Background Stevens-Johnson syndrome and toxic epidermal necrolysis are rare but severe mucocutaneous hypersensitivity reactions. Ocular involvement is common and represents one of the major determinants of long-term morbidity. Acute ocular findings, including conjunctival hyperemia, pseudomembrane formation, and corneal epithelial loss, may progress to chronic complications such as severe dry eye, lid margin keratinization, symblepharon, limbal stem cell deficiency, and irreversible visual loss. Aims This narrative review aims to summarize current evidence on the epidemiology, pathophysiology, clinical spectrum, acute management, and long-term rehabilitation of ocular involvement in Stevens-Johnson syndrome and toxic epidermal necrolysis. Methods A narrative literature review was conducted to synthesize current data on ocular involvement in Stevens-Johnson syndrome and toxic epidermal necrolysis. The review focused on mechanisms of ocular surface injury, acute and chronic clinical manifestations, therapeutic strategies, and approaches to visual rehabilitation. Results Ocular damage in Stevens-Johnson syndrome and toxic epidermal necrolysis reflects the interaction between genetic susceptibility and a T cell mediated cytotoxic response involving Fas/FasL signaling, perforin/granzyme activity, and granulysin. Early manifestations may include conjunctival inflammation, pseudomembranes, epithelial defects, and corneal involvement. Without timely intervention, these changes may lead to chronic ocular surface disease, severe dry eye, symblepharon, lid margin keratinization, limbal stem cell deficiency, corneal scarring, and permanent visual impairment. Early discontinuation of the causative drug, prompt ophthalmological assessment, targeted topical therapy, and timely amniotic membrane transplantation are central components of acute management. Chronic care focuses on preservation and reconstruction of the ocular surface. Conclusions Ocular involvement in Stevens-Johnson syndrome and toxic epidermal necrolysis requires early recognition, multidisciplinary management, and long-term ophthalmological follow-up. Timely treatment during the acute phase is essential to reduce the risk of chronic ocular sequelae and irreversible visual loss.