of the options to perform distal splenorenal shunt with splenopancreatic and gastric disconnection in addition to shunt closure if a remarkable increase of portal vein pressure is observed by the shunt occlusion test.
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4/26. Usefulness of magnetic resonance spectroscopy for diagnosis of hepatic encephalopathy in a patient with relapsing confusional syndrome.

    magnetic resonance spectroscopy allows the assessment of several metabolites in brain tissue. In patients with hepatic encephalopathy, this technique shows a rise in glutamine and a decrease in myoinositol in brain tissue. However, the role of magnetic resonance spectroscopy in the diagnosis of hepatic encephalopathy is not known. We report the case of a patient with a relapsing confusional syndrome who underwent magnetic resonance spectroscopy. Previously, hepatic encephalopathy was ruled out because of the negative results of a transjugular liver biopsy and normal hepatic venous pressure gradient. The results of magnetic resonance were characteristic of hepatic encephalopathy. Abdominal computed tomography demonstrated large portosystemic shunts associated with cirrhosis of the liver. This case shows that magnetic resonance spectroscopy is an useful technique for the diagnosis of hepatic encephalopathy in selected cases, such as those without clinical signs of cirrhosis and/or large portosystemic shunts.
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5/26. hepatic encephalopathy secondary to a large-caliber porto-hepatic venous shunt. A case report.

    A case of hepatic encephalopathy secondary to a large-caliber porto-hepatic venous shunt in a 61-year-old woman with gastric cancer is reported. Mild confusion, flapping tremor and hyperammonemia were noted preoperatively. Abdominal ultrasonography showed a large-caliber porto-hepatic venous shunt in the left lateral segment of the liver. Percutaneous transhepatic portography and superior mesenteric angiography were confirmatory. Intraoperative portal scintigraphy was performed before and after temporary shunt occlusion to measure the intrahepatic shunt rate, which decreased markedly after occlusion. portal pressure was also measured, and increased only slightly after occlusion. Left lateral hepatic segmentectomy, and subtotal gastrectomy with splenectomy were performed. hepatic encephalopathy resolved postoperatively. The shunt was thought to be acquired. The relevant reports on large-caliber porto-hepatic venous shunts in the literature are reviewed.
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6/26. Obliteration of portal systemic shunts as therapy for hepatic encephalopathy in patients with non-cirrhotic portal hypertension.

    The effects of obliteration of portal systemic shunts (PSS) in 5 patients with non-cirrhotic hepatic encephalopathy is reported. All patients had a history of disturbance of consciousness for several years, and examinations revealed large PSS, most of which connecting the left gastric vein to the left renal vein. After the obliteration of PSS, portal vein pressure elevated, the shunt ratio of the portal blood flow decreased, the indocyanine green disappearance rate increased, and serum albumin increased. Blood ammonia (NH3) decreased significantly accompanied by disappearance of hepatic encephalopathy. This treatment may open a way to improve the quality of life in patients with large PSS without severe hepatic injury.
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7/26. Noncardiogenic pulmonary edema induced by a molecular adsorbent recirculating system: case report.

    Noncardiogenic pulmonary edema is a well-recognized manifestation of acute lung injury which has been related, among others, to blood or blood-product transfusion, intravenous contrast injection, air embolism, and drug ingestion. We describe two cases of noncardiogenic pulmonary edema after use of a molecular adsorbent recirculating system, a cell-free dialysis technique. patients in this series presented at our institution to be evaluated for liver transplantation. Subsequently, they developed an indication for the molecular adsorbent recirculating system. Two patients of 30 (6.6%) treated with the molecular adsorbent recirculating system for acute-on-chronic liver failure and intractable pruritus had normal chest x-rays before treatment and developed severe pulmonary edema, in the absence of cardiogenic causes, following use of the molecular adsorbent recirculating system. For each patient we reviewed the history of blood or blood-product transfusion, echocardiograms if available, daily chest x-rays, and when available pre- and postmolecular adsorbent recirculating systemic blood pressure, central venous pressure, pulmonary arterial pressures, cardiac output, cardiac index, systemic vascular resistance index, and arterial blood gas. Our data suggest that the molecular adsorbent recirculating system may cause noncardiogenic pulmonary edema, possibly by an immune-mediated mechanism.
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8/26. Stage IV hepatic encephalopathy associated with acute blindness after liver transplantation.

    A 5-yr-old boy who diagnosed acute liver failure and Stage IV hepatic encephalopathy underwent living related liver transplantation and awakened with persistent hand motions visual loss. Serum tacrolimus, electrolytes, magnesium levels were normal as well as blood pressure. His neurologic and opthamologic examinations were otherwise normal. Visual evoked potential (VEP) was prolonged and brain magnetic resonance immaging (MRI) revealed bilateral parietooccipital white matter signal abnormalities with gliosis. During follow up his visual loss resolved spontoneously as well as the VEP and MRI abnormalities. In this case we aimed to point out hepatic encephalopathy might be a cause of postoperative visual loss and serial VEP analysis is an important diagnostic tool for monitoring visual function of liver graft recipients in the post-operative period.
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9/26. Intrahepatic portosystemic venous shunt: occurrence in a child patient without liver cirrhosis.

    There are multiple reports of intrahepatic portosystemic venous shunt (PSVS) cases in adult patients. We report the case of a 4-year-old child with PSVS and pulmonary arteriovenous malformation (PAVM). Abdominal sonography and computed tomography (CT) revealed the presence of PSVS. T1-weighted magnetic resonance imaging (MRI) demonstrated multiple intracranial hyperintense lesions, mainly in the globus pallidus, which suggested portosystemic encephalopathy. Tc-99m labeled microsphere study showed diffusely increased uptake in the thyroid and kidneys. The scan suggested the existence of PAVM. Pulmonary angiography was performed in order to evaluate pulmonary hypertension, and pulmonary venous pressure was slightly elevated. Contrast echocardiography suggested the presence of an intrapulmonary arteriovenous malformation with significant right-to-left shunt, as evidenced by rapid filling of the left atrium with dissolved bubbles. In this case, contrast echocardiography was helpful in diagnosing the patient's PAVM. In conclusion, we present the case of PSVS with PAVM in childhood. The incidence of PSVS is low, and data from the literature remain limited. However, further investigation is required to clarify the possible correlation between PSVS and PAVM.
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10/26. Portosplenic blood flow separation in a patient with portosystemic encephalopathy and a spontaneous splenorenal shunt.

    A patient with portosystemic encephalopathy, hyperammonemia, and a spontaneous splenorenal shunt was admitted to the authors' institution after a failed attempt at transvenous retrograde shunt obliteration. As an alternative approach, the authors separated splenic and portal flows by embolizing only the proximal splenic vein while leaving the shunt intact. Thus, the splenic flow could escape into the systemic circulation and an extreme increase in portal pressure was avoided. The procedure could provide rapid decreases in blood ammonia levels and a fast resolution of symptoms, but repeated interventions were required.
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