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Floppy eyelid syndrome: ocular and systemic associations.


Purpose of review

To summarize the ocular and systemic associations of floppy eyelid syndrome (FES) as well as provide an up-to-date review on the pathogenesis and treatment strategies.

Recent findings

Virtually all patients with FES have obstructive sleep apnea (OSA). However, a significantly lower proportion of patients with OSA have FES. Although some studies demonstrate no association between OSA and FES, almost all show at least an association with increased eyelid laxity, which may be a less severe form of FES. FES has also been associated with keratoconus (KCN) and glaucoma. Decreased corneal hysteresis has been found in FES, KCN, glaucoma, and OSA and may be related to matrix metalloproteinase (MMP) upregulation. Hypoxia-reperfusion injury, leptin resistance, and mechanical forces all may lead to increased MMP activity, contributing to elastin breakdown in the tarsus and other tissues throughout the body. Management of FES begins with investigation for OSA. Treating OSA with continuous positive airway pressure (CPAP) or surgical uvulopalatoplasty may improve FES. Surgical treatments for FES should reduce horizontal eyelid laxity while maximizing the stability of the tarsus. Collagen crosslinking may prove a helpful modality for stabilizing the tarsus in the future.


FES is associated with OSA, glaucoma, and KCN. MMP upregulation and lower corneal hysteresis have been found in these conditions, pointing toward a potential common pathogenesis.

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