Treatment of Hepatic Encephalopathy in Patients with Cirrhosis of the Liver

Abstract

The treatment of hepatic encephalopathy is predominantly an empirical approach because the process pathogenesis of this syndrome is uncertain. Many treatment trials have been published, but few fullfil the usually accepted criteria for optimum study design. Lack of placebo controls, inadequate sample size and the difficulty in assessing the severity of encephalopathy are noteworthy examples. Treatments based on reducing ammoniagenic factors in the intestinal tract and promoting urinary waste nitrogen elimination are discussed. Other forms of therapy based on the false neurotransmitter and γ-aminobutyric hypotheses are reviewed before outlining a practical approach to treatment of hepatic encephalopathy in clinical practice.

Prospective evaluation of the impact of covert hepatic encephalopathy on quality of life and sleep in cirrhotic patients

“…Hepatic encephalopathy (HE) is a frequent and devastating complication of end‐stage liver disease. It is defined as a reversible brain dysfunction which manifests with a wide spectrum of neuropsychiatric abnormalities caused by liver insufficiency and portosystemic shunting . Clinically, it includes neurological and psychiatric abnormalities ranging from subclinical alterations to coma.…”

Medical Foods from Natural Sources

“…Therefore, the glutamine content of the enteral foods was increased by about 3.5% of the total amino acids. Branched chain amino acids (BCAA) are the major skeletal muscle proteins, which help localized metabolism besides improving the liver function (Ferrando et al, 1995;Ferenci, 1996). In addition, recently, Kakazu et al (2007) have reported the immune-enhancing effect of BCAA in cirrhotic patients.…”

“…Moreover, in severely hypercatabolic conditions BCAA are utilized as a source of locally available energy in the skeletal muscle. The formulae enriched with BCAA help normalize the amino acid profile, improve protein synthesis, and maintain nitrogen balance (Ferenci, 1996). These products are often recommended for patients under major metabolic stress (Cerra et al, 1983;Mobarhan et al, 1990;Ferando et al, 1995).…”

“…While formulating enteral foods, besides the overall nutritional quality, other factors such as the nutrient density, electrolytes concentrations, content of specific nutrients such as branched chain amino acids (Bower et al, 1986;Ferrando et al, 1995;Kato and Suzuki, 2004), aromatic amino acids (Ferenci, 1996), arginine (Barbul, 1986;Farreras et al, 2005), glutamine (Souba et al, 1990;Gianotti et al, 1995;Van den Berg et al, 2005), nucleotides (Van Buren et al, 1983;Farreras et al, 2005), and shadow nutrients (Menon and Natraj, 1984) among others require considerations, depending on the requirement of patients. Similarly, the composition of lipid, namely the proportion of polyunsaturated fatty acids (PUFA) with special reference to the ratio between n-6 and n-3 fatty acids (Narshimha Rao, 1993;Turley and Strain, 1993;Grester, 1995;Roy et al, 2004;Farreras et al, 2005), structured glycerides (Sandstorm et al, 1995;Roy et al, 2004), and medium-chain triglycerides (Ledeboer et al, 1995) is required to be incorporated in appropriate proportion.…”

Probable Local Anesthetic Systemic Toxicity in a Postpartum Patient with Acute Fatty Liver of Pregnancy After a Transversus Abdominis Plane Block

“…Although she comprehended questions and was oriented to situation, time, and place, she was lethargic and was a grade 2 per the West Haven Criteria for hepatic encephalopathy. 5 The patient weighed 51 kg, and her height was 150 cm (body mass index = 22.7 kg/m 2 ). Initial laboratory tests showed white blood count 20,000/µL, hematocrit 41%, platelets 141,000/µL, international normalized ratio 4.1, fibrinogen 50 mg/dL, a 2+ proteinuria, elevated creatinine 2.1 mg/dL, hypoglycemia 48 mg/dL, direct bilirubinemia 9.0 mg/dL, aspartate aminotransferase/alanine aminotransferase 59/63 U/L, alkaline phosphatase 1000 IU/L, and ammonia 101 mg/dL.…”