A basic understanding of lower eyelid anatomy is pertinent to understand the pathogenesis of involutional entropion. The lower eyelid retractors are a definite double layer, and both layers are responsible for maintaining the stability of the tarsal plate. Because of a motor component contribution from the inferior rectus muscle, the posterior layer of the lower lid retractors is also responsible for a lower eyelid excursion or vertical traction of 3 to 5 mm in downgaze.¹,⁴,⁵ In younger patients, the pretarsal muscle is normally firmly adherent to the tarsus, while its preseptal counterpart is weakly adherent to the septum, and involution makes these connections even weaker.¹

Progressive age-related thinning and attenuation of eyelid tissues predispose the preseptal orbicularis muscle to migrate upward and override its pretarsal counterpart so that the lower eyelid turns in.²,⁶,⁷,⁸,⁹ This is mediated by a combination of horizontal and vertical lower eyelid laxity in the form of lateral canthal tendon laxity, attenuation, dehiscence, or disinsertion of the lower eyelid retractors, and age-related atrophy of orbital fat and enophthalmos. Involutional entropion and ectropion are characterized by their “mirrored” clinical presentation, and they share similar age-related changes on both the anatomical as well as the ultrastructural levels,¹⁰,¹¹ see Chapter 18 for a detailed review and a more thorough discussion of those collective predisposing factors.

The involutional type is by far the commonest type of entropion,¹² except in regions of the world where trachoma is endemic. An unprecedented number of people around the world are growing older, and the current number is expected to double by 2050.¹³ The prevalence of involutional entropion in the elderly is currently 2.1%, and likewise is also on the rise.¹⁴ This figure surges to 7.6% in patients older than 80 years.¹⁴ Involutional entropion, which is more frequently bilateral, is slightly more common in white females, with a prevalence of 2.4%, compared with 1.9% in men. The incidence is very low in elderly blacks (0.8%).¹⁴ The difference in sex prevalence could be attributed to tarsal size, axial globe position, or possibly the size of the globe itself.¹⁰,¹⁴,¹⁵,¹⁶,¹⁷

Patients typically present with significant ocular irritative symptoms and discharge. But because the symptoms and signs are initially intermittent, some cases may remain undiagnosed for months or even years or be mislabeled as dry eye or meibomian gland dysfunction.³ The frequency of the attacks gradually increases over time, and entropion becomes more permanent.³,¹⁸ Similar to other types of entropion, the entire mucocutaneous border of the eyelid, together with the eyelashes, is directed toward the globe, with subsequent corneal touch secondary to the eyelid malposition (Figure 20.1). Other eyelid and ocular surface abnormalities in patients with involutional entropion include lower retractor laxity, lateral canthal tendon laxity, chronic blepharitis, chronic conjunctivitis, dry eyes, and superficial punctate keratopathy. If left untreated, entropion could potentially lead to corneal ulceration.³,¹⁴,¹⁵ A specific variant of involutional entropion, the so-called “spastic entropion,” typically follows a definitive inflammatory ocular event in the elderly, like intraocular surgery. This initiates a vicious cycle of ocular irritation,
reflex blepharospasm, and entropion. The resulting mechanical irritation exacerbates the eyelid malposition problem even further.¹⁹,²⁰