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hepatic encephalopathy

Hello.  I’m making this thread for my niece Mallory that was born with PKD Polycystic Kidney Disease with fibrotic liver (recessive).  At the time of her birth, her condition was considered not to be text book. This may get a little wordy, so please bear with me. I’m aware there are threads that already exist about PKD. But due to the rarity of her condition and her present age of 23 years, I thought it was justified.  She has baffled doctors by surviving this long, since her parents were told not to expect her to live only a few years at best.
Last week, she became very ill due to a rather large bleeding varacie in her stomach.  The gastro intestinal doctor that performed the endoscopy on her said that this varacie he found was the largest he has ever encountered and was going to submit the pictures to be used in medical text books. The only option she had was the T.I.P.S. procedure, and at best it would only last for one year.  Less than a week after her T.I.P.S. procedure, she started showing signs of hepatic encephalopathy.  She is currently on a list for a liver transplant and was admitted to the hospital today due to a fever. There have been a plethora of other complications she has endured over the years that I won’t get into since I feel they are not relevant to my query here.
Initially we were told that it is possible to treat the encephalopathy with meds and diet. She has not been put on meds for this yet. I’m guessing it is because she wasn’t showing signs of it until today. It has only been a little over a week now, so we are still trying to figure a lot of things out.
I’ve been to quite a few different medical sites looking for specific information on the best foods to eat and the worst foods as well. We are aware that a low protein diet is needed, but I’ve read that there are good proteins and bad proteins, as well as good and bad fats that can/will help or hurt. My intention here is to gather specific information related to diet and nutrition relating to her current condition. If there are specific foods to be eaten or avoided, certain fruits and vegetables that work better than others, vitamins and minerals that would be beneficial , either from personal and or professional experience, any help would be greatly appreciated .
B. Jones
2 Responses
Avatar universal
Energy and Protein Requirements
Protein Supplementation

The primary goal for a patient suffering from ESLD should be to maintain their weight, avoid by all means possible intentional or unintentional weight loss and sustain a diet rich in macro- and micronutrients. For reasons mentioned earlier, this effort may be considered a mission impossible.

Patients with liver cirrhosis should receive 35–40kcal/kg per day[9] with a protein intake up to 1.6g/kg per day.[1,9] For those with compensated liver cirrhosis this goal can be achieved with a normal diet without any restrictions in carbohydrates, proteins or fat. In the case of uncompensated liver cirrhosis supplementary meals are often recommended and prescribed.[27]

According to the ESPEN consensus report in 2006,[9] low-grade hepatic encephalopathy (grades I and II) is not regarded a reason for diet or protein restriction, pointing to the fact that malnutrition is certainly considered a negative prognostic factor. There is an exception, however, for those patients with severe hepatic encephalopathy (grades III and IV) who should be deprived of protein intake.[1] The above negates the longstanding belief that protein intake can easily deteriorate hepatic encephalopathy. Perhaps overuse of this restriction has been, up to now, unjustified. Two recently conducted studies in Australia in New South Wales and the Australian Capital Territory have surprisingly depicted that 58% and 36%, respectively, of the dieticians questioned continued to restrict protein intake in patients with hepatic encephalopathy one year after the 2006 ESPEN guidelines.[28] Apart from this, deprivation of food intake for long periods of time during hospitalization with the exceptions of variceal bleeding and severe hepatic encephalopathy should be avoided. Early enteral feeding should be started.[2] Physicians should also keep in mind not to deprive patients of regular meals and should organize examinations and procedures in a way that will not keep their patients starving for long. These patients are quite often hospitalized and this risk is real.

In ESLD, the liver has lost some of its capacity to synthesize and metabolize protein, glycogen and very low-density lipoprotein (VLDL). As a consequence, the liver can no longer regulate metabolism and therefore a continuous offer of nutrients is mandatory. Owen etal. have shown that an overnight fast in cirrhotic patients has lead to a metabolic state similar to that of healthy individuals after a 3-day fast.[19,20] This study is very interesting because it shows that hepatic glycogen reserves are extremely low in the affected liver and, as a consequence, an early switch to gluconeogenesis from amino acids originating from body protein is a status quo in cirrhosis. This means that in order to maintain proper body composition, the patient should receive a late evening snack to compensate for the overnight fasting period and to avoid gluconeogenesis.[29–32] Regular meals are mandatory and a program with specific meals is advisable.

Energy requirements consist of 35–40kcal/kg per day[9] with a protein intake of up to 1.2–1.6g/kg per day.[1,9] This means that a 75kg patient should ingest 2625–3000kcal per day with approximately 90–120g protein per day, which means that 360–480kcal of the total amount of energy should be of protein origin. The exact amount of protein recommended depends on the severity of malnutrition and the compliance of the affected patients. Of course, the role of the physician is to lead his patient to an anabolic state.
Carbohydrates and Fat

In the prescribed diets there should be no restriction on carbohydrate intake,[14] even in patients that suffer from diabetes mellitus or belong to the subgroup of patients with insulin resistance. This situation is not rare. In fact, 40–50% of all patients with ESLD suffer from insulin-resistant diabetes mellitus.[14,33] The exact causes differ from patient to patient with the most prominent being chronic hyperinsulinemia, an affected pancreas due to alcohol toxicity, diminished glycogen storage capacity of the liver, and impaired glucose uptake from the skeletal muscles.[14] When cirrhosis reaches levels at which 80% of hepatocytes are dysfunctional, hypoglycemia is a frequent event due to hyperinsulinemia. However, correction of hypoglycemia with glucose administration can lead to resistant hyperglycemia.[33]

Therefore, multiple meals are required in order to provide a continuous and regulated flow of nutrients. Four to six meals containing food rich in carbohydrates are recommended.[27]

Further nutritional support is needed in cirrhotic patients with ongoing alcohol abuse because of the danger of hypoglycemia due to the alcohol-induced restriction in gluconeogenesis. It is important to state that alcohol abstinence should be seriously considered. Alcohol intake not only aggravates liver function but has a potential negative role in deteriorating malnutrition. Alcohol-induced anorexia, the ingestion of empty calories, and the loss of meals are some of the reasons that alcohol should be banned for life in patients with liver diseases.

An increased absorption of fat in patients with impaired liver function can aggravate the hepatic inflammation and fibrogenesis. Fat is absorbed through the portal route[34] and consequently is directed to the liver. The rich offer of fat in combination with an impaired hepatic VLDL release can result in an increased hepatic fat storage and an already suffering liver cannot tolerate an excess fat inflow.
Enteral Versus Parenteral Feeding

Another issue that should be discussed is the method of feeding cirrhotic patients who are hospitalized. Enteral nutrition via a nasogastric tube, parenteral feeding and oral intake are used in severely ill patients with ESLD. The majority of attending physicians don't initiate enteral feeding promptly on the grounds that many of the patients start spontaneous dietary intake with amelioration of general health and liver function after a few days. Oral feeding with the addition of oral supplements is generally the rule in many hospital units as far as cirrhotic patients are concerned. As was shown by the study of Campillo etal., oral dietary intake improved after a long hospital stay with oral nutritional support and the help of a dietician within a period of 2–3 weeks in the majority of patients.[35]

However, in severely ill patients, supplemental enteral nutrition is advisable. According to the ESPEN recommendations, patients that cannot meet their caloric requirements through oral food intake, despite adequate individualized nutritional support, are candidates for supplemental enteral nutrition. Tube feeding even in the presence of esophageal varices is suggested. In patients with ascites the use of whole protein formulae and concentrated high energy formulae is recommended. Branched chain amino acid (BCAA)-enriched formulae are used in patients with hepatic encephalopathy arising during enteral nutrition.[9]

When deciding between enteral or parenteral nutrition in critically ill patients the risk of repeated vomiting or diarrhea and bronchopulmonary aspiration during feeding through a nasogastric tube[4] must be weighed against the complications of parenteral feeding. Septic complications and a supply of an excessive fluid load are often observed during total parenteral feeding.[36]

For more information.
See:  Malnutrition in End Stage Liver Disease: Recommendations and Nutritional Support


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Good luck,
Avatar universal
Rifaximin for the Prevention of Hepatic Encephalopathy Breakthrough and Hospitalization
Robert S. Brown, Jr., MD, MPH
Posting Date: August 12, 2010

Frank Cardile Professor of Medicine
Chief, Center for Liver Disease
Columbia University College of Physicians & Surgeons
NewYork-Presbyterian Hospital
New York, New York

Effective therapeutics for the prevention and management of hepatic encephalopathy (HE) are lacking. Heretofore, the only widely used drug for HE has been lactulose, which is associated with extensive adverse effects and suboptimal effectiveness. This large unmet need has prompted the desire for improved HE therapeutics, with an eye toward rifaximin (a nonabsorbable antibiotic currently approved for the treatment of traveler’s diarrhea) based on encouraging data from Europe.[1-6] A recent trial of rifaximin conducted in the United States evaluated its use during acute exacerbation of HE to determine whether the agent could effectively lower ammonia levels and other known correlates of HE (Capsule Summary).[7] Bass and colleagues[8] have now added to these findings with the current study, which is the first randomized controlled trial assessing the efficacy of rifaximin for the maintenance of HE remission—or, alternatively, for the prevention of what the researchers call “breakthrough HE episodes” (Capsule Summary).

In this large, placebo-controlled trial, 299 patients with recurrent HE who were in remission at entry were randomly assigned to receive rifaximin 550 mg twice daily or placebo for 6 months. Rifaximin significantly reduced the risk of a breakthrough HE episode—the primary endpoint—by 58%. Indeed, breakthrough HE episodes were observed in 22.1% vs 45.9% of patients in the rifaximin and placebo arms, respectively (hazard ratio [HR]: 0.42; 95% confidence interval [CI]: 0.28-0.64; P  91%) did. Therefore, the study results essentially reflect treatment with rifaximin plus lactulose vs lactulose alone, with the control arm illustrating the natural history of disease with what many clinicians consider to be the HE standard of care, lactulose monotherapy. The data show that among patients treated with lactulose alone, even with high (≥ 80%) compliance to therapy, nearly 25% ended up back in the hospital for HE-related events during a 6-month period. When considered in this light, the additional risk reduction in HE breakthrough and hospitalization conferred by the addition of rifaximin to lactulose becomes all the more impressive. Although the addition of rifaximin to the standard of care greatly improved clinical outcomes, one cannot ignore that approximately 14% of patients who received combination therapy required hospitalization for HE-related events, highlighting the need for even better therapeutics for this disabling disease.

In this same vein, this study illustrates that HE is indeed a serious disease since 20 of 299 patients (6.7%) died during 6 months of preventive treatment despite having fairly low model for end-stage liver disease (MELD) scores (≤ 24). These data imply that nearly 15% of patients with HE could die within 1 year. Therefore, the presence of HE—even in patients with low MELD scores—must be viewed as a harbinger of poor clinical outcomes, thereby necessitating prompt referral for liver transplantation in this patient population.

Despite the robust findings reported in this study, a few weaknesses must be mentioned. First, it remains unclear what additional benefit is provided by concomitant lactulose, and as a result, we cannot assess the true treatment efficacy of rifaximin monotherapy. The number of patients who were not on lactulose was too small to reach any conclusions about rifaximin use in this group. Second, this study provides no information on the efficacy of rifaximin in the sickest HE patients with the highest MELD scores (25-40)—patients who are probably most in need of preventive HE therapy. The number of patients with MELD scores between 19-25 was also too small to draw statistically significant conclusions, although the HR in this group was similar to other cohorts. Third, these data only extend out to 6 months. With any antibiotic used long term, there is concern that resistance may develop or the agent may lose its effectiveness. Although the ongoing, open-label extension phase of the trial will provide a glimpse at the longer-term efficacy and safety of rifaximin, there will be no control arm against which to compare the findings to fully gauge the long-term outcomes.

When this trial was initiated, many clinicians primarily used rifaximin as salvage therapy in patients with HE who failed or were intolerant to lactulose. However, the high failure rate of lactulose and the ability of rifaximin to dramatically decrease that failure rate in the current study will fuel interest in the potential role of rifaximin in the frontline treatment setting, likely in combination with other agents, such as lactulose. When coadministering rifaximin and lactulose, it should be further studied whether a lower dose of lactulose can be administered to minimize its adverse effects while still retaining effectiveness for the prevention of breakthrough HE and hospitalization.


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