Hepatic Encephalopathy

2017 ◽  
Author(s):  
Allison R Schulman ◽  
Nikroo Hashemi

Hepatic encephalopathy (HE) is one of the most debilitating manifestations of acute or chronic liver disease and/or portosystemic shunting. The clinical manifestations of HE span a wide spectrum of neurologic or psychiatric abnormalities, ranging from subclinical neuropsychological disturbances to coma. HE severely affects the lives of patients and their caregivers and results in the use of more health care resources in adults than other manifestations of hepatic dysfunction. To date, there are insufficient clinical studies and standardized definitions, making the diagnosis, classification, and treatment of HE challenging. This review covers the epidemiology, pathophysiology and pathogenesis, diagnosis, differential diagnosis, treatment, and follow-up of HE. Figures show the numerous processes and mechanisms involved in the pathogenesis of HE and ammonia trafficking and metabolism within the body. Tables list the four factors that dictate categorization and grading of HE, differential diagnosis of HE, summary of testing used for minimal HE and covert HE with associated advantages and/or disadvantages, and precipitating causes of HE in patients with cirrhosis. This review contains 2 highly rendered figures, 4 tables, and 77 references. Key words: chronic liver disease; covert hepatic encephalopathy; hepatic encephalopathy; minimal hepatic encephalopathy; overt hepatic encephalopathy; transjugular intrahepatic portosystemic shunt 

2020 ◽  
Vol 53 (4) ◽  
pp. 299
Author(s):  
Opeyemi F Bamidele ◽  
Abdulfatai B Olokoba ◽  
Matthew O Bojuwoye ◽  
Richard O. Akintayo ◽  
Oluwakemi Bamidele

2020 ◽  
pp. 3080-3089
Author(s):  
Paul K. Middleton ◽  
Debbie L. Shawcross

Hepatic encephalopathy (HE) is a significant complication of both acute and chronic liver disease, causing much morbidity and mortality. It is a complex neuropsychological condition, associated with hyperammonaemia and systemic inflammation, with a wide spectrum of symptoms. The West Haven criteria describe grades of severity from 0 (subclinical) and I (changes in awareness, mood, attention, cognition, and sleep pattern) through to IV (coma). It is further classified by the underlying aetiology: type A, due to acute liver failure; type B, secondary to portosystemic shunting; and type C, occurring in chronic liver disease in association with precipitating factors including infections, gastrointestinal bleeding, and electrolyte disorders, particularly hyponatraemia. There is no definitive test or set of diagnostic criteria to establish a diagnosis of HE, which remains primarily a clinical diagnosis of exclusion in patients with a history or clinical evidence of liver disease. Management depends on the type of HE, but for type C (the commonest type) typically includes lactulose and rifaximin. Patients with cirrhosis with ongoing overt HE despite optimal medical management have a dismal outlook and should be considered promptly for liver transplantation.


2018 ◽  
Vol 30 (4) ◽  
pp. 217
Author(s):  
GhadaA Mohamed ◽  
MohammadEltaher Abdelrahman ◽  
SaadZaky Mahmoud ◽  
AnwarM Ali ◽  
Haitham Ahmed AbdallaT El-Khateeb

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Mohamed Abdelftah Elmaltawy ◽  
Ahmed Saady Khayyal ◽  
Mohamed Osama Aly ◽  
Hisham Ashraf Elhussieny Elghandour

Abstract Background Hepatic Encephalopathy (HE) is defined as alteration of mental state in the absence of other causes of encephalopathy due to liver failure and/or abnormal shunting of blood from portal to systemic circulation often accompanied by elevated blood ammonia. Objectives The aim of this study was to determine the relation between the Helicobacter pylori infectionand minimal hepatic encephalopathy (MHE) in cirrhotic patients and to assess the outcome after treatment of H. pylori. Patients and Methods This study was can•ied out at Egyptian Railway Medical Centre at the in-patients section at Gastroenterology and Hepatology Medicine Department with chronic liver disease who agreed to participate in the study. After performing the psychometric tests the patients were allocated in one of the two groups according to test results: Group I: consisted of 30 consecutive patients who have chronic liver disease and presented with evidence of Minimal hepatic encephalopathy (MHE), as recognized by positive psychometric tests, Group Il: included 30 consecutive patients who presented with chronic liver disease and did not have Minimal hepatic encephalopathy, as confirmed by negative psychometric test. Results In this study a significant reduction was found in blood ammonia levels in MHE and non- MHE after triple-drug anti-H. pylori treatment (p < 0.001). This reduction was more marked in patients with MHE group compared to non-MHE group with % improvement in ammonia level 26.1 ± 8.36 umol/L and 17.79 ± 7.308 for MHE and non-MHE respectively. This finding indicates that H. pylori may contribute to the development of hyperammonemia in patients with liver disease and MHE. The role of H. pylori in the pathogenesis of hyperammonemia has been shown in previous studies which showed a reduction in blood ammonia levels after eradication of H.pylori infection. Conclusion Helicobacter Pylori infection was more prevalent in patients with MHE than without MHE. Serum arnrnonia levels were significantly higher in MHE patients than without MHE and even higher in H.pylori positive patients than without H.pylori infection. Helicobacter Pylori eradication treatment significantly improves ammonia levels, results of psychometric tests and improves manifestations of MHE.


2021 ◽  
Vol 16 (1-2) ◽  
pp. 32-40
Author(s):  
Dagmara Bogdanowska-Charkiewicz ◽  
Paweł Rogalski ◽  
Andrzej Dąbrowski ◽  
Jarosław Daniluk

2017 ◽  
Author(s):  
Anna Hadjihambi ◽  
Ian F. Harrison ◽  
Natalia Arias ◽  
Rocío Gallego-Durán ◽  
Patrick S. Hosford ◽  
...  

AbstractNeuronal function is exquisitely sensitive to alterations in extracellular environment. In patients with hepatic encephalopathy (HE), accumulation of metabolic waste products and noxious substances in the interstitial fluid of the brain may contribute to neuronal dysfunction and cognitive impairment. In a rat model of chronic liver disease, we used an emerging dynamic contrast-enhanced MRI technique to assess the efficacy of the glymphatic system, which facilitates clearance of solutes from the brain. We identified discrete brain regions (olfactory bulb, prefrontal cortex and hippocampus) of altered glymphatic flow, which aligned with cognitive/behavioural deficits. Although the underlying pathophysiological mechanisms remain unclear, this study provides the first experimental evidence of impaired glymphatic clearance in HE.


1993 ◽  
Vol 14 (11) ◽  
pp. 436-443
Author(s):  
Catherine Mews ◽  
Frank Sinatra

Chronic liver disease encompasses a wide spectrum of disorders, including infectious, metabolic, genetic, drug-induced, idiopathic, structural, and autoimmune diseases. The clinical presentation and initial laboratory data in many of these diseases are similar, and a definitive diagnosis often relies on specialized laboratory investigation and histologic examination of liver tissue. The aim of this article is to: 1) Define chronic hepatitis and cirrhosis; 2) Review briefly the clinical presentation, pathophysiology, diagnosis, and management of the more common pediatric causes of chronic liver disease; 3) Review the complications associated with chronic liver disease and discuss their appropriate management; and 4) Review the indications for hepatic transplantation. Chronic Hepatitis Chronic hepatitis is defined as ongoing inflammation within the liver that is capable of progression to cirrhosis, liver failure, and death. The presence of continued hepatic inflammation, as confirmed by clinical manifestations and laboratory studies, for a period of greater than 10 weeks usually excludes a self-limited hepatitis and implies chronicity. However, to fulfill the international criteria for chronic disease strictly, evidence of continued hepatic inflammatory activity needs to be present for a period of at least 6 months. Most pediatricians, however, allow 3 months for an acute liver insult to clear before undertaking specialized laboratory investigations and invasive studies.


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