The Treatment of Hepatic Encephalopathies – Gastrointestinal System Example

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"The Treatment of Hepatic Encephalopathies" is a great example of a paper on the gastrointestinal system.   The liver is one of the most important organs of the body involved in the metabolism of substances and detoxification. It has an interaction with the major bodily systems including the central nervous system. It detoxifies substances that are produced in the brain as well as other organs which can be harmful and disrupt the normal functioning of the body. Thus any alterations in the functioning of the liver can also affect the working of the major systems of the body which includes the central nervous system (Butterworth 2003).

Hepatic encephalopathy is one such pathology that affects the central nervous system due to the inability of the liver to detoxify ammonia which leads to an increase in its levels and hence this affects the functioning of the brain. “ Hepatic encephalopathy is regarded as a disorder of neurotransmission in the central nervous system and neuromuscular system” (Butterworth 2005). It results in neurologic symptoms which include altered levels of staying conscious and the patient is confused and in further stages, this may proceed to coma and then death (Kumar et al 2005).                       Hepatic encephalopathy occurs due to loss of proper functioning of the liver which may be due to alcohol consumption which may result in hepatitis, fibrosis, or cirrhosis of the liver.

This leads to a decreased number of cells in the liver and hence the liver is unable to perform its functions efficiently which includes the function of detoxification. Another mechanism is known as “ portal-systemic shunting” might also result in which the blood does not enter the liver through the portal vein due to its decreased function and it rather enters directly into the circulation which causes an increase in the toxic metabolites leading to an increase in their levels (Butterworth 2003).

Other factors that may aggravate the condition include loss of renal function, bleeding with the gastrointestinal tract, and due to certain medications which include benzodiazepines and diuretics (Cash et al 2010).                       Electroencephalography (EEG) is one of the tests used in the diagnosis of this condition and research by Bucci et al in the year 1991 has served to prove the fact that EEG pattern alterations are seen in hepatic encephalopathy.

Hepatic encephalopathy is categorized into 5 stages starting from stage 0 to stage with stage 0 showing no symptoms and stage 4 representing the stage when the patient goes in a coma. Electroencephalography is not useful in the initial stages of the disease but it is only of assistance in the later stages (Davies et al 2001). There are believed to be decreased waves of the brain noticed in the electroencephalography (Butterworth 2003).

In stage 0 EEG does not present with any disturbances despite the fact that encephalopathy might be there at a very low level. In the following three stages that are 1, 2, and 3 disturbances are seen in the form of waves which are triphasic waves. These are found in the frontal section of the brain with a frequency of 5 Hz. In the final stage of hepatic encephalopathy, the EEG pattern shows delta waves which have a reduced frequency (Cash et al 2010). Hepatic encephalopathy has neurologic presentations along with other signs and symptoms.

It leads to alterations in the sleeping patterns along with altered mood as well changes are seen in the personality of the patient. The ability to concentrate also decreases and depressive disorders might also accompany the condition. Asterixis is also observed which results due to alterations in the functioning of the motor system. This is basically a “ flapping tremor” . The diagnosis of the condition can be done by confirming the presence of previous liver pathologies along with the results of electroencephalography. Tests that assess the motor functioning of the patients should also be performed.

The patient has decreased attentiveness and alertness. The smell of the breath of the patient is also bad due to the liver condition and the breathing rate is also high along with the presence of high levels of ammonia in the blood (Butterworth 2003). The treatment of hepatic encephalopathy requires many measures. The patient should be intubated via the nasogastric tube for the provision of diet if he is suffering from severe hepatic encephalopathy. It is also essential that a proper diet is to be given with amino acids which are branched so that the patient gets the right amount of energy.

Lactulose is another form of treatment that is given to the patients because it is a sugar that is not absorbed from the gastrointestinal tract and it also relieves constipation which is considered to be one of the reasons that lead to the condition.   Antibiotics are also employed for the treatment of the condition with rifaximin being the treatment of choice (Cash et al 2010). Research has also proved the fact that treatment with rifaximin has been very helpful in the management of the condition resulting in a reduction in hospital admissions as well as episodes of hepatic encephalopathy (Bass et al 2010).

Treatment with LOLO which is a combination therapy of L-ornithine and L- aspartate is also useful in this condition (Cash et al 2010). In cirrhosis, liver transplantation is considered to be the last treatment of choice which can increase life expectancy (Blei et al 2001).             The prognosis of hepatic encephalopathy is not considered to be very good.

Though it is believed that it can be cured by treating the underlying liver disease which leads to it (Kumar et al 2005) but a research conducted by Bustamante and his colleagues in the year 1999 concluded the fact that patients who develop hepatic encephalopathy as a result of liver cirrhosis do not have a very good prognosis rate. According to the research, 74 percent of the patients following treatment did not survive. There are major factors which are associated with the decreased rate of prognosis with a greater preponderance towards males and high levels of certain substances which include serum bilirubin, the enzyme alkaline phosphatase, as well as raised potassium ions and the level of blood urea nitrogen, are also related to lower rates of treatment success.

The lower success rate of treatment is also seen if the levels of albumin in the serum are low and the action of prothrombin is also reduced. The research also presented the fact that if the liver is transplanted in the patients of cirrhosis who have hepatic encephalopathy the prognosis may be improved (Bustamante et al 1999).

References

Bass, NM, KD Mullen, A Sanyal, F Poordad, G Neff, CB Leevy, S Sigal, MY Sheikh, K Beavers, T Frederick, L Teperman, D Hillebrand, S Huang, K Merchant, A Shaw, E Bortey, and WP Forbes. "Rifaximin Treatment in Hepatic Encephalopathy." The New England Journal of Medicine. 362.12 (2010): 1071-81. Print.

Blei, Andres T, and Juan Córdoba. "Hepatic Encephalopathy." American Journal of Gastroenterology. 96.7 (2001): 1968-1976. Print.

Bucci, L, and R Chiaverelli. "Hepatic Encephalopathy Eeg and Octopamine." The Journal of Clinical Psychiatry. 41.5 (1980): 175-7. Print.

Bustamante, J, A Rimola, PJ Ventura, M Navasa, I Cirera, V Reggiardo, and J Rodés. "Prognostic Significance of Hepatic Encephalopathy in Patients with Cirrhosis."Journal of Hepatology. 30.5 (1999): 890-5. Print.

Butterworth, Roger F. "Hepatic Encephalopathy." Alcohol Research & Health : the Journal of the National Institute on Alcohol Abuse and Alcoholism. 27.3 (2003): 240. Print.

Butterworth, RF. "Complications of Cirrhosis Iii. Hepatic Encephalopathy." Journal of Hepatology. 32.1 (2000): 171-80. Print.

Cash, WJ, P McConville, E McDermott, PA McCormick, ME Callender, and NI McDougall. "Current Concepts in the Assessment and Treatment of Hepatic Encephalopathy." Qjm : Monthly Journal of the Association of Physicians. 103.1 (2010): 9-16. Print.

Davies, MG, MJ Rowan, and J Feely. "Eeg and Event Related Potentials in Hepatic Encephalopathy." Metabolic Brain Disease. 6.4 (1991): 175-86. Print.

Kumar, Vinay, Abul K. Abbas, Nelson Fausto, Stanley L. Robbins, and Ramzi S. Cotran. Robbins and Cotran Pathologic Basis of Disease. Philadelphia: Elsevier Saunders, 2005. Print.

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