Abstract ID: 26-263
Changing Concepts on the Etiology and Management of Involutional Entropion
Author: Philip Custer Base Hospital / Institution: WashU Medicine, St louis, MO, USA
Presentation Type: Video Presentation
Purpose
Involutional entropion has traditionally been attributed to horizontal eyelid laxity, orbicularis muscle override, and lower eyelid retractor laxity. Evidence will be presented supporting alternative etiologies of the condition. Modified surgical techniques will be presented.
Methods
Information from the author’s clinical research, patient observations and videos, and published studies will be presented.
Results
Lower eyelid retractor laxity causes tarsal instability and loss of deep anterior lamellar fixation. Most patients have marked lateral canthal instability, likely related to laxity of the lateral rectus capsulopalpebral fascia and loss of deep fixation. This facilitates inferior migration of the canthus and lid margin with blink. The preseptal lid remains well attached at the lateral raphe, giving the false impression of override. Enophthalmos enables the lower lid to displace the eye superiorly as it inverts underneath the axis of the globe. The lid is seldom horizontally elongated. The perception of horizontal eyelid laxity is caused be poor retractor and canthal fixation, rather than lid redundancy. Tarsal atrophy reduces appositional pressure between the lid and globe, while fat prolapse may alter orbicularis dynamics in some cases.
Conclusion
Involutional entropion has a multifactorial etiology. Lid retractor laxity, lateral canthal instability, and enophthalmos frequently contribute. Tarsal atrophy and fat prolapse are factors in some patients. Surgery should be individualized. Retractor fixation to the tarsus and orbicularis, and lateral canthal stabilization (lateral tarsal strip and/or lateral retractor fixation) should be considered in most repairs. Marked horizontal eyelid shortening is seldom indicated.