Observations on the Etiology of Involutional Entropion.

Abstract

Purpose: To review evidence supporting proposed anatomic etiologies of involutional entropion and propose additional potential contributing factors.

Methods: A literature review was performed to identify publications describing possible etiologies of involutional entropion. The author's clinical observations and information supporting new proposed causes are presented.

Results: The frequency of perceived anatomic causes of entropion listed in modern publications include retractor dehiscence (97%), horizontal eyelid laxity (89%), orbicularis override (89%), enophthalmos (33%), tarsal atrophy (16%), and fat prolapse (10%). Evidence suggests attenuation of the retractors is a predominant factor in most patients. Tarsal atrophy, enophthalmos, and fat prolapse likely play a role in some individuals. The eyelid distraction test often shows horizontal margin laxity, although the eyelids typically are not elongated. Poor deep fixation and increased inferior mobility of the lateral canthus may contribute to marginal laxity and predispose patients to entropion. Lateral rectus capsulopalpebral fascia attenuation could lead to this canthal instability and reduced horizontal stability of the tarsal base.

Conclusions: Various age-related anatomic changes predispose patients to involutional entropion. Findings may vary among individuals. Tarsal atrophy and relative enophthalmos reduce appositional tension between the eyelid and globe. Lower eyelid retractor dehiscence causes poor anterior lamellar fixation and rotary instability of the tarsal base. Orbital fat prolapse may displace the tarsal base and alter orbicularis mechanics. Dysfunction of the lateral rectus capsulopalpebral fascia may contribute to both canthal instability and reduced horizontal tension near the tarsal base. Each patient's findings should be considered when individualizing surgical repair.