Evolving Concepts: The Negative Effect of Minimal Hepatic Encephalopathy and Role for Prophylaxis in Patients With Cirrhosis (original) (raw)
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Management of hepatic encephalopathy in patients with cirrhosis
Best Practice & Research Clinical Gastroenterology, 2007
The term hepatic encephalopathy encompasses a spectrum of neuropsychiatric abnormalities seen in patients with liver dysfunction. Distinct syndromes are identified in acute liver failure and cirrhosis. Rapid deterioration in consciousness level and increased intracranial pressure that may result in brain herniation and death are a feature of acute liver failure whereas manifestations of hepatic encephalopathy in cirrhosis include psychomotor dysfunction, impaired memory, increased reaction time, sensory abnormalities, poor concentration and in severe forms, coma. In patients with acute-on-chronic liver failure the pathophysiology remains undefined. Ammonia has been considered central to its pathogenesis. In the brain, the astrocyte is the main site for ammonia detoxification, during the conversion of glutamate to glutamine. An increased ammonia level raises the amount of glutamine within astrocytes, causing an osmotic imbalance resulting in cell swelling and ultimately brain oedema. Recent studies suggest that inflammation and it modulators may play a synergistic role with ammonia in the pathogenesis of hepatic encephalopathy. Therapy of hepatic encephalopathy is directed primarily at reducing ammonia generation and increasing its detoxification. The currently accepted regimens to treat hepatic encephalopathy such as lactulose and protein restricted diets need further clinical trials and therefore placebo controlled clinical trials in hepatic encephalopathy are justified. In liver failure, ammonia metabolism involves multiple organs and therefore ammonia reduction will require simultaneous targeting of these organs. The present review describes the pathophysiological basis of hepatic encephalopathy and evaluates the available therapies.
Zagazig University Medical Journal, 2020
Background: Minimal hepatic encephalopathy (MHE) has a mild neurocognitive impairment that includes neuropsychological and neurophysiological alterations that can not be detected by clinical examination. This study aims to assess the frequency and risk factors for developing minimal hepatic encephalopathy in patients with compensated cirrhosis. Methods: This cross sectional study was conducted on 60 patients with compensated cirrhosis in Zagazig University Hospital and elmatarya Teaching Hospital from December 2017 to June 2018, diagnosis of minimal hepatic encephalopathy was established by using mini mental status examination test and psychometric studies, they underwent full history, laboratory investigations and abdominal doppler ultrasonography by professional radiologist assessing the presence of any porto systemic shunts and measuring serum ammonia level. Results: About 37% had MHE. Female represented 65% with mean age 49.82 years. There is statistically significant relation between MHE and smoking, comorbid diabetes, hypertension, high ammonia level and portosystemic shunt. Smoking, being single, illiterate, portosystemic shunt, comorbid diabetes and hypertension increased risk of MHE by 4.57, 3.05, 2.31, 25.94, 3.29 and 3.55 folds. Male gender and normal ammonia level were protective factors. There is significant relation between MHE and age, platelet count, serum albumin, ammonia and INR. Older patients, low platelet count and serum albumin, high ammonia level and INR were detected among patients with MHE. Increasing ammonia level was significant independent risk factor for MHE. Conclusions: MHE is a prevalent condition among patients with compensated cirrhosis with high ammonia level and portosystemic shunts as a strong risk factors for its development.
Pathogenesis, diagnosis, and treatment of hepatic encephalopathy
Journal of clinical and experimental hepatology, 2011
Hepatic encephalopathy (HE) is a neuropsychiatric disorder seen in patients with advanced liver disease or porto-systemic shunts. Based on etiology and severity of HE, the World Congress of Gastroenterology has divided HE into categories and sub-categories. Many user-friendly computer-based neuropsychiatric tests are being validated for diagnosing covert HE. Currently, emphasis is being given to view HE deficits as a continuous spectrum rather than distinct stages. Ammonia is believed to play crucial role in pathogenesis of HE via astrocyte swelling and cerebral edema. However, evidence has been building up which supports the synergistic role of oxidative stress, inflammation and neurosteroids in pathogenesis of HE. At present, treatment of HE aims at decreasing the production and intestinal absorption of ammonia. But as the role of new pathogenetic mechanisms becomes clear, many potential new treatment strategies may become available for clinician.
Prevention and treatment of hepatic encephalopathy: focusing on gut microbiota
World journal of gastroenterology : WJG, 2012
The gut flora plays an important role in the pathogenesis of the complications of cirrhosis. Hepatic encephalopathy (HE) represents a broad continuum of neuropsychological dysfunction in patients with acute or chronic liver disease and/or porto-systemic shunting of blood flow and it manifests with progressive deterioration of the superior neurological functions. The pathophysiology of this disease is complex, as it involves overproduction and reduced metabolism of various neurotoxins, particularly ammonia. Management of HE is diversified and requires several steps: elimination of precipitating factors, removal of toxins, proper nutritional support, modulation of resident fecal flora and downregulation of systemic and gut-derived inflammation. This review will provide an overview of gut barrier function and the influence of gut-derived factors on HE, focusing on the role of gut microbiota in the pathogenesis of HE and the recent literature findings on its therapeutic manipulation.
Minimal hepatic encephalopathy and extrapyramidal signs in patients with cirrhosis
American Journal of Gastroenterology, 2003
OBJECTIVES: Two types of neurological dysfunction can occur in compensated cirrhosis: 1) extrapyramidal signs related to the accumulation of manganese in the basal ganglia and 2) milder degrees of cognitive impairment known as minimal hepatic encephalopathy (mHE). We assessed whether there was any relationship between both disorders in 42 patients with compensated cirrhosis.
Hepatic encephalopathy: a critical current review
Hepatology international, 2018
Hepatic encephalopathy (HE) is a serious neuropsychiatric complication of cirrhosis and/or porto-systemic shunting. The clinical symptoms are widely variable, extending from subtle impairment in mental state to coma. The utility of categorizing the severity of HE accurately and efficiently serves not only to provide practical functional information about the current clinical status of the patient but also gives valuable prognostic information. In the past 20-30 years, there has been rapid progress in understanding the pathophysiological basis of HE; however, the lack of direct correlation between pathogenic factors and the severity of HE make it difficult to select appropriate therapy for HE patients. In this review, we will discuss the classification system and its limitations, the neuropsychometric assessments and their challenges, as well as the present knowledge on the pathophysiological mechanisms. Despite the many prevalent hypotheses around the pathogenesis of the disease, mo...