Hepatic encephalopathy is a neuropsychiatric dysfunction an advanced form of the liver disease characterized by an altered level of consciousness which happens as a result of liver failure. It has profound effects on brain function, which may be sudden or gradual. It is common in 30 to 40% of patients with liver cirrhosis. In those who are able to get a liver transplant, the risk of death is less than 30% over the subsequent five years. This condition is life-threatening inducing neuropsychiatric abnormalities ranging from subclinical alterations to coma. It has the different characteristic of electroencephalographic abnormalities with increased blood ammonia level which are the most frequent manifestations. In spite of more than ten decades of medical research, the pathogenesis of hepatic encephalopathy is still not well understood.
Hepatic Encephalopathy in the USA and Their Types
In the United States, hepatic encephalopathy accounts for 22,931 cases of hospitalizations with an average stay of 8.5 days and an average cost of each stay ranging from $46,663–$63,108. The American Association for the Study of Liver Disease classified hepatic encephalopathy according to the underlying disease, the severity of clinical manifestations, and precipitating factors. They referred as A, B, and C type of hepatic encephalopathy. Type A is an acute form occur because of acute liver failure, type B is due to portosystemic shunting without any intrinsic liver disease and type C is a most life-threatening condition known as cirrhosis.
Is Hepatic Encephalopathy Life Threatening?
Hepatic encephalopathy is a reversible condition if the underlying liver disease is successfully treated. The manner of development of hepatic encephalopathy is multifactorial. Ammonia and dysregulation of the urea cycle are often associated with the cause of the disease. Nitrogenous compounds excreted by intestinal bacteria are transported to the liver through the portal circulation along with endogenous nitrogen, which enters the urea cycle. The end process is the generation of urea, which is subsequently excreted in urine. In advanced liver disease, damaged hepatocytes cause the ammonia to accumulate in the systemic circulation. This ammonia imbalance is responsible for astrocytes swelling and neuron dysfunction.
Negative Impact of The Condition
Ammonia considered as neurotoxin associated in inducing hepatic encephalopathy. It is directly involved in altering the neuronal electric activity by inhibiting the generation of both excitatory and inhibitory postsynaptic potentials and cortical hemichannels. GABA-benzodiazepine-ergic, dopaminergic, serotoninerergic and glutamate-ergic neurotransmitter systems are altered in individuals suffering from hepatic encephalopathy. 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.
Hepatic Encephalopathy Easily Manageable
Patients with higher grades of hepatic encephalopathy who are at risk need more intensive monitoring and are ideally managed in an intensive-care setting. The 90% of hepatic encephalopathy patients can be treated with just correction of the precipitating factor. In addition, specific drug treatment is part of the management. Rifaximin added to lactulose is the best-recognized agent to maintain a reduction in patients who have already experienced one or more sessions of overt hepatic encephalopathy. Neomycin, vancomycin, and metronidazole have been historically used in the setting of hepatic encephalopathy.
Nutritional Modification Can Improve Hepatic Encephalopathy
Maintaining adequate nutrition is vital in patients with hepatic encephalopathy. Protein-calorie malnutrition is commonly found in hepatic encephalopathy patients and has been associated with poor prognosis. If patients are intolerant of dietary protein, branched-chain amino acid supplementation is an alternative to consider. Multivitamin use can be considered in patients admitted for decompensated cirrhosis with the addition of specific treatments for clinically apparent vitamin deficiencies.
Conclusion
Hepatic encephalopathy disease is a reversible condition if the underlying liver disease is successfully treated on time. Early recognition of hepatic encephalopathy is essential for timely management. Liver transplant remains the only option for recurrent overt hepatic encephalopathy, which is the indication of liver failure.
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