VIRAL ENCEPHALITIS: STABILIZATION AND SUPPORT PROTOCOLS IN THE INTENSIVE CARE UNIT

Abstract

Viral encephalitis (VE) represents a critical neurological emergency, with herpes simplex virus type 1 (HSV-1) being a prevalent pathogen associated with high mortality rates and sequelae, despite standard antiviral therapy with acyclovir. The pathophysiology is complex and dynamic, involving direct neuronal damage, regulated cell death pathways such as ferroptosis, and an exacerbated host immunoinflammatory response mediated by Toll-like receptors. Management in Intensive Care Units (ICUs) requires not only control of viral replication but also management of secondary complications such as cerebral edema and prevention of persistent post-virological neuronal injury. The narrative literature review points to the inadequacy of acyclovir in preventing structural damage and highlights injury mechanisms such as Tumor Necrosis Factor (TNF) activation and virus-induced ferroptosis. The use of adjuvant corticosteroids remains controversial, with no significant reduction in mortality in meta-analyses, but with possible functional benefit in subgroups (HSV-1 encephalitis). The use of intravenous immunoglobulin (IVIg) lacks robust evidence from controlled clinical trials. There is a trend towards abandoning the therapeutic model focused exclusively on viral suppression in favor of an approach that considers inflammatory modulation, neuroprotection (such as ferroptosis inhibitors), and surveillance for post-infectious autoimmune complications, such as anti-NMDAR encephalitis. Future studies are crucial to delineate the timing and efficacy of combined therapies.