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Background
Portosystemic encephalopathy is also known as hepatic encephalopathy. It is a neurological disease. It occurs due to the complication of liver dysfunction. It can be identified by the neuropsychiatric symptoms from mild cognitive impairment to severe neurological dysfunction. The conditions which are associated with the accumulation of toxins, ammonia in the blood. Affected liver cannot eliminate those substances. Factors like gastrointestinal bleeding, infections, electrolyte imbalances and medications can trigger worsen portosystemic encephalopathy.
Epidemiology
Cirrhosis is a liver disease. It is the major cause of the death between 45 to 55 years of age in America. It is more common in populations with high chronic liver disease. The factors which lead to portosystemic encephalopathy are like alcohol consumption, viral hepatitis and metabolic syndrome. The risk increases with age. Males are high risk of liver diseases as per the studies. Portosystemic encephalopathy is a major cause of hospitalizations with cirrhosis. Patients may be admitted for episodes of encephalopathy or complications related to liver disease. The death rate depends on the severity of the disease and effectiveness of the treatment. In severe cases, it leads to the coma and death.
Anatomy
Pathophysiology
Hepatic encephalopathy is caused by the increased level of the blood ammonia. It is affected by the like tyramine, mercaptans, octopamine, GABA, and manganese. The process to determine blood ammonia levels is complex because of the various organ reactions. Ammonia metabolism occurs in the gastrointestinal tract, liver, muscles, kidney, and brain. The urea cycle retains the majority of ammonia released during amino acid metabolism. It leads to the abnormal blood ammonia. Liver eliminates most of the ammonia from the gastrointestinal tract in healthy individuals. People with liver cirrhosis or trans jugular shunts miss the early metabolic process of ammonia. It leads to the hyperammonemia. This increases the ammonia level and accumulates in the brain cells. This leads to the neuropsychiatric syndrome associated with hepatic encephalopathy.
Etiology
Liver Cirrhosis:Â The main cause of portosystemic encephalopathy is liver cirrhosis. It is caused by the severe scarring of the liver tissue. Cirrhosis is associated with the chronic liver diseases like chronic vital hepatitis B and C, alcoholic liver disease, non-alcoholic fatty liver disease (NAFLD) and autoimmune liver diseases.
Portal Hypertension:Â Cirrhosis leads to increased pressure in the portal vein. It is known as portal hypertension. This increased pressure can cause the portosystemic shunts formation.
Bacterial Overgrowth and Toxin Production:Â Patients who have cirrhosis and portal hypertension are at the increased risk of the bacterial overgrowth in the small intestine. This can lead to the production of the neurotoxins like ammonia, short-chain fatty acids and mercaptans.
Ammonia Buildup:Â Ammonia is the main substance for the prognosis of the portosystemic encephalopathy. Impaired liver function leads to an accumulation of ammonia in the blood. Increased level of the ammonia is associated with the neurotoxicity. It contribute to the cognitive and neurological symptoms of portosystemic encephalopathy.
Genetics
Prognostic Factors
Hepatic encephalopathy has a poor prognosis. It reduces the survival rate. The recurrence of the disease affects the quality of the patient life.
Clinical History
Portosystemic encephalopathy (PSE) is a neurological condition. The associated symptoms include including cognitive impairment, motor dysfunction, and sleep disturbances. It is often linked to a liver disease like cirrhosis. The clinical history of the patient is necessary to understand the liver disease etiology, duration and risk factors. Some people have intermittent or reversible episodes and some have chronic encephalopathy. The duration of the episode is affected by the liver disease and the effectiveness of the management.
Physical Examination
Patients with this disease may have symptoms like confusion, impaired orientation, difficulty concentrating, cognitive impairments from mild to severe. Neurological symptoms like fine tremors in the hand and asterixis. This indicates the neurological dysfunction. Patient may feel difficulty in motor skills like writing or buttoning a shirt. Muscle tone may increase. Articulation affects and this can lead to the slurred speech. Behavioral and personality changes, mood swings may occur. A musty or sweet odor may be present because of the volatile substances.
Age group
Associated comorbidity
Associated activity
Acuity of presentation
Differential Diagnoses
Laboratory Studies
Imaging Studies
Procedures
Histologic Findings
Staging
Treatment Paradigm
Hepatic encephalopathy (HE) is a serious condition. It leads to the severe health issues. The treatment involves like lactulose. It can reduce the risk of recurrence to 50%. If lactulose is intolerance, rifaximin is used as an alternative. Combination of the lactulose and rifaximin can reduce the recurrence. The main goal is to identify and eliminate the shunt. The main approach is to manage and prevent the future HE. Regular monitoring and adjustments can improve the overall health.
by Stage
by Modality
Chemotherapy
Radiation Therapy
Surgical Interventions
Liver transplantation is used to replace a damaged liver with a healthy liver. It is used for the patient who has advanced liver disease like cirrhosis. The procedure involves the assessment of medical and psychological factors. This will ensure that the patient is suitable for the procedure. The procedure may involve the whole liver transplant or partial liver transplant.
Hormone Therapy
Immunotherapy
Hyperthermia
Photodynamic Therapy
Stem Cell Transplant
Targeted Therapy
Palliative Care
use-of-non-pharmacological-approach
Patient who has hepatic encephalopathy should take the snacks between meals and before the bedtime. It reduces the gluconeogenesis and protein catabolism. They should reduce the meat protein intake and increase the milk protein. High fiber is also suggested. Vitamin and mineral supplements and probiotics are also suggested
Role of Antibiotics
Role of Zinc
primary-prophylaxis-phase
Primary prophylaxis for HE includes treatments like avoid alcohol, antiviral drugs administration, proper nutrition intake, manage the overload of iron. Gliading with non-absorbable disaccharides or mannitol can reduce the risk of HE.
secondary-prophylaxis-phase
This treatment is recommended to those who are at the high risk of this disease. Lactulose is used to reduce the risk by 50%. If lactulose is intolerance, rifaximin is used as an alternative. Combination of the lactulose and rifaximin can reduce the recurrence. The main goal is to identify and eliminate the shunt.
Medication
Future Trends
Portosystemic encephalopathy is also known as hepatic encephalopathy. It is a neurological disease. It occurs due to the complication of liver dysfunction. It can be identified by the neuropsychiatric symptoms from mild cognitive impairment to severe neurological dysfunction. The conditions which are associated with the accumulation of toxins, ammonia in the blood. Affected liver cannot eliminate those substances. Factors like gastrointestinal bleeding, infections, electrolyte imbalances and medications can trigger worsen portosystemic encephalopathy.
Cirrhosis is a liver disease. It is the major cause of the death between 45 to 55 years of age in America. It is more common in populations with high chronic liver disease. The factors which lead to portosystemic encephalopathy are like alcohol consumption, viral hepatitis and metabolic syndrome. The risk increases with age. Males are high risk of liver diseases as per the studies. Portosystemic encephalopathy is a major cause of hospitalizations with cirrhosis. Patients may be admitted for episodes of encephalopathy or complications related to liver disease. The death rate depends on the severity of the disease and effectiveness of the treatment. In severe cases, it leads to the coma and death.
Hepatic encephalopathy is caused by the increased level of the blood ammonia. It is affected by the like tyramine, mercaptans, octopamine, GABA, and manganese. The process to determine blood ammonia levels is complex because of the various organ reactions. Ammonia metabolism occurs in the gastrointestinal tract, liver, muscles, kidney, and brain. The urea cycle retains the majority of ammonia released during amino acid metabolism. It leads to the abnormal blood ammonia. Liver eliminates most of the ammonia from the gastrointestinal tract in healthy individuals. People with liver cirrhosis or trans jugular shunts miss the early metabolic process of ammonia. It leads to the hyperammonemia. This increases the ammonia level and accumulates in the brain cells. This leads to the neuropsychiatric syndrome associated with hepatic encephalopathy.
Liver Cirrhosis:Â The main cause of portosystemic encephalopathy is liver cirrhosis. It is caused by the severe scarring of the liver tissue. Cirrhosis is associated with the chronic liver diseases like chronic vital hepatitis B and C, alcoholic liver disease, non-alcoholic fatty liver disease (NAFLD) and autoimmune liver diseases.
Portal Hypertension:Â Cirrhosis leads to increased pressure in the portal vein. It is known as portal hypertension. This increased pressure can cause the portosystemic shunts formation.
Bacterial Overgrowth and Toxin Production:Â Patients who have cirrhosis and portal hypertension are at the increased risk of the bacterial overgrowth in the small intestine. This can lead to the production of the neurotoxins like ammonia, short-chain fatty acids and mercaptans.
Ammonia Buildup:Â Ammonia is the main substance for the prognosis of the portosystemic encephalopathy. Impaired liver function leads to an accumulation of ammonia in the blood. Increased level of the ammonia is associated with the neurotoxicity. It contribute to the cognitive and neurological symptoms of portosystemic encephalopathy.
Hepatic encephalopathy has a poor prognosis. It reduces the survival rate. The recurrence of the disease affects the quality of the patient life.
Portosystemic encephalopathy (PSE) is a neurological condition. The associated symptoms include including cognitive impairment, motor dysfunction, and sleep disturbances. It is often linked to a liver disease like cirrhosis. The clinical history of the patient is necessary to understand the liver disease etiology, duration and risk factors. Some people have intermittent or reversible episodes and some have chronic encephalopathy. The duration of the episode is affected by the liver disease and the effectiveness of the management.
Patients with this disease may have symptoms like confusion, impaired orientation, difficulty concentrating, cognitive impairments from mild to severe. Neurological symptoms like fine tremors in the hand and asterixis. This indicates the neurological dysfunction. Patient may feel difficulty in motor skills like writing or buttoning a shirt. Muscle tone may increase. Articulation affects and this can lead to the slurred speech. Behavioral and personality changes, mood swings may occur. A musty or sweet odor may be present because of the volatile substances.
Hepatic encephalopathy (HE) is a serious condition. It leads to the severe health issues. The treatment involves like lactulose. It can reduce the risk of recurrence to 50%. If lactulose is intolerance, rifaximin is used as an alternative. Combination of the lactulose and rifaximin can reduce the recurrence. The main goal is to identify and eliminate the shunt. The main approach is to manage and prevent the future HE. Regular monitoring and adjustments can improve the overall health.
Liver transplantation is used to replace a damaged liver with a healthy liver. It is used for the patient who has advanced liver disease like cirrhosis. The procedure involves the assessment of medical and psychological factors. This will ensure that the patient is suitable for the procedure. The procedure may involve the whole liver transplant or partial liver transplant.
Patient who has hepatic encephalopathy should take the snacks between meals and before the bedtime. It reduces the gluconeogenesis and protein catabolism. They should reduce the meat protein intake and increase the milk protein. High fiber is also suggested. Vitamin and mineral supplements and probiotics are also suggested
Primary prophylaxis for HE includes treatments like avoid alcohol, antiviral drugs administration, proper nutrition intake, manage the overload of iron. Gliading with non-absorbable disaccharides or mannitol can reduce the risk of HE.
This treatment is recommended to those who are at the high risk of this disease. Lactulose is used to reduce the risk by 50%. If lactulose is intolerance, rifaximin is used as an alternative. Combination of the lactulose and rifaximin can reduce the recurrence. The main goal is to identify and eliminate the shunt.
Portosystemic encephalopathy is also known as hepatic encephalopathy. It is a neurological disease. It occurs due to the complication of liver dysfunction. It can be identified by the neuropsychiatric symptoms from mild cognitive impairment to severe neurological dysfunction. The conditions which are associated with the accumulation of toxins, ammonia in the blood. Affected liver cannot eliminate those substances. Factors like gastrointestinal bleeding, infections, electrolyte imbalances and medications can trigger worsen portosystemic encephalopathy.
Cirrhosis is a liver disease. It is the major cause of the death between 45 to 55 years of age in America. It is more common in populations with high chronic liver disease. The factors which lead to portosystemic encephalopathy are like alcohol consumption, viral hepatitis and metabolic syndrome. The risk increases with age. Males are high risk of liver diseases as per the studies. Portosystemic encephalopathy is a major cause of hospitalizations with cirrhosis. Patients may be admitted for episodes of encephalopathy or complications related to liver disease. The death rate depends on the severity of the disease and effectiveness of the treatment. In severe cases, it leads to the coma and death.
Hepatic encephalopathy is caused by the increased level of the blood ammonia. It is affected by the like tyramine, mercaptans, octopamine, GABA, and manganese. The process to determine blood ammonia levels is complex because of the various organ reactions. Ammonia metabolism occurs in the gastrointestinal tract, liver, muscles, kidney, and brain. The urea cycle retains the majority of ammonia released during amino acid metabolism. It leads to the abnormal blood ammonia. Liver eliminates most of the ammonia from the gastrointestinal tract in healthy individuals. People with liver cirrhosis or trans jugular shunts miss the early metabolic process of ammonia. It leads to the hyperammonemia. This increases the ammonia level and accumulates in the brain cells. This leads to the neuropsychiatric syndrome associated with hepatic encephalopathy.
Liver Cirrhosis:Â The main cause of portosystemic encephalopathy is liver cirrhosis. It is caused by the severe scarring of the liver tissue. Cirrhosis is associated with the chronic liver diseases like chronic vital hepatitis B and C, alcoholic liver disease, non-alcoholic fatty liver disease (NAFLD) and autoimmune liver diseases.
Portal Hypertension:Â Cirrhosis leads to increased pressure in the portal vein. It is known as portal hypertension. This increased pressure can cause the portosystemic shunts formation.
Bacterial Overgrowth and Toxin Production:Â Patients who have cirrhosis and portal hypertension are at the increased risk of the bacterial overgrowth in the small intestine. This can lead to the production of the neurotoxins like ammonia, short-chain fatty acids and mercaptans.
Ammonia Buildup:Â Ammonia is the main substance for the prognosis of the portosystemic encephalopathy. Impaired liver function leads to an accumulation of ammonia in the blood. Increased level of the ammonia is associated with the neurotoxicity. It contribute to the cognitive and neurological symptoms of portosystemic encephalopathy.
Hepatic encephalopathy has a poor prognosis. It reduces the survival rate. The recurrence of the disease affects the quality of the patient life.
Portosystemic encephalopathy (PSE) is a neurological condition. The associated symptoms include including cognitive impairment, motor dysfunction, and sleep disturbances. It is often linked to a liver disease like cirrhosis. The clinical history of the patient is necessary to understand the liver disease etiology, duration and risk factors. Some people have intermittent or reversible episodes and some have chronic encephalopathy. The duration of the episode is affected by the liver disease and the effectiveness of the management.
Patients with this disease may have symptoms like confusion, impaired orientation, difficulty concentrating, cognitive impairments from mild to severe. Neurological symptoms like fine tremors in the hand and asterixis. This indicates the neurological dysfunction. Patient may feel difficulty in motor skills like writing or buttoning a shirt. Muscle tone may increase. Articulation affects and this can lead to the slurred speech. Behavioral and personality changes, mood swings may occur. A musty or sweet odor may be present because of the volatile substances.
Hepatic encephalopathy (HE) is a serious condition. It leads to the severe health issues. The treatment involves like lactulose. It can reduce the risk of recurrence to 50%. If lactulose is intolerance, rifaximin is used as an alternative. Combination of the lactulose and rifaximin can reduce the recurrence. The main goal is to identify and eliminate the shunt. The main approach is to manage and prevent the future HE. Regular monitoring and adjustments can improve the overall health.
Liver transplantation is used to replace a damaged liver with a healthy liver. It is used for the patient who has advanced liver disease like cirrhosis. The procedure involves the assessment of medical and psychological factors. This will ensure that the patient is suitable for the procedure. The procedure may involve the whole liver transplant or partial liver transplant.
Patient who has hepatic encephalopathy should take the snacks between meals and before the bedtime. It reduces the gluconeogenesis and protein catabolism. They should reduce the meat protein intake and increase the milk protein. High fiber is also suggested. Vitamin and mineral supplements and probiotics are also suggested
Primary prophylaxis for HE includes treatments like avoid alcohol, antiviral drugs administration, proper nutrition intake, manage the overload of iron. Gliading with non-absorbable disaccharides or mannitol can reduce the risk of HE.
This treatment is recommended to those who are at the high risk of this disease. Lactulose is used to reduce the risk by 50%. If lactulose is intolerance, rifaximin is used as an alternative. Combination of the lactulose and rifaximin can reduce the recurrence. The main goal is to identify and eliminate the shunt.

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