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Importance Floppy eyelid syndrome "plasty" (FESplasty) is a surgical technique that addresses underlying superior tarsal plate and lateral canthal instability in floppy eyelid syndrome (FES) and aims to restore normal anatomical and physiological function to the upper eyelid. Background To describe the use of FESplasty in the surgical management of FES, and to report outcomes in an initial patient cohort. Design Retrospective study. Participants Seven patients (nine eyelids) with FES undergoing FESplasty. Methods A single surgeon (G.W.) performed all procedures. FESplasty utilizes a periosteal flap based at the inferolateral orbital rim, and applied to the anterior surface of the upper tarsal plate. It is combined with a titrated shortening procedure of the upper eyelid. Patient demographics, comorbidities and ocular symptoms and signs were recorded preoperatively. Pre- and postoperative upper eyelid distractibility were graded and documented. Main outcome measures Postoperative improvement in upper eyelid distractibility and symptomatology, operative complications and FES recurrence. Results FES symptoms and upper eyelid laxity improved at last follow-up (average 24 weeks) in all patients, with no FES recurrences after a maximum follow-up of 36 weeks. One patient, in whom FESplasty exacerbated his pre-existing aponeurotic ptosis, required definitive ptosis surgery subsequently. There was one case of postoperative wound infection. Obstructive sleep apnoea was present in four of the seven patients. The remaining three patients were awaiting assessment. Conclusions and relevance FESplasty is likely to confer long-term effective stabilization of the lateral canthal tendon, lateral commissure and superior tarsal plate. Anatomical and functional results appeared to have been successfully achieved.

Necrotising fasciitis is a fulminant, rapidly progressive infection associated with extensive tissue destruction and significant mortality. Given the robust blood supply of the face, periorbital necrotising fasciitis is rare in this region. Traditional management consists of prompt initiation of antibiotics and adequate surgical debridement. This report documents the outcome of Type 2 periorbital necrotising fasciitis in a 49-year-old, immunocompetent man, in whom negative pressure wound therapy, was combined with conventional measures. The negative pressure wound therapy was applied directly to the involved orbit, suggesting its safety and efficacy in relation to use over the orbit. Negative pressure wound therapy may be a useful adjunct to the armamentarium of the oculoplastic surgeon for the reconstruction of periorbital defects produced by the surgical debridement of periorbital necrotising fasciitis.

Compression of anterior visual pathway (AVP) structures by intracranial arteries is observed not infrequently on neuroimaging. Whether or not such compression results in damage to these structures, however, remains unclear. This information is important to define as AVP compression by intracranial arteries may be a causative factor in patients with otherwise unexplained visual dysfunction. In a single centre, 37 patients with evidence of intracranial artery AVP compression demonstrated on magnetic resonance imaging were identified by retrospective review of case records over the period 2011–2017. Variables were collected, including patient demographics, visual acuity, visual fields, pupillary reactions and optic disc appearance for patients in the case series. Visual field deficits correlated with compression sites in the 37 patients examined. Internal carotid artery-optic nerve compression was the most frequent (unilateral compression n = 9, bilateral compression n = 14), followed by chiasmal compression by the anterior cerebral artery (n = 8) and a combination of optic nerve and chiasmal compression (n = 5). Visual acuity and visual fields were stable on follow-up (mean 4 years) in 24 of 26 cases (93%). We conclude that AVP compression by intracranial arteries may be a causative factor in unexplained visual dysfunction. The visual defects are largely non-progressive.