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Ophthalmology – Entropion
Entropion is defined as an inward rotation of the eyelid margin, causing the eyelashes and periocular skin to rub against the ocular surface. This results in chronic irritation and can lead to corneal damage if untreated. It may be classified into four types: congenital, involutional (most common), spastic, and cicatricial.
Epidemiologically, involutional entropion increases with age and is the most frequently encountered type. Spastic entropion is typically temporary, often triggered by trauma, ocular irritation, or blepharospasm. Cicatricial entropion is less common but more severe, frequently associated with ocular cicatricial pemphigoid (OCP), which tends to affect older adults (age 60–70) and occurs more often in females. OCP has a prevalence of approximately 1 in 15,000–20,000 individuals.
The pathophysiology involves multiple mechanical and structural changes. These include increased orbicularis muscle tone and override, weakening or dehiscence of the lower eyelid retractors, horizontal eyelid laxity, and atrophy of the tarsal plate. In cicatricial cases, scarring of the conjunctiva leads to inward rotation of the lid margin.
Etiologically, entropion may result from aging changes, chronic use of certain topical medications (e.g., pilocarpine, timolol, epinephrine), or systemic autoimmune conditions such as ocular cicatricial pemphigoid, a type II hypersensitivity reaction with genetic predisposition (associated with HLA-DQB1*0301). Other associated conditions include Stevens–Johnson syndrome, trachoma, trauma, and chemical burns, all of which can lead to conjunctival scarring.
Patients typically present with foreign body sensation, tearing, redness, and irritation.
On examination, the eyelid margin is visibly inverted, with eyelashes rubbing against the cornea. Findings may include conjunctival injection, superficial punctate keratopathy, corneal abrasions, and in advanced cases, corneal scarring, thinning, ulceration, or neovascularization. In cicatricial entropion, additional features such as symblepharon (adhesion between palpebral and bulbar conjunctiva) and forniceal shortening may be present.
Diagnosis is primarily clinical. Laboratory testing is generally not required unless an autoimmune etiology such as OCP is suspected. In such cases, conjunctival biopsy with immunofluorescence can confirm the diagnosis, showing antibody deposition in over 80% of cases. Ancillary markers such as ANA or inflammatory mediators may also be elevated.
The differential diagnosis includes conditions that mimic eyelash irritation, such as epiblepharon (common in children), trichiasis (misdirected lashes), and distichiasis (extra row of lashes).
Management initially focuses on protecting the ocular surface. First-line treatment includes frequent lubrication with artificial tears and ointments. Temporary measures such as taping the lower eyelid to the cheek may help reposition the lid. In cases associated with OCP, systemic immunosuppressive therapy (e.g., prednisone, methotrexate, cyclophosphamide) may be required.
Definitive treatment is surgical, and most patients will eventually require it. Procedures include horizontal eyelid tightening, retractor repair, orbicularis muscle repositioning, or marginal rotation techniques. Simple suture repairs can be performed but have a higher recurrence rate.
Close follow-up is essential, typically within one week, to monitor for corneal complications. Patients should be educated to seek urgent care if they experience increased pain, redness, tearing, or photophobia, as these may indicate corneal involvement.
The prognosis is generally good with timely surgical correction. However, cicatricial causes like OCP may follow a chronic relapsing course and can lead to progressive vision loss if not adequately managed. Serious complications include corneal ulceration, scarring, perforation, and even loss of the eye, making early recognition and treatment critical.
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