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Summary Table

Feature	Trichiasis	Distichiasis
Risk Factors	Trachoma (leading infectious cause worldwide), chronic blepharitis, herpes zoster ophthalmicus, cicatricial pemphigoid, Stevens-Johnson syndrome, chemical burns, prior eyelid surgery	Congenital (autosomal dominant, linked to FOXC2 mutations), lymphedema-distichiasis syndrome, chronic inflammatory lid disease
Etiology	Misdirection of normally positioned lashes inward due to scarring or inflammation of the lid margin	Accessory row of lashes arising from meibomian gland orifices (aberrant differentiation of meibomian glands into hair follicles)
Patient Presentation	Foreign body sensation, tearing (epiphora), photophobia, recurrent eye redness	Often asymptomatic in mild cases; similar irritative symptoms when aberrant lashes contact the globe
Classic Physical Exam	Normal lash row origin but lashes curve inward and contact the cornea/conjunctiva; corneal punctate epithelial erosions on fluorescein staining	Extra row of lashes emerging posterior to the normal lash line (from or near meibomian gland openings); lashes are often thinner and less pigmented
Key Diagnostic Results	Slit-lamp examination showing misdirected lashes with corneal epitheliopathy; fluorescein staining highlights corneal damage	Slit-lamp biomicroscopy revealing a second row of lashes at the meibomian gland orifices; eversion of the lid may be needed
Management	Epilation (temporary), electrolysis, cryotherapy, radiofrequency ablation, or surgical lid margin rotation for recurrent/severe cases	Epilation for mild cases; cryotherapy or surgical excision of the aberrant follicles for definitive treatment
Keywords	"Lashes touching the cornea," "corneal abrasion from lashes," "trachoma complication," "cicatricial lid changes"	"Extra row of eyelashes," "lashes from meibomian gland openings," "lymphedema-distichiasis," "congenital double row of lashes"

1. Pathophysiology

Trichiasis refers to the acquired misdirection of eyelashes from their normal position so that they turn inward and abrade the ocular surface. The lash follicles themselves are in the correct anatomical location along the anterior lid margin, but the direction of lash growth has changed. This distinction is critical: the problem is not an extra row of lashes or a malpositioned lid, but rather lashes growing in the wrong vector.

The most common global cause is trachoma, a chronic conjunctival infection caused by Chlamydia trachomatis. Repeated cycles of infection and inflammation lead to conjunctival scarring (Arlt line on the upper tarsal conjunctiva), which contracts the posterior lamella of the eyelid. This traction distorts the lid margin architecture and redirects the lash follicles posteriorly toward the globe. The World Health Organization classifies trichiasis as a late-stage complication in the FISTO grading system for trachoma (TT = trachomatous trichiasis). In non-endemic settings, any process that scars the lid margin or tarsal conjunctiva can produce the same result: cicatricial pemphigoid, Stevens-Johnson syndrome, chemical or thermal burns, herpes zoster ophthalmicus, and prior lid surgeries.

The clinical consequence of trichiasis is mechanical trauma to the corneal and conjunctival epithelium. Repeated contact between the misdirected lash and the ocular surface produces punctate epithelial erosions, which are best visualized with fluorescein staining under cobalt blue light. If left untreated, chronic abrasion leads to corneal vascularization, scarring, and ultimately corneal opacification with visual loss. This is the mechanism by which trachoma remains one of the leading infectious causes of preventable blindness worldwide.

Distichiasis is fundamentally different in origin. It is defined by the presence of an accessory row of eyelashes arising from the meibomian gland orifices on the posterior lid margin. This occurs because of aberrant differentiation: cells that should form meibomian (sebaceous) glands instead differentiate into pilosebaceous units capable of producing hair. The congenital form follows an autosomal dominant inheritance pattern and is strongly linked to mutations in the FOXC2 transcription factor gene on chromosome 16q24. This same gene is responsible for lymphedema-distichiasis syndrome, a condition in which patients develop bilateral lower-extremity lymphedema (typically around puberty) alongside the accessory lash row. Acquired distichiasis can arise from chronic meibomian gland inflammation (posterior blepharitis) or other inflammatory lid diseases that trigger metaplastic change.

The aberrant lashes in distichiasis tend to be finer, shorter, and less pigmented than normal lashes, which is why mild cases may go undetected for years. When these lashes are long enough or stiff enough to contact the cornea, they produce the same irritative symptoms and epithelial damage as trichiasis.

A commonly tested distinction is separating both conditions from entropion, where the entire lid margin rotates inward. In entropion, the lashes contact the globe because the lid itself is malpositioned; in trichiasis, the lid position is normal but individual lashes are misdirected; in distichiasis, both the lid and the normal lash row are correctly positioned, but an additional row exists in an abnormal location.

2. Classification and Clinical Manifestation

Classification	Definition	Clinical Features
Trichiasis (minor)	Fewer than 5 misdirected lashes	Intermittent foreign body sensation, mild tearing; may be managed with periodic epilation
Trichiasis (major)	5 or more misdirected lashes, or lashes touching the cornea in the central visual axis	Persistent pain, photophobia, corneal erosions, early scarring; warrants definitive surgical intervention
Congenital distichiasis	Present from birth; autosomal dominant (FOXC2 mutation)	Often bilateral; fine, pale lashes from posterior lid margin; may be asymptomatic until childhood or adolescence; screen for associated lymphedema
Acquired distichiasis	Secondary to chronic lid inflammation or metaplasia	Usually localized; arises in the context of chronic blepharitis, chemical injury, or Stevens-Johnson syndrome
Lymphedema-distichiasis syndrome	Distichiasis + primary lymphedema (lower extremities)	Distichiasis present at birth but lymphedema appears later (puberty); may also have cardiac defects, cleft palate, or varicose veins

Trichiasis vs Distichiasis vs Entropion

Feature	Trichiasis	Distichiasis	Entropion
Lash follicle location	Normal (anterior lid margin)	Abnormal (posterior lid margin / meibomian orifices)	Normal
Lid margin position	Normal	Normal	Inverted (turned inward)
Number of lash rows	Single row, misdirected	Two rows (normal + accessory)	Single row
Primary mechanism	Scarring redirects lash vector	Metaplastic follicle development	Lid margin rotation

3. Diagnostic Workup

Test	Purpose	Findings
Slit-lamp biomicroscopy (Best Initial Test)	Direct visualization of lash position, number, and contact with the globe	Trichiasis: lashes from normal origin touching cornea/conjunctiva. Distichiasis: second row of lashes at meibomian orifices
Fluorescein staining with cobalt blue light	Assess corneal epithelial damage	Punctate epithelial erosions or frank corneal abrasion in the area of lash contact
Lid eversion	Examine tarsal conjunctiva for scarring (trachoma workup) and identify posterior lash row in distichiasis	Arlt lines (linear scarring on upper tarsal conjunctiva) in trachomatous trichiasis; visible accessory follicles in distichiasis
*Genetic testing (FOXC2)*	Confirm lymphedema-distichiasis syndrome when clinical suspicion exists	Mutation in FOXC2 on chromosome 16q24
Lymphoscintigraphy	Evaluate lymphatic function if lymphedema-distichiasis syndrome is suspected	Delayed or absent lymphatic drainage in lower extremities

The diagnosis of both trichiasis and distichiasis is fundamentally clinical, made at the slit lamp. No advanced imaging or laboratory test is required in straightforward cases. The slit-lamp examination serves as both the best initial test and the most accurate test for identifying the lash abnormality itself.

The critical slit-lamp finding in trichiasis is one or more lashes originating from the correct anterior lid margin but directed posteriorly toward the globe. In severe cases, lashes may be embedded in the corneal epithelium. Always perform fluorescein staining to document the extent of corneal damage, as this determines urgency of intervention.

For distichiasis, careful inspection of the posterior lid margin is essential. The accessory lashes exit from meibomian gland orifices and are often easy to miss because they are thin and lightly pigmented. Lid eversion is frequently necessary to bring the posterior row into clear view, particularly on the upper lid.

When trichiasis is identified, the examiner should always assess the underlying etiology. In endemic regions, this means grading for trachoma using the WHO simplified grading system (looking for follicles, papillae, Arlt lines, and Herbert pits at the limbus). In non-endemic settings, the clinician should look for signs of cicatricial pemphigoid (symblepharon, progressive conjunctival shrinkage), Stevens-Johnson syndrome history, or chronic blepharitis.

When distichiasis is found in a young patient, screening for lymphedema-distichiasis syndrome is warranted. This includes a lower extremity examination for edema, a family history assessment (autosomal dominant), and consideration of genetic testing for FOXC2 mutations if additional syndromic features are present.

4. Management and Treatment

Intervention	Indication	Mechanism	Recurrence Rate
Epilation (manual removal)	First-line temporizing measure for few lashes	Forceps removal of offending lash	High (4 to 6 weeks regrowth)
Electrolysis	Recurrent trichiasis or distichiasis involving few lashes	Electrical current destroys the follicle via a fine needle	Moderate (may need repeat sessions)
Radiofrequency ablation	Similar to electrolysis; fewer lashes involved	Radiofrequency energy applied to follicle	Moderate
Cryotherapy	Multiple aberrant lashes; distichiasis with a full accessory row	Freeze-thaw cycle destroys follicles (double freeze-thaw at $-20°C$ to $-30°C$)	Lower than epilation; risk of lid depigmentation and notching
Argon laser photoablation	Small number of lashes; precise targeting needed	Laser energy directed at the lash root	Comparable to electrolysis
Bilamellar tarsal rotation surgery	Trachomatous trichiasis with lid margin distortion	Full-thickness lid incision with outward rotation of the distal margin (corrects the lash vector by repositioning the margin)	Low when performed correctly
Tarsal wedge resection / direct follicle excision	Localized distichiasis	Surgical removal of the segment of tarsus harboring accessory follicles	Low
Bandage contact lens	Adjunct while awaiting definitive treatment	Mechanical barrier protecting the cornea from lash contact	N/A (temporary)

Acute management begins with removing the immediate threat to the corneal surface. Epilation is the fastest intervention and can be performed in any clinic setting with fine forceps. However, students must understand that epilation is purely temporary: lashes regrow within 4 to 6 weeks, and repeated epilation does not destroy the follicle. It is appropriate as a bridge to definitive therapy or when only one or two lashes are involved and the patient can return for regular removal.

For definitive treatment of trichiasis, the choice depends on the number of lashes and the underlying pathology. When fewer than 5 lashes are involved and the lid margin architecture is preserved, electrolysis or radiofrequency ablation of the individual follicles is preferred. The procedure involves inserting a fine needle or probe into the follicle and applying current to destroy the germinal cells. Multiple sessions may be required.

When trichiasis is secondary to trachomatous scarring with lid margin distortion, the gold standard surgical treatment is bilamellar tarsal rotation (also called the Trabut procedure or its modifications). This involves a full-thickness horizontal incision through the upper lid, 3 mm above the lid margin, followed by eversion and suturing of the distal segment to rotate the lash-bearing margin away from the globe. The WHO endorses this procedure for trachomatous trichiasis and it should be performed when at least one lash touches the globe or there is evidence of corneal damage.

For distichiasis, the approach depends on the extent of the accessory row. If only a few lashes are symptomatic, cryotherapy is the treatment of choice. A double freeze-thaw cycle at $-20°C$ to $-30°C$ effectively destroys the aberrant follicles. The main complications of cryotherapy are lid margin depigmentation (particularly notable in darker-skinned patients), lid notching, and damage to meibomian glands (which can worsen dry eye). For localized segments, direct surgical excision of the tarsal plate harboring the accessory follicles (tarsal wedge resection with or without mucous membrane grafting) provides definitive results.

In all cases, concurrent corneal damage should be treated with preservative-free lubricating drops and, if epithelial defects are present, topical antibiotic ointment (e.g., erythromycin ophthalmic ointment) to prevent secondary infection. A bandage contact lens may be placed as a temporary corneal shield when definitive treatment is not immediately available.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
Entropion	Lashes touch the globe, causing corneal irritation and foreign body sensation	In entropion, the entire lid margin is turned inward; in trichiasis, the lid margin position is normal but individual lashes are misdirected
Epiblepharon	Common in East Asian children; lower lid skin fold pushes lashes against the cornea	The lash follicles and lid margin are normal in position; excess pretarsal skin and orbicularis muscle override pushes lashes vertically against the globe; usually self-resolves with facial growth
Ectopic cilia	Aberrant lash(es) growing through the conjunctival surface (usually upper lid, away from the lid margin)	The cilia emerge through the palpebral conjunctiva, not from the lid margin at all; rarer than trichiasis/distichiasis and typically presents in younger patients
Blepharitis (chronic)	Causes foreign body sensation, lid irritation, and lash crusting	No misdirection of lashes toward the globe; findings include collarettes at the base of lashes (anterior blepharitis) or meibomian gland plugging (posterior blepharitis) without an accessory lash row
Madarosis	Eyelid pathology affecting lashes	Madarosis is loss of lashes (the opposite problem); may coexist with conditions that also cause trichiasis (e.g., chronic blepharitis)
Chalazion / hordeolum	Lid lesion causing discomfort and tearing	A focal nodule or abscess, not a lash misdirection issue; no corneal abrasion from lash contact

6. Traps and High-Yield Pearls

The single most tested concept around eyelash abnormalities is the distinction between trichiasis, distichiasis, and entropion. Many students conflate these three because all result in lashes contacting the cornea. The vignette will differentiate them by describing the lid margin: if the lid is turned inward, it is entropion; if the lid position is normal but lashes are misdirected, it is trichiasis; if the lid is normal and there is an accessory row of lashes at the posterior margin, it is distichiasis. Read the stem carefully for descriptions of "normal lid position" versus "inturned lid."

A second common trap involves trachoma staging. Students may recognize trichiasis in a vignette set in an endemic region but fail to connect it to trachomatous scarring. When the stem mentions a patient from sub-Saharan Africa, South Asia, or the Middle East with recurrent childhood conjunctivitis, upper tarsal scarring, and now corneal irritation from inward lashes, the expected answer chain is: trachoma led to conjunctival scarring, which led to trichiasis, which is causing corneal damage. The management is bilamellar tarsal rotation, not just epilation.

A third pearl is the association between distichiasis and lymphedema-distichiasis syndrome. If a vignette describes a teenager with bilateral accessory lash rows and lower extremity swelling, the answer is lymphedema-distichiasis syndrome caused by FOXC2 mutation. Students who do not recognize this syndromic association may focus only on the eye findings and miss the underlying genetic diagnosis.

Finally, remember that epilation is never a definitive answer on an exam asking for the best long-term management. It is a temporizing measure. If the question asks for the "next best step" in a patient with ongoing corneal damage from trichiasis who has already undergone epilation multiple times, the answer shifts to a permanent follicle-destructive procedure (electrolysis, cryotherapy) or surgical correction.

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