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ALF remains associated with high morbidity and mortality, largely driven by profound metabolic instability, systemic inflammation, and multiorgan dysfunction. The liver's central role in carbohydrate, protein, and lipid metabolism makes metabolic derangements an early and defining feature of ALF. Hypoglycemia, hyperlactatemia, and hyperammonemia reflect impaired hepatic bioenergetic and detoxifying capacity and directly contribute to cerebral edema, intracranial hypertension, and neurological deterioration. Simultaneously, a cytokine-mediated hypercatabolic state promotes accelerated skeletal muscle wasting and alters amino acid homeostasis, further complicating nutritional management. Lipid metabolism is also profoundly disrupted, with reduced lipoprotein synthesis, altered fatty acid profiles, and impaired innate immune functions. In parallel, intestinal barrier dysfunction and gut microbiota dysbiosis exacerbate systemic inflammation through bacterial translocation and endotoxemia, reinforcing the gut\u2013liver axis as a key modulator of disease severity. Nutritional support therefore represents a cornerstone of intensive care management in ALF, extending beyond caloric provision to influence metabolic control, immune competence, and neurological safety. This review provides a practical, evidence-based framework for nutritional management of patients with ALF admitted to the intensive care unit. Key aspects discussed include assessment of energy expenditure, timing and route of nutritional support, macronutrient composition, and the management of micronutrient deficiencies. Particular attention is given to balancing protein delivery against the risk of hyperammonemia, optimizing glucose control to avoid neurological harm, and selecting lipid formulations that minimize proinflammatory effects. Nutritional therapy in ALF must be individualized, dynamically reassessed, and closely integrated with hemodynamic stabilization, renal replacement therapy, and neuroprotective strategies. 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