Entropion

01Pathophysiology

Entropion is the inward inversion of the eyelid margin so that the lashes and keratinized skin contact the cornea and conjunctiva. The mechanism differs across the four classifications, but the end result is mechanical trauma to the ocular surface, producing the patient's symptoms.

In involutional (senile) entropion, three age-related changes converge: horizontal eyelid laxity (loss of canthal tendon tone), disinsertion or attenuation of the lower eyelid retractors, and override of the preseptal orbicularis muscle over the pretarsal orbicularis. When the orbicularis contracts during blinking, the upper portion of the muscle rolls over the lower portion and flips the tarsal plate inward. Coexisting enophthalmos from orbital fat atrophy removes the posterior support that normally keeps the lid apposed to the globe.

In cicatricial entropion, scar tissue on the posterior lamella (tarsoconjunctival surface) contracts and pulls the lid margin posteriorly toward the globe. This is the dominant mechanism in trachoma worldwide, and is also seen in ocular cicatricial pemphigoid, Stevens-Johnson syndrome, chemical burns, and prior surgery.

In spastic entropion, sustained orbicularis contraction from ocular irritation (postoperative inflammation, conjunctivitis) overrides normal lid position. It often resolves once the underlying irritant is treated, but it can become involutional if laxity already exists.

In congenital entropion, the tarsal plate is malformed or the lower lid retractors fail to attach properly, producing a true rolled-in lid. This is distinct from epiblepharon, in which the lid position is normal but a horizontal skin fold pushes the lashes against the globe (commonly seen in East Asian children and frequently self-resolving).

The downstream sequence is consistent: lashes contact the cornea, producing reflex tearing, foreign body sensation, and corneal epithelial defects. Untreated, this progresses to corneal ulceration, neovascularization (pannus), scarring, and vision loss, which is the chief reason entropion is treated rather than observed.

02Classification and Clinical Manifestation

03Diagnostic Workup

Entropion is a clinical diagnosis made at the slit lamp. The best initial step is direct inspection of the eyelid margin in primary gaze followed by forceful blinking, because mild involutional entropion may only manifest with orbicularis contraction. Fluorescein staining is mandatory in every suspected case because the most consequential complication, corneal ulceration, must be identified before definitive repair is planned.

The snap-back test is performed by pulling the lower lid downward and releasing it without allowing the patient to blink. A normal lid snaps back immediately; in involutional entropion the lid returns slowly or only after a blink. The distraction test measures how far the lid can be pulled anteriorly from the globe, with greater than 6 to 8 mm indicating clinically meaningful laxity.

When the upper lid is involved, or when the patient has a history compatible with autoimmune or infectious scarring, the upper tarsal conjunctiva must be everted to look for the diagnostic features of trachoma (Arlt's line, Herbert's pits) or cicatricial pemphigoid (subepithelial fibrosis, symblepharon, fornix shortening). Conjunctival biopsy with immunofluorescence is the confirmatory test for ocular cicatricial pemphigoid and is the only way to distinguish it reliably from other scarring conjunctivitides.

04Management and Treatment

Acute stabilization focuses on protecting the cornea. Preservative-free artificial tears are dosed every 2 to 4 hours during the day, with a lubricating ointment such as carboxymethylcellulose or paraffin at bedtime. If a corneal abrasion or early ulcer is present, a bandage soft contact lens is placed and prophylactic topical antibiotics (moxifloxacin 0.5% four times daily, or ofloxacin 0.3% four times daily) are added until the epithelium heals. Lid taping, with adhesive strips drawing the lid skin inferolaterally toward the cheek, can immediately reverse the inversion as a bridge to surgery.

Botulinum toxin type A, injected at 2.5 to 5 units into the pretarsal orbicularis, paralyzes the overriding muscle and corrects the lid position for roughly 3 to 4 months. It is the treatment of choice for spastic entropion and is useful for patients who are poor surgical candidates.

Definitive management is surgical in involutional and cicatricial cases. For involutional entropion, the lateral tarsal strip combined with lower eyelid retractor reinsertion addresses both horizontal laxity and the disinserted retractors and is the standard definitive procedure. Quickert sutures, three full-thickness everting sutures placed through the lower fornix and out through the skin, provide a quick repair under local anesthesia and are favored in elderly or medically frail patients, although recurrence rates are higher.

Cicatricial entropion requires posterior lamellar lengthening. Options include tarsal fracture (tarsotomy with anterior rotation) for milder cases and mucous membrane grafting (typically buccal mucosa or hard palate) for advanced posterior lamellar shortening. Critically, cicatricial entropion is never treated with anterior lamellar tightening alone; doing so worsens the inversion. In autoimmune disease, systemic immunosuppression must be initiated before surgery because operating on inflamed tissue accelerates scarring. Dapsone, methotrexate, mycophenolate, or rituximab are used depending on severity for ocular cicatricial pemphigoid.

The next best step in any patient presenting with suspected entropion and ocular pain is slit-lamp examination with fluorescein staining to rule out corneal ulceration, because identifying an ulcer changes the immediate management to include a bandage contact lens and topical antibiotics before surgical referral.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The most common error is confusing entropion with trichiasis. Both produce the identical symptom of "lashes rubbing the eye," but the management is different. In entropion, the entire lid margin is rotated inward and the lid itself must be repositioned surgically. In isolated trichiasis, the lid margin is normal and the misdirected lashes are treated locally with epilation, electrolysis, or cryotherapy. Picking surgical lid repair for pure trichiasis, or simple lash removal for true entropion, is the test-writer's favorite trap.

A second high-yield pearl is the distinction between involutional and cicatricial entropion, because this drives the surgical plan. A vignette featuring an elderly patient with intermittent lid inversion, chronic tearing, and a positive snap-back test points to involutional disease and a lateral tarsal strip with retractor reinsertion. A vignette featuring a patient from a trachoma-endemic region, a history of Stevens-Johnson syndrome, or visible conjunctival scarring points to cicatricial disease and the answer becomes a posterior lamellar lengthening procedure, never simple horizontal tightening.

A third trap is forgetting fluorescein staining. Any patient with entropion and ocular pain or decreased vision needs the cornea examined for ulceration before definitive repair, and the question stem will often hide a corneal ulcer in the description ("greenish-yellow infiltrate," "hypopyon"). The next best step in that scenario is bandage contact lens with topical antibiotic coverage, not immediate surgery.

Finally, epiblepharon should never be repaired surgically as a first step in a young child. It typically resolves as facial bones mature, and conservative management with lubrication is correct unless persistent corneal damage develops past age 5 to 6.

The core competency tested is recognizing the mechanism behind a malpositioned eyelid, mapping that mechanism to the correct surgical approach, and protecting the cornea before doing anything else.