Nutrition in Acute Liver Failure and Severe Acute Pancreatitis

Gastrointestinal activity, beyond nutrient absorption, is essential for modulating endocrine and immune function. Its impairment sets off a pathophysiological cascade involving gastroparesis, modifications in the microbiome, bacterial translocation, and an infectious stimulus to the lymphatic system, resulting in bowel edema and related ischemia-reperfusion damage. Given the close relationship between gastrointestinal function and liver and pancreatic metabolic regulation, it is significantly influenced by the nutritional approach to acute liver and pancreatic dysfunction. Acute liver failure is characterized by rapid hepatic injury, coagulopathy derangements, and hepatic encephalopathy in patients without previous liver disease. It can be categorized as hyperacute, acute, or subacute based on the speed of encephalopathy development. Encephalopathy dictates the necessity and timing of nutrition, playing a minor role in hyperacute cases. In acute and subacute grades, encephalopathy guides both the feeding route and the need for BUN monitoring to balance the risk of exacerbating encephalopathy due to hyperammonemia and the need to counter hypercatabolism-induced sarcopenia. Glucose control is crucial to offset impaired gluconeogenesis and hypoglycemia with continuous glucose infusion and prevent hyperglycemia and its consequences on intracranial pressure. Acute pancreatitis is the acute inflammation of pancreas tissue, occurring as a severe disease in 20–25% of cases. Enteral nutrition has been shown to yield better outcomes compared to parenteral nutrition. Oral feeding is preferred whenever possible, with a transition to nasogastric or nasojejunal routes based on intraabdominal pressure and neurological status, resorting to parenteral nutrition only when enteral feeding is absolutely contraindicated.