Your kidneys change these toxins into safer substances that are then removed through urination. Toxins can then build up in your bloodstream and potentially get into your brain. Toxic buildup can also damage other organs and nerves. A complete blood count checks your red blood cells , white blood cells , and platelets. A low red blood cell count indicates blood loss and a lack of oxygen.
Blood tests may also be used to check your blood levels of sodium , potassium , and ammonia. Having too much of these substances is a sign of impaired liver function. An imaging test, such as a CT scan or MRI , can check for bleeding in your head or abnormalities in your brain.
Liver function tests check for raised enzyme levels. An increase in enzymes indicates stress on your liver or liver damage. Tell your doctor if you have kidney disease or liver disease.
Hepatic encephalopathy is divided into stages based on the severity of the symptoms. Treatment options for hepatic encephalopathy depend on the severity and underlying cause of the condition. High-protein foods to avoid include:. Medications can also help slow the rate at which your blood absorbs toxins. Your doctor may prescribe antibiotics and lactulose Enulose , a synthetic sugar.
These medications can draw ammonia, created by intestinal bacteria from your blood, into your colon. Your body will then remove the blood from your colon. In severe cases that cause difficulty breathing , a ventilator or oxygen mask may be necessary. Some people with the condition may be eligible to receive a liver transplant.
People with chronic hepatic encephalopathy have better recovery rates than those with the acute version of the condition. The rate of recovery increases if you receive treatment before the condition gets worse. The best way to prevent hepatic encephalopathy is to prevent or manage liver disease.
You can lower your chances of getting liver disease by taking these steps:. Cirrhosis is the severe scarring and poor function of the liver caused by long-term exposure to toxins such as alcohol or viral infections. This decline usually takes place over days or weeks. The most common cause of ALF is acetaminophen overdose.
Some other causes include:. Type B HE results from a portal-systemic bypass. This involves blood flowing around the liver when it would ordinarily flow to the liver.
The redirection prevents the liver from effectively filtering toxins from the blood. Type C HE results from severe scarring — cirrhosis — of the liver. Cirrhosis develops during late stage liver disease.
Over time, as scar tissue increasingly replaces healthy tissue, the liver is less able to remove toxins from the blood and perform its other functions. According to the American Liver Foundation , the most common causes of cirrhosis are:.
The following tips can help people protect their livers from disease and infection, thereby helping reduce the risk of developing HE:. In some cases, a doctor may be able to diagnose HE using these methods alone. Examples of such tests include:. Some treatments will target the underlying cause of HE. Depending on the cause, these treatments may involve:. The doctor may also prescribe medication to help reduce levels of ammonia and other toxins in the blood.
Because these toxins are often produced in the intestines, this type of treatment targets the gut. For example, the doctor may prescribe lactulose, a synthetic sugar, to speed up digestion and prevent the intestines from absorbing toxins. Lactulose also reduces the amount of ammonia-producing bacteria in the intestines. In terms of other treatments, people who experience breathing difficulty as a result of HE may require oxygen or a ventilator.
When severe liver damage or disease has caused severe HE, a person may require a liver transplant. However, most of these drugs can safely be used despite their limited proven efficacy. Metabolic ammonia scavengers : such drugs have been used for treatment of inborn errors of the urea cycle for many years. Different forms are available and now present as promising investigational agents.
Ornithine phenylacetate has been studied for HE but further clinical reports are awaited [ 96 ]. More clinical studies on the same principle are under way and, if confirmed, may lead to clinical recommendations. Oral supplementation with LOLA is ineffective. Probiotics : a recent open-label study of either lactulose, probiotics or no therapy in cirrhosis patients who recovered from HE found fewer episodes of HE in the lactulose or probiotic arms compared to placebo, but were no different between either intervention.
There was no difference in rates of readmission in any of the arms of the study [ 99 ]. Flumazenil : this drug is not frequently used. It transiently improves the mental status in overt HE without improvement in recovery or survival. The effect may be of importance in marginal situations to avoid assisted ventilation.
Likewise, the effect may be helpful in difficult differential diagnostic situations by confirming reversibility, e. Laxatives : simple laxatives alone do not have the prebiotic properties of disaccharides, and no publications have been forthcoming on this issue.
The use of polyethylene glycol preparation [ ] needs further validation. Lactulose is frequently used for the maintenance of remission from overt HE. A single-center, open-label RCT of lactulose demonstrated less recurrence of HE in patients with cirrhosis [ ]. Rifaximin added to lactulose is the best documented agent to maintain remission in patients who have already experienced one or more bouts of overt HE while on lactulose treatment after their initial episode of overt HE [ 90 ].
If it occurs, shunt diameter reduction can reverse the HE [ ]. The latter is associated with more bouts of encephalopathy [ ]. Recurrent bouts of overt HE in patients with preserved liver function consideration should lead to a search for large spontaneous portosystemic shunts.
Certain types of shunts, such as spleno-renal shunts, can be successfully embolized with rapid clearance of overt HE in a fraction of the patients in a good liver function status, despite the risk for subsequent variceal bleeding [ ].
While it is not standard to offer therapy for minimal and covert HE, several studies used a variety of agents including probiotics, lactulose and rifaximin in minimal HE. Trials span the gamut from small open-label trials to larger, randomized—controlled studies using various treatments. Most studies have shown an improvement in the underlying cognitive status but the mode of diagnosis has varied considerably among studies.
A minority of studies used clinically relevant endpoints. It was shown in an open-label study that lactulose can prevent development of the first episode of overt HE but the study needs to be replicated in a larger study in a blinded fashion before firm recommendations can be made [ ]. Studies using lactulose and rifaximin have shown improvement in quality of life [ , ] and also in driving simulator performance [ , ]. Probiotics have also been used but the open-label nature, varying amounts and types of organisms and different outcomes make them difficult to recommend as therapeutic options at this time [ — ].
Owing to the multiple methods used to define minimal and covert HE, varying endpoints, short-term treatment trials and differing agents used in trials to date, routine treatment for minimal HE is not recommended at this stage.
Modulation of nitrogen metabolism is crucial to the management of all grades of HE and nutritional options are relevant. Detailed recent guidelines for nutrition of patients with HE are given elsewhere [ ]. Sarcopenia has been proven to be an important negative prognostic indicator in cirrhotic patients [ ]. The therapy is refeeding by moderate hyperalimentation. Small meals evenly distributed throughout the day and a late-night snack [ ] should be encouraged, with avoidance of fasting.
The hyperalimentation should be given orally to patients who can cooperate, by gastric tube to patients who cannot take the required amount and parenterally to other patients.
There is consensus that low protein nutrition should be avoided for patients with HE. Some degree of protein restriction may be inevitable in the first few days of overt HE treatment but should not be prolonged. National Center for Biotechnology Information , U. Journal List Gastroenterol Rep Oxf v. Gastroenterol Rep Oxf. Published online Apr Peter Ferenci. Author information Article notes Copyright and License information Disclaimer.
Corresponding author. Email: ta. Received Mar 16; Accepted Mar For commercial re-use, please contact journals. This article has been cited by other articles in PMC. Abstract Hepatic encephalopathy HE is a reversible syndrome of impaired brain function occurring in patients with advanced liver diseases.
Keywords: Hepatic encephalopathy, pathophysiology, diagnostic tests, management strategy. Introduction Hepatic encephalopathy HE or portosystemic encephalopathy PSE is a reversible syndrome of impaired brain function occurring in patients with advanced liver failure.
Pathogenesis In spite of more than years of research, the pathogenesis of HE is still not well understood. Neurotoxins Ammonia is the best characterized neurotoxin linked to HE. Impairment of neurotransmission Several neurotransmitter systems have been studied in various experimental models of mostly acute liver failure, including investigations of neurochemical, neurobehavioral and electro phy si ological methods. Systemic response to infections and neuroinflammation Other possible causes of brain dysfunction include alterations in cerebral blood flow, brain metabolites and the release of inflammatory mediators; importantly, these processes occur without the direct infection of brain tissue [ 9 , 26 ].
Clinical presentation HE produces a wide spectrum of nonspecific neurological and psychiatric manifestations [ 34 ]. Classification HE should be classified according to all of the following four factors [ 50 ]: According to the underlying disease: Type A due to a cute liver failure; Type B due predominantly to portosystemic bypass or shunting; Type C due to c irrhosis.
Table 1. West-Haven criteria WHC for hepatic encephalopathy and clinical description. Open in a separate window. Diagnosis and testing Judging and measuring the severity of HE is approached as a continuum [ 64 ]. Diagnosis and testing for overt HE The diagnosis of overt HE is based on a clinical examination and a clinical decision.
Testing for minimal and covert HE Minimal and covert HE is defined as the presence of test-dependent or clinical signs of brain dysfunction in patients with chronic liver disease who are not disoriented or display asterixis. The most established testing strategies are: Portosystemic encephalopathy PSE —Syndrome—Test consists of five paper—pencil tests that evaluate cognitive and psychomotor processing speed and visuomotor coordination.
Laboratory testing High blood ammonia levels alone do not add any diagnostic, staging or prognostic value in HE patients with chronic liver disease [ 80 ]. Treatment General principles At this time, only overt HE is routinely treated [ 10 ].
Therapy for episodes of overt HE In addition to the other elements of the four-pronged approach to treatment of HE, specific drug treatment is part of the management. Non-absorbable disaccharides Lactulose is usually used as initial treatment for overt HE [ 82 ]. Antibiotics Rifaximin has been used for the therapy of HE in a number of trials comparing it with placebo, other antibiotics, non-absorbable disaccharides and in dose-ranging studies [ 89 ].
Other therapies Many drugs have been used for treatment of HE but data to support their use are limited, preliminary or lacking.
Treatment of minimal and covert HE While it is not standard to offer therapy for minimal and covert HE, several studies used a variety of agents including probiotics, lactulose and rifaximin in minimal HE. Nutrition Modulation of nitrogen metabolism is crucial to the management of all grades of HE and nutritional options are relevant. Conflict of interest statement : none declared.
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