Extractions: (advertisement) Home Specialties CME PDA ... Patient Education Articles Images CME Patient Education Advanced Search Link to this site Back to: eMedicine Specialties Medicine, Ob/Gyn, Psychiatry, and Surgery Gastroenterology Last Updated: January 8, 2003 Rate this Article Email to a Colleague Synonyms and related keywords: portosystemic encephalopathy, PSE, hepatic encephalopathy, HE, liver disease, advanced liver disease, portosystemic shunt, portal-systemic shunt, neurotoxicity, neuropsychosis, hyperammonemia, transjugular intrahepatic portosystemic shunt, TIPS, nonselective portocaval shunts AUTHOR INFORMATION Section 1 of 10 Author Information Introduction Clinical Differentials ... Bibliography Author: Blake A Jones, MD , New Hampshire Gastroenterology Blake A Jones, MD, is a member of the following medical societies: American Association for the Study of Liver Diseases American College of Gastroenterology American Gastroenterological Association American Medical Association ... Royal College of Physicians and Surgeons of Canada , and Texas Medical Association Editor(s): Ann Ouyang, MBBS
Extractions: (advertisement) Synonyms, Key Words, and Related Terms: portosystemic encephalopathy, PSE, hepatic encephalopathy, HE, liver disease, advanced liver disease, portosystemic shunt, portal-systemic shunt, neurotoxicity, neuropsychosis, hyperammonemia, transjugular intrahepatic portosystemic shunt, TIPS, nonselective portocaval shunts Background: Portosystemic encephalopathy (PSE) is a neuropsychiatric syndrome associated with advanced liver disease. Portosystemic shunting of ill-defined substances is suspected to result in neurotoxicity. This has led to many investigative and therapeutic efforts aimed at identifying and eliminating the putative poisons that originate from the gut lumen. A fluctuating level of consciousness is common, and progression to coma may occur rapidly. A high index of clinical awareness is critical for anticipating and recognizing complications. A precipitating cause usually is discovered after clinical and laboratory evaluation. Although elevated plasma ammonia levels often are seen and therapy based on this observation generally is effective, poor correlation exists between plasma ammonia levels and the degree of encephalopathy. Multiple mechanisms contribute to the pathogenesis of this disorder. Discrete neuropathological features are described in PSE but may represent epiphenomena. Treatment with lactulose is the mainstay of therapy, but novel developmental approaches show promise.
Postgraduate Medicine: Hepatic Encephalopathy Often, the term "portalsystemic encephalopathy" is used to emphasize the failure of the Butterworth RF. portal-systemic encephalopathy a disorder of neurone-astrocytic metabolic http://www.postgradmed.com/issues/2001/02_01/assi.htm
Extractions: Souheil Abou-Assi, MD; Z. Reno Vlahcevic, MD* VOL 109 / NO 2 / FEBRUARY 2001 / POSTGRADUATE MEDICINE CME learning objectives The authors disclose no financial interests in this article. Supported by a grant from the National Institutes of Health and a grant from the Department of Veterans Affairs. *Deceased. This is the first of three articles on cirrhosis This page is best viewed with a browser that supports tables. Preview : Hepatic encephalopathy is characterized by neuropsychiatric manifestations ranging from a slightly altered mental status to coma, and neuromuscular symptoms may be present. This complication of chronic or acute liver disease is a result of the failure of the liver to detoxify toxins originating in the intestine. The pathogenesis probably is multifactorial, although the predominant causative agent appears to be ammonia. In this article, Drs Abou-Assi and Vlahcevic discuss the timely recognition and correction of factors contributing to this often reversible condition.
Volume 96, Number 7, July 2001 in the treatment of acute portalsystemic encephalopathy. A controlled, double-blind water) to treat acute portal-systemic encephalopathy A double-blind randomized clinical 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 (
Encephalopathy-drugs.html with hepatodepressive syndrome and portalsystemic encephalopathy. MEDLINE ACCESSION NUMBER Mental state gradation, portal systemic encephalopathy index (PSEI), and fasting http://www.indiana.edu/~pietsch/encephalopathy-drugs.html
Extractions: The following MEDLINE items were compiled by SilverPlatter and are presented here with their generous co-operation and permission. ( See SilverPlatter's Worldwide Library for bibliographic search information Record 1 of 55 in MEDLINE EXPRESS (R) 1999/01-1999/02 TITLE: [Thiamine treatment today] AUTHOR(S): Tallaksen-CM; Bovim-G ADDRESS OF AUTHOR: Nevrologisk avdeling, Rikshospitalet, Oslo. SOURCE (BIBLIOGRAPHIC CITATION): Tidsskr-Nor-Laegeforen. 1998 Oct 20; 118(25): 3946-9 INTERNATIONAL STANDARD SERIAL NUMBER: 0029-2001 LANGUAGE OF ARTICLE: NORWEGIAN; NON-ENGLISH ABSTRACT: This article reviews some of the established data on thiamin and the most common symptoms of deficiency. Guidelines for appropriate therapy are offered. Thiamin or vitamin B1 was among the first vitamins to be discovered. Beriberi was the first disease to be associated with thiamin deficiency, and Wernicke's encephalopathy was shown to respond to thiamin treatment a few years later. However, thiamin treatment remains inadequate or delayed. Treatment is efficient in the early stages, but delays often causes permanent damage. It is important that all physicians are aware of what patients are susceptible to develop thiamin deficiency and that they recognize the symptoms as early as possible. MEDLINE ACCESSION NUMBER: 99048032 Record 2 of 55 in MEDLINE EXPRESS (R) 1999/01-1999/02
THE MERCK MANUAL, Sec. 4, Ch. 38, Clinical Features Of Liver Disease portalsystemic encephalopathy" is a more descriptive term of the pathophysiology than "hepatic portal-systemic encephalopathy may occur in fulminant hepatitis caused by viruses http://www.merck.com/pubs/mmanual/section4/chapter38/38f.htm
Extractions: (Hepatic Encephalopathy; Hepatic Coma) A neuropsychiatric syndrome caused by liver disease and usually associated with portal-systemic shunting of venous blood. "Portal-systemic encephalopathy" is a more descriptive term of the pathophysiology than "hepatic encephalopathy" or "hepatic coma," but clinically all three are used interchangeably. Etiology Portal-systemic encephalopathy may occur in fulminant hepatitis caused by viruses, drugs, or toxins, but it more commonly occurs in cirrhosis or other chronic disorders when extensive portal-systemic collaterals have developed as a result of portal hypertension. The syndrome also follows portacaval shunt or similar portal-systemic anastomoses. In patients with chronic liver disease, encephalopathy is usually precipitated by specific, potentially reversible causes (eg, GI bleeding; infection; electrolyte imbalance, especially hypokalemia; alcoholic debauches) or iatrogenic causes (tranquilizers, sedatives, analgesics, diuretics).
THE MERCK MANUAL, Sec. 4, Ch. 38, Clinical Features Of Liver Ascites. portalsystemic encephalopathy. Other Symptoms And Signs Of Liver Disease. Portal-SystemicEncephalopathy (Hepatic Encephalopathy; Hepatic Coma). http://www.merck.com/mrkshared/mmanual/section4/chapter38/38f.jsp
THE MERCK MANUALSECOND HOME EDITION, Liver Encephalopathy In Ch. Liver encephalopathy (portalsystemic encephalopathy, hepatic encephalopathy, hepaticcoma) is a disorder in which brain function deteriorates because toxic http://www.merck.com/mrkshared/mmanual_home2/sec10/ch135/ch135g.jsp
Extractions: Section 10. Liver and Gallbladder Disorders Chapter 135. Clinical Manifestations of Liver Disease Topics: Introduction Jaundice Cholestasis Liver Enlargement ... Liver Failure Liver encephalopathy (portal-systemic encephalopathy, hepatic encephalopathy, hepatic coma) is a disorder in which brain function deteriorates because toxic substances normally removed by the liver build up in the blood. Substances absorbed into the bloodstream from the intestines pass through the liver, where toxins are normally removed. Many of these toxins are normal breakdown products of the digestion of protein. In liver encephalopathy, toxins are not removed because liver function is impaired. Also, some toxins may bypass the liver altogether through connections formed between the portal venous system (which supplies blood to the liver) and the general (systemic) venous system as a result of liver disease. A surgical bypass (portal-systemic shunt) to correct portal hypertension may have the same effect. Whatever the cause, the outcome is the same: Toxins can pass to the brain and affect its function. Exactly which substances are toxic to the brain is not known; however, high levels of protein breakdown products in the blood, such as ammonia, appear to play a role. In a person with long-standing (chronic) liver disease, encephalopathy is usually triggered by an event such as an acute infection or an alcoholic binge, which increases liver damage. Or encephalopathy may be triggered by eating too much protein, which increases the levels of protein breakdown products in the blood. Bleeding in the digestive tract, such as from dilated, twisted veins in the esophagus (esophageal varices), can also lead to a buildup of protein breakdown products, which may directly affect the brain. Certain drugsespecially some sedatives, analgesics, and diureticsmay also trigger encephalopathy. When such a precipitating cause is removed, the encephalopathy may disappear.
Best Practice Of Medicine -Portal-systemic Encephalopathy - Print portalsystemic encephalopathy. portal-systemic encephalopathy can present in thechronic form as acquired non-Wilsonian hepatolenticular degeneration 11. http://merck.praxis.md/index.asp?page=bpm_viewall&article_id=CPM02HP377&show_ban
Best Practice Medicine-Professional Reference - Portal-systemic portalsystemic encephalopathy. by Sanjay Sandhir, MD and Fredrick L Weber Jr,MD, Best Practice of Medicine. January 2000. Last modified October 12, 2001. http://merck.micromedex.com/index.asp?page=bpm_brief&article_id=CPM02HP377
Hep C Vets, Hepatic Encephalopathy Chronic Hepatitis C Hep C Vets Home page is a source of information about the world pandemic Hepatitis C. Often, the term "portalsystemic encephalopathy" is used to emphasize the failure of the http://www.hepcvets.com/se/enceph.html
Extractions: What's New? Our Latest Additions Hepatitis C Biopsy Books On Liver Disease (Recommended) Clinical Trials Depression Drugs Used In Treatment Fibrosis/Cirrhosis Genotypes Hepatitis B HEP C INFO Only List Sign Up HEP C INFO Only Full Text Medical Articles Herbals / Alternative Medicine Insurance Issues Liver Disease Glossary Miscellaneous Vaccine Information Veterans Table Of Contents Viral Loads What The Heck Is....VERY INFORMATIVE 2002 NIH Hepatitis C Consensus Hep C Vets Bulletin Board Hepatitis C Bulletin Board Our Favorite Links Poetry/Short Stories Metabolic consequence of cirrhosis often is reversible Souheil Abou-Assi, MD; Z. Reno Vlahcevic, MD* VOL 109 / NO 2 / FEBRUARY 2001 / POSTGRADUATE MEDICINE CME learning objectives The authors disclose no financial interests in this article.
Entrez PubMed portalsystemic encephalopathy presence of basal ganglia lesions withhigh signal intensity on MR images. Inoue E, Hori S, Narumi http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2
Hepatic Encephalophaty Hepatic encephalopathy for healthcare personel (contains medical terms).portal-systemic encephalopathy - (Hepatic Encephalopathy; Hepatic Coma). http://home3.inet.tele.dk/omni/encephalopathy.htm
Extractions: The Danish Hepatitis C website Hepatic encephalopathy (for patients and relatives): The typical symptoms of hepatic encephalopathy include The typical symptoms of hepatic encephalopathy include ... Ascites Hepatic encephalopathy (for patients and relatives): Hepatic encephalopathy refers to the changes in the brain that occur in patients with advanced acute or chronic liver disease. If liver cells are damaged, certain substances that are normally cleansed from the blood by the healthy liver are not removed (ammonia mainly, and other toxins). A patient with chronic hepatic encephalopathy may develop progressive loss of memory, disorientation, untidiness, and muscular tremors, leading to a form of chronic dementia. The ingestion of protein invariably aggravates these symptoms. The treatment of hepatic encephalopathy involves, first, the removal of all drugs that require detoxification in the liver and, second, the reduction of the intake of protein. Restricting the amount of protein in the diet will generally lower the levels of amino acids and ammonia in the bloodstream and brain. Most physicians advise their patients with this condition to eat only about 40 grams of protein a day, and will prescribe lactulose or neomycin to lower amino acid production. Non-meat proteins, such as those found in vegetables and milk, are preferred. Certain amino acids are used in treatment, since they are considered less likely to cause mental impairment. A dietary supplement rich in these amino acids is used at many liver treatment centers.
Chapter 2 - Workbook: First Principles Of Gastroenterology Section 6 Dietary Therapy in Liver Disease 6.1 Discuss appropriate dietarytherapy for a. Ascites b. portalsystemic encephalopathy c. Cirrhosis. http://gastroresource.com/GITextbook/En/chapter2/workbook.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
Lactulose containing both lactose and galactose; causes a decrease in the blood concentrationof ammonia in clients suffering from portalsystemic encephalopathy. http://www.healthdigest.org/drugs/lactulose.html
Extractions: Pregnancy Category: B Acilac Cephulac Cholac Chronulac Constilac Constulose Duphalac Gen-Lac Enulose Evalose Heptalac Lactulax Laxilose PMS Lactulose (Rx) Classification: Ammonia detoxicant, laxative Action/Kinetics: A disaccharide containing both lactose and galactose; causes a decrease in the blood concentration of ammonia in clients suffering from portal-systemic encephalopathy. Due to bacteria-induced degradation of lactulose in the colon, resulting in an acid medium. Ammonia will then migrate from the blood to the colon to form ammonium ion, which is trapped and cannot be absorbed. A laxative action due to increased osmotic pressure from lactic, formic, and acetic acids then expels the trapped ammonium. The decrease in blood ammonia concentration improves the mental state, EEG tracing, and diet protein tolerance of clients. The increased osmotic pressure also results in a laxative effect, which may take up to 24 hr. Partly absorbed from the GI tract. Onset: 24-48 hr.
Extractions: Clinical Resources by Topic: Gastroenterology Hepatic Encephalopathy Clinical Resources Emergency Pediatrics Pathology Clinical Guidelines ... Miscellaneous Resources See also: Chapter 299: Cirrhosis and its Complications: Table of contents Chapter 376: Critical Care Neurology: Table of contents Feldman: Sleisenger and Fordtran's Gastrointestinal and Liver Disease 7th Ed.-2002 (MD Consult):
Volume 93, Number 5, May 1998 4. Gitlin N. Subclinical portalsystemic encephalopathy. Comparison of lactuloseand neomycin in the treatment of chronic portal-systemic encephalopathy. http://www-east.elsevier.com/ajg/issues/9305/ajg214fla.htm
Extractions: Pages Analysis of Risk Factors for Chronic Hepatic Encephalopathy: The Role of Helicobacter pylori Infection Bharat M. Dasani , M.D., a Samuel H. Sigal , M.D., a and Charles S. Lieber , M.D. a Objective: Elevated blood ammonia is an important pathogenic factor of hepatic encephalopathy. Although colonic bacteria are considered the main source of ammonia, the stomach in subjects with urease-producing Helicobacter pylori H. pylori ) is an alternative site. The objective of this study was to determine whether H. pylori is associated with this complication. Methods: After assessing liver function and portal hypertension, 55 cirrhotics were evaluated for encephalopathy and H. pylori infection. Response to 2 weeks of amoxicillin (2 g/day) and omeprazole (40 mg/day) was then assessed in 17 (13 H. pylori -positive, four H. pylori -negative) encephalopathic subjects. Results: H. pylori infection was more common (67% vs p vs p vs p vs p vs p vs p vs p = 0.001). When adjusted for severity of cirrhosis and age, H. pylori continued to demonstrate a statistical association ( p = 0.039). After anti-
Penn State Faculty Research Expertise Database (FRED) Hepatocerebral Encephalopathy, portalsystemic encephalopathy. Coma, Hepatic,Comas, Hepatic. Hepatocerebral Encephalopathies, Portal Systemic Encephalopathy. http://fred.hmc.psu.edu/ds/retrieve/fred/meshdescriptor/D006501
