Definition

Acute liver failure (ALF) is caused by acute liver injury and is defined as follows:

• Two- to three-fold increase in transaminases, indicating acute liver injury
• Decreased liver function (coagulopathy [INR >1.5], jaundice [icterus], hepatic encephalopathy)
• No history of chronic liver disease ^1,2

Based on the time between the onset of jaundice and hepatic encephalopathy, a distinction is made between hyperacute (≤7 days), acute (8-28 days), and subacute (5-12 weeks) liver failure ². The incidence of ALF is low, with one case per 100,000 to 1,000,000 inhabitants ^3,4. In general, a distinction is made between paracetamol-induced ALF and ALF caused by other factors (e.g., hepatotoxic medications, infections, and autoimmune disorders) ². This is also important because the criteria for evaluating an emergency liver transplant differ between these two groups ¹. In severe cases, a liver transplant is often the only life-saving treatment.

Impact on Nutritional Status

Patients with ALF usually have severe disturbances in carbohydrate, protein, and lipid metabolism. Hypoglycemia often occurs due to depletion of hepatic glycogen stores, impaired hepatic gluconeogenesis, and hyperinsulinemia ⁵. Increased protein catabolism results in a 3- to 4-fold increase in plasma amino acids and hyperammonemia ⁶. Resting energy expenditure (REE) in these patients is 1.2 to 1.3 times higher than normal and comparable to other critically ill patients. Therefore, whenever possible, the exact energy requirement should be measured using indirect calorimetry ⁷. Hyponatremia is particularly common in hyperacute liver failure and is associated with increased morbidity and mortality, as well as severe ascites and increased intracranial pressure ^2,8,9. The pathogenesis of ALF is multifactorial and may involve increased antidiuretic hormone (ADH) secretion, leading to excessive water reabsorption in the kidneys ¹⁰.

Nutrient requirements of patients with acute liver failure. Adjustments are necessary for malnourished patients, physical activity and age of the patient. The weight used is the adjusted body weight (ADJ) from BMI 28, otherwise the body weight before admission to hospital. 
BW = body weight; d = day 

Aims of Nutritional Therapy

• Maintenance/improvement of nutritional status and body function
• Prevention of malnutrition and nutrient deficiencies through the administration of glucose, lipids, and trace elements
• Reduction of acidosis
• Prevention of metabolic complications: achieving euglycemia, optimizing protein synthesis rates, and preventing hyperammonemia and hypertriglyceridemia

Whenever possible, energy and protein requirements should be met through oral nutrition. If oral supplementation, snacks, or sip feeds cover less than 75% of the requirements, enteral nutrition should be initiated within five days. Complementary parenteral nutrition should be considered if enteral and/or oral nutrition together provide less than 75% of the requirement. For more details, refer to the chapter on enteral and parenteral nutrition.

General Nutrition Recommendations

Patient needs can vary significantly over the course of the disease; thus, energy requirements should ideally be determined by indirect calorimetry. Nutrient requirements are similar to those of other critically ill patients.

To prevent or treat hypoglycemia, 2-3 g glucose/kg body weight per day should be administered intravenously ⁷. An optimal protein synthesis rate can be achieved by an adequate supply of proteins or amino acids ⁷. In hyperacute patients with encephalopathy and at risk of cerebral edema, protein administration can be delayed for 24–48 hours until hyperammonemia has been controlled ¹¹.

Oral Nutrition

In cases of mild encephalopathy, food can be administered orally, provided there are no contraindications such as a lack of cough or swallowing reflex ⁷. In cases of advanced encephalopathy, nutritional therapy should be tailored individually by the treating medical team in collaboration with nutrition counseling.

Enteral and Parenteral Nutrition

Both enteral and parenteral nutrition should begin at a low rate and be gradually increased to enhance gastrointestinal tolerance and reduce the risk of metabolic complications. Enteral nutrition is usually administered via a nasogastric or nasojejunal tube ¹¹. Nasogastric nutrition should be avoided in patients with progressive encephalopathy ². The use of standard solutions for enteral and parenteral nutrition is recommended, since no study to date has shown an increased efficacy of specialized products (e.g., BCAA-rich parenteral nutrient solutions) ¹¹. Physical mixtures of LCT (long-chain triglycerides) and MCT (medium-chain triglycerides) are commonly used as lipid components in nutrient solutions ².

Monitoring

• Monitoring of blood ammonia levels should be conducted during nutritional therapy, particularly in patients in a hyperacute state with encephalopathy ¹¹.
• Any acidosis should be corrected either medically or, if necessary, through renal replacement therapy. Acidosis may be caused by an increase in blood lactate levels or by reduced acid excretion ².