Glossary portalsystemic encephalopathy - Refers to a condition of mental status changes,ranging from mild confusion to a coma-state resulting from increased ammonia http://liver.bsd.uchicago.edu/html/body_glossary.html
Extractions: Glossary of Terms for Hepatobiliary Diseases ALBUMIN - Main circulating protein in bloodstream synthesized by liver. Measured in blood by laboratory to assess function of liver. ALCOHOLIC HEPATITIS - Hepatitis with unique pathologic liver injury varying widely in severity and caused by chronic, heavy alcohol ingestion. ALKALINE PHOSPHATASE - Enzyme or protein synthesized by the liver in large amounts when there is obstruction of the bile ducts to the normal flow of bile. Measured in blood by laboratory to assess function of liver. ALT (Alanine Aminotransferase) - Enzyme or protein that leaks from the damaged liver. Measured in blood to assess liver injury. ANTI-NUCLEAR ANTIBODY TEST - Laboratory test, when positive suggests the presence of some form of autoimmune illness. ASCITES - Fluid accumulation around the liver and other abdominal organs resulting from portal hypertension. AST (Aspertate Aminotransferase) - Enzyme or protein that leaks from the damaged liver. Measured in blood to assess liver injury. AZATHIOPRINE - Drug marketed with trade name Imuran. Used to treat a number of diseases of unknown or autoimmune cause. Also used to treat organ transplant recipients to help prevent graft rejection.
Best Practice Of Medicine - Evaluated Links 52. portalsystemic encephalopathy - Children's Hospital, Boston Fulminant hepaticfailure - hepatic encephalopathy edema - Extensive review thanks to an http://praxis.md/praxislinks/links.asp?action=specialty&specialty=HP
Extractions: Introduction Impairment of intellectual functions is a classic symptom of portal-systemic encephalopathy in humans. The hippocampal system is important for learning and memory both in humans and animals. Different subcortical neurotransmitter systems participate in the regulation of hippocampal activity and thus play a role in the cognitive process. It has been suggested that endogenous histamine, particularly neuronal histamine in the hippocampus and hypothalamus, may be involved in the process of learning and memory in rats. Long-term portacaval anastomosis in the rat results in dramatic, region-selective changes in the brain histamine system, characterized by a marked increase in the tissue levels and a moderate elevation in the extracellular concentrations of histamine, and an increase in the tissue concentrations of tele -methylhistamine, most evident in the hypothalamus.
ICD-9-CM From Code 570 encephalopathy; Hepatocerebral intoxication; portalsystemic encephalopathy.572.3 Portal hypertension; 572.4 Hepatorenal syndrome Excludes that http://www.cpmc.columbia.edu/homepages/hripcsa/icd9/1tabular570.html
Veröffentlichungen 2001 Elevated serum levels of astroglial S100beta in patients with liver cirrhosisindicate early and subclinical portalsystemic encephalopathy. http://www.gwdg.de/~egogoll/Pub 2000.htm
Extractions: Veröffentlichungen 2000 Ringe B, Braun F, Wietzke P, Oellerich M, Ramadori G. Replacement of corticosteroids by mycophenolate mofetil in liver graft recipients on initial tacrolimus immunosuppression. Transplant Proc 2000; 32(7):2543. Wietzke P, Braun F, Ringe B, Ramadori G. Interferon Alfa-2A and ribavirin therapy for hepatitis C recurrence after liver transplantation. Transplant Proc 2000; 32(7):2539-2542. Schwörer H, Ramadori G. [Acute pancreatitisadverse effect of 5-aminosalicylic acid (mesalazine) in various galenic dosage forms]. Dtsch Med Wochenschr 2000; 125(44):1328-1330. Meier V, Mihm S, Ramadori G. MxA gene expression in peripheral blood mononuclear cells from patients infected chronically with hepatitis C virus treated with interferon- alpha. J Med Virol 2000; 62(3):318-326. Sebestyen A, Gallai M, Knittel T, Ambrust T, Ramadori G, Kovalszky I. Cytokine regulation of syndecan expression in cells of liver origin. Cytokine 2000; 12(10):1557-1560. Lorf T, Ramadori G, Ringe B, Schworer H. The effect of pantoprazole on tacrolimus and cyclosporin A blood concentration in transplant recipients.
Volume 96, Number 7, July 2001 Neomycinsorbitol and lactulose in the treatment of acute portal-systemic encephalopathy. Portalhemodynamics in chronic portal-systemic encephalopathy. http://www-east.elsevier.com/ajg/issues/9607/ajg3964fla.htm
Extractions: Pages Hepatic Encephalopathy Andres T. Blei a rdoba b and The Practice Parameters Committee of the American College of Gastroenterology Cite this article as: a Department of Medicine, Lakeside VA Medical Center and Northwestern University, Chicago, Illinois b Unidad de Hepatologia, Hospital Vall d'Hebron and Autonomous University of Barcelona, Barcelona, Spain Introduction Hepatic encephalopathy (HE) may be defined as a disturbance in central nervous system function because of hepatic insufficiency. This broad definition reflects the existence of a spectrum of neuropsychiatric manifestations related to a range of pathophysiological mechanisms. Present in both acute and chronic liver failure, these neuropsychiatric manifestations are potentially reversible. Clinical Considerations Pathophysiology The main tenet of all theories of the pathogenesis of HE is firmly accepted: nitrogenous substances derived from the gut adversely affect brain function. These compounds gain access to the systemic circulation as a result of decreased hepatic function or portal-systemic shunts. Once in brain tissue, they produce alterations of neurotransmission that affect consciousness and behavior. Abnormalities in glutamatergic, serotoninergic, -aminobutyric acid-ergic (GABA-ergic), and catecholamine pathways, among others, have been described in experimental HE (
Journal Of Hepatology Changes in the portalsystemic encephalopathy (PSE) index on entry and at theend of the study were used to evaluate the efficacy of the two therapies. http://www.hepatoweb.com/pda/jhepatol08.html
Extractions: Post-transplant hepatitis C recurs universally and results in patient and graft loss Abstract: With the dramatic improvement in results, liver transplantation is now recognized as the best form of therapy for end stage liver disease. With the continued success, there are now more than 3,000 liver transplants performed yearly in the United States alone. One year survival rates of 80% to 90% are now expected and the rate-limiting step in the application of transplantation in liver disease has become donor availability. Table I Liver Transplantation: Indications
EDPnet 1998 Dec;13(4)27390. 2. Layrargues GP, et al. Role of manganese in the pathogenesisof portal-systemic encephalopathy. Metab Brain Dis. 1998 Dec;13(4)311-7. http://www.devolder.be/brl/Case of month/cases 1999/oplmarch99.htm
>LITERATUR (SHE STUDIE) Trailmaking and numberconection tests in the assessment of mental state in portalsystemic encephalopathy. Subclinical portal-systemic encephalopathy. http://www.medipol.de/she/h-literatur.html
Extractions: Ackermann H (1994) Medizinische Normbereiche. medwelt; 45: 448-456 Araki K, Ueda Y, Kagawa K, Kashima K, Kono I, Nakajima K (1994) Subcortical impairment in subclinical hepatic encephalopathy. J Neurol Sci ; 126: 162-167 Banz K, Rohrbacher R, Schwicker D (1993) Die Sozioökonomie der chronischen Lebererkrankungen in Deutschland: Epidemiologie, Diagnostik, Therapie, Kosten. Band 5; HealthEcon; Bern, Frankfurt A/M, New York; (1993) Beckmann G, Rüffer A, Sonnenschein B (1996) Lactulose und Darmmilieu. Können intestinale Hefen Lactulose verwerten? Ärztezeitschrift für Naturheilverfahren 10; 37:775-780 Bianchi CP, Marchesini G (1993) Vegetable versus animal protein diet in cirrhotic patiens with chronic encephalopathy. A randomized cross-over comparison. J Intern Med; 233(5): 385-392 Brockelhurst J, Fulton J (1994) Klinische Aspekte der Lactulose. durpahr med sccipt Brockhaus A, Ewers U, Janke W, Krämer U, Kujanek G, Lechner H, Winneke G (1983) Neurophysiological studies with elevated tooth-lead concentrations. II. Extended study. Int Arch Occup Environ Health; 51: 231-252 Butterworth RF (1996) The neurobiology of hepatic encephalopathy. In: Rothschild MA (Hrsg.), Berk PD (Hrsg.): Hepatic encephalopathy. Seminars in liver desease; Thieme; Stuttgart, New York; Vol.16: 235-244
Portal-systemic Shunt Procedures - General Practice Notebook portalsystemic shunts have a high intraoperative mortality and a poor 5 year survival,particularly The most common problem is chronic hepatic encephalopathy. http://www.gpnotebook.co.uk/cache/-1804926932.htm
Extractions: portal-systemic shunt procedures The use of portal-systemic shunt procedures for the treatment of acutely bleeding oesophageal varices is now reserved for the 5-10% of patients who fail to respond to pharmacotherapy or sclerotherapy. Portal-systemic shunts have a high intraoperative mortality and a poor 5 year survival, particularly in patients with significant hepatic decompensation. The most common problem is chronic hepatic encephalopathy. There are two types of portal-systemic shunt procedures: Transjugular intrahepatic portal-systemic shunting (TIPSS) is a new procedure which is particularly useful in the treatment of acutely bleeding oesophageal varices if liver transplantation is being considered.
Portal-Systemic Shunts portalsystemic Shunts Portosystemic Shunt The shunt may lead to episodic developmentof hepatic encephalopathy (seizures or bizarre behavior) associated with http://www.cah.com/library/ps.html
Extractions: Portosystemic Shunt Congenital Portal Shunts are due to a defect in the circulation around the liver-instead of blood entering the liver to be de-toxified it is bypassed. The liver usually eliminates toxins derived from the gut. There is a bridging between the veins around the liver and the toxic material bypasses the liver causing an elevation of ammonia in the circulation. This defect may be within the liver (intrahepatic) or occur outside of the liver (extrahepatic)- most are single vessels Acquireddevelops subsequent to portal hypertension (high blood pressure); typically multiple-This occurs due to a lack of valves in the portal vein permits circulatory accommodation through the shunt. Portal hypertensionusually associated with liver scarring or cirrhosis) The shunt may lead to episodic development of hepatic encephalopathy (seizures or bizarre behavior) associated with ingestion of high- protein food, and administration of certain drugs. Another effect of the shunt is the development of bladder stones due to inability of the liver to delete uric acid from the blood. SYSTEMS AFFECTED Nervous system signs include episodic hepatic encephalopathy (seizures).
STI: Transjugular Intrahepatic Portal-Systemic Shunt Procedure The transjugular intrahepatic portalsystemic shunt, or TIPS, procedure is not asurgical operation a radiologist performs the procedure in encephalopathy. http://www.sti.upmc.edu/STI_Patient_web/sti/l-1c5.TIPS.asp
Extractions: The Transjugular Intrahepatic Portal-Systemic Shunt (TIPS) Procedure The transjugular intrahepatic portal-systemic shunt, or TIPS, procedure is not a surgical operation a radiologist performs the procedure in the x-ray room under x-ray guidance. During the TIPS procedure, a radiologist places a stent (a tubular device) in the middle of the liver to reroute blood flow from the portal vein, which leads to the liver, directly into the hepatic veins and to the vena cava (the largest vein leading from the liver to the heart). The TIPS procedure reroutes blood flow around the liver and reduces pressure in all abnormal veins not only in the stomach and esophagus, but also in the bowel and liver. TIPS provides immediate control of variceal bleeding in more than 90 percent of patients. Needless to say, innumerable TIPS procedures have been performed successfully at the Thomas E. Starzl Transplantation Institute. The procedure lasts from 1 to 3 hours. Patients usually remain in the hospital for two to three days after the procedure. Before discharge, the physician orders a repeat Doppler sonogram to determine whether the shunt is functioning properly.
Chapter 14 - Section 13: First Principles Of Gastroenterology Common precipitants of hepatic encephalopathy. Superimposed acute liver disease Progressiveliver disease Transjugular intrahepatic portalsystemic shunt (TIPS). http://gastroresource.com/GITextbook/En/Chapter14/14-13.htm
Extractions: - Select a chapter - 1. Symptoms and Signs 2. Nutrition 3. Ethics 4. Research/Clinical Trials 5. Esophagus 6. Stomach and Duodenum 7. Small Intestine 8. Intestinal Ischemia 9. H.I.V. 10. Inflammatory Bowel 11. Colon 12. Pancreas 13. Biliary System 14. Liver 15. Paediatrics 16. Video Endoscopic Images Search 13. Hepatic Encephalopathy / L.J. Worobetz page 537 Hepatic encephalopathy (HE) is a complex, potentially reversible neuropsychiatric condition that occurs as a consequence of acute or chronic liver disease. It is characterized by changes of personality, consciousness, behavior and neuromuscular function ( Table 20 ). Early features include reversal of sleep pattern, apathy, hypersomnia, irritability and personal neglect. In later stages, delirium and coma may occur. Neurologic signs may include hyperreflexia, rigidity, myoclonus and asterixis. Asterixis is not specific to hepatic encephalopathy and may be present in other causes of metabolic encephalopathy. Seizures and lateralizing signs are uncommon and are more commonly seen in acute than chronic liver failure. Clinically, a number of encephalopathic patterns can be observed: acute, acute recurrent, chronic recurrent and chronic permanent encephalopathy (the last often forms part of the spectrum of acquired hepatocerebral degeneration).
P set up over the surface of heart and liver, portalsystemic shunting index artificialvessel was 8mm), the morbidity o f postoperative encephalopathy and the http://www.wjgnet.com/1007-9327/5/525.htm
Extractions: cirrhotic portal hypertensive patients Zhu JY, Leng XS, Dong N, Qi GY, Du RY Subject headings liver volume; hypertension, portal; liver ci rrhosis; prognosis Zhu JY, Leng XS, Dong N, Qi GY, Du RY. Measurement of liver volume and its clinical significance in cirrhotic portal hypertensive patients. World J Gastroentero, 1999;5(6):525-526 Accurate assessment of hepatic reserve function in cirrhotic portal hypertensive patients is important for selection of surgical proc edure and evaluation of prognosis. The measurement of liver volume has been applied in clinic as widely as Child s class . Limited by technical condition, measurement of liver volume in vivo has seldom been reported in China. Using double helix spiral CT (Elscint CT Twin), the liver volume of 25 cirrhoti
Hepatic Encephalopathy of hepatic encephalopathy should be considered when six major factors are present(1) acute or chronic hepatocellular disease and/or extensive portalsystemic http://www.geocities.com/twisted_artist/Medecine/hepatic_encephalopathy.htm
Extractions: Hepatic Encephalopathy DEFINITION: Hepatic encephalopathy is a syndrome seen in patients with cirrhosis of the liver. It is characterized by personality changes, intellectual impairment, and a depressed level of consciousness , fluctuating neurologic signs, asterixis or "flapping tremor," and distinctive electroencephalographic changes. An important prerequisite for the syndrome is diversion of portal blood into the systemic circulation through porto-systemic collateral vessels. Indeed, hepatic encephalopathy may develop in non-cirrhotic patients who have undergone portocaval shunt surgery. The development of hepatic encephalopathy is explained to some extent by the effect of neurotoxic substances, which occurs in the setting of cirrhosis and portal hypertension. Subtle signs of hepatic encephalopathy are seen in nearly 70% of patients with cirrhosis. Symptoms may be debilitating in a significant number of patients and are seen in 24-53% of patients who undergo portosystemic shunt surgery. About 30% patients dying of end-stage liver disease will experience significant encephalopathy, approaching coma. Encephalopathy may be acute and reversible or chronic and progressive . In severe cases, irreversible coma and death may occur. Acute episodes may recur with variable frequency
Liver And Biliary Tract 17.Riggio O, Balducci G, Ariosto F. Lactitol in prevention of recurerent episodesof hepatic encephalopathy in cirrhotic patients with portalsystemic shunt. http://www.geocities.com/gastroyu/jan2001/article2.htm
Extractions: ( accepted March 31st, 2001 ) Institute of Digestive Diseases, Clinic for Gastroenterology and Hepatology, Clinical Center of Serbia, Belgrade, Institute for Cardiovascular Diseases Dedinje , Belgrade. Address correspondence to: Professor Dr Rada Clinic for Gastroenterology and Hepatology, Institute of Digestive Diseases, Clinical Center of Serbia, YU-11000 Belgrade, Serbia, Yugoslavia. Tel + 381 11 361 777/ Ext. 3733 Surgery of portal hypertension Gastroenterolo ABSTRACT s hemodynamic characteristics, clinical condition, and aetiology of portal hypertension. Distal spleno-renal shunt was made in 20 patients. In six patients this was combined with partial splenic resection. Fifteen cases underwent mesocaval shunt with H-graft, while in 4 patients coronaro-caval shunt was made. Postoperative follow-up studies demonstrated stable liver function tests in 36 cases. Variceal size was greatly reduced in 27 patients. No variceal bleeding occurred during the immediate postoperative period. Haematologic indices of hypersplenism were reversed in 18 cases. Ascites did not recur in 27 patients. In 4 cases shunts became thrombosed. In the very first 2 cases this occurred during immediate postoperative period, in another 2 after couple of years. Acute postoperative encephalopathy was recorded in 3 patients, while chronic in 4 cases. Hepatic perfusion index was slightly decreased in 4 patients. Thirty-four patients survived from 2.5 to 4.5 years in average.
Tulane Center For Abdominal Transplant: Liver The encephalopathy can usually be controlled with medication, but some Shunt TIPSis an abbreviation for Transjugular Intrahepatic portalsystemic Shunt, and http://www.tulanetransplant.com/li_varices.htm
Extractions: Esophageal varices are the enlarged veins (varicose veins) located in the lower end of the esophagus (swallowing tube). These veins develop because cirrhosis blocks blood from flowing freely through the liver. Once the blood is blocked from flowing through the liver, it must find another way to return to the heart. The veins surrounding the esophagus and stomach provide a pathway for blood to return to the heart. Over time, these veins become larger and develop into varicose veins or varices. The enlarged veins surrounding the esophagus are esophageal varices, and the veins surrounding the stomach are gastric varices. If the pressure within these veins becomes high enough the veins can rupture, leading to life threatening bleeding. Bleeding from varices is generally brisk and associated with symptoms. The most frequent symptoms include: weakness, light-headedness, nausea, vomiting of blood or coffee colored material, and passage of bowel movements that are bloody or black (like tar). Bleeding from varices represents a life-threatening medical emergency. If you develop signs of bleeding, someone should take you to the nearest hospital immediately.
Portal Systemic Encephalopathy For Medical Professionals only. Portal systemic encephalopathy, http://www.amersham-health.com/medcyclopaedia/Volume%20VI%201/PORTAL%20SYSTEMIC%
Extractions: portal systemic encephalopathy Hepatic encephalopathy is a metabolic disorder of the central nervous system and neuromuscular system that may complicate liver failure from any cause. It is particularly associated with advanced cirrhosis on account of the diffuse parenchymal damage and portosystemic shunting. The features depend on the aetiology and precipitating factors, eventually developing into stupor and then coma. Some aetiologies of the hepatic failure, for example paracetamol overdose, can precipitate this condition within three or four days, with a very rapid progression through the grades of encephalopathy. Other aetiologies, for example viral hepatitis, are associated with a much more variable onset. The grade of the encephalopathy can be used to predict the prognosis - for example grades I and II have and excellent prognosis, grades III and IV have poorer prognoses with the development of complications.
