Liver Dysfunction in Patients with Neurotrauma

Traumatic brain injury (TBI) has emerged as a leading cause of morbidity and mortality around the world, often instigating systemic complications. An underappreciated consequence of TBI is hepatic dysfunction, which can potentiate neuroinflammation and worsen the patient's prognosis. This mini-review describes how neurotrauma drives liver dysfunction mechanisms, alongside the involvement of the systemic inflammatory response and possible treatment modalities to prevent secondary organ injury. A literature review was performed to assess current evidence on TBI-induced hepatic dysfunction, inflammatory mediators, and liver–brain interactions. Neurotrauma activates the systemic acute-phase response that brings hepatocellular injury, metabolic disruption, and immune dysfunction. Changes in the gut–liver–brain axis, an increase of oxidative stress, and changes in cytokine signaling altogether result in secondary liver injury following TBI. Liver dysfunction should be considered a secondary complex consequent with TBI to derive better management for patients. Future studies should be directed toward brain–liver axis-targeted therapeutic interventions to manage systemic inflammatory responses.