Eyelashes exist to help protect the ocular surface, but can certainly cause problems, from trivial to very serious.
Worldwide, trachoma is one of the leading causes of blindness, essentially caused by infection which leads to scarring, eventually in turn causing lashes to abrade and scar the cornea. Fortunately, such severe trachoma is uncommon in New Zealand and the South Pacific, but there are many other reasons why lash problems may drive a patient to consult you.
Key to managing troublesome lashes is understanding the normal eyelid anatomy and accurately determining why the lashes are causing symptoms, so that you can target treatment in acute and chronic cases. Epilation is not always the best thing to do.
The eyelid margin anatomy should be constant along its entire length. The key points to appreciate are:
- Well-defined posterior lid margin with a near 90-degree angle
- Orderly line of meibomian gland orifices
- The “grey line” separating the meibomian glands from the lashes
- Two to three orderly rows of lashes arching away from the cornea
Distortion of these normal anatomical patterns must be documented, with a diagram or photo, paying particular attention to the extent of the changes.
Fig 1. Normal lid margin. Note the regular lamellar arrangement along the entire lid margin
Too many lashes
Distichiasis is a rare condition where an extra row of lashes arises from the meibomian glands (not to be confused with the common situation of a loose lash getting stuck in a meibomian gland orifice). It is almost always congenital and definitive treatment is surgical, with either a lid split and posterior lamellar cryotherapy or meticulous dissection and ablation of each individual lash follicle.
Lashes in the wrong place
Trichiasis refers to isolated lashes or groups of lashes arising in an abnormal position in an otherwise normal lid margin. It is usually the result of inflammatory scarring distorting the underlying lash follicle. This is most commonly seen secondary to chronic meibomian gland dysfunction and lid margin inflammation. Epilation is a reasonable first treatment, as long as careful note is made of the position of the removed lash(es), so that their recurrence can be monitored. Treatment of the underlying inflammation is also important. Epilation should be performed carefully so that the entire lash is removed intact. Breaking the shaft of the lash at or even slightly below the lid margin will usually make the situation much worse.
Entropion is a generalised inward rotation of the lid margin towards the cornea, so that lashes and/or skin abrade the inferior cornea. Involutional entropion is when the lid margin is unstable and turns in when the patient blinks or closes their eyes. It can have an acute onset and may be secondary to reactive blepharospasm after eye surgery or other trauma.
The diagnosis is often obvious, but not always and should be considered in any patient with intermittent foreign body sensation. Provocative tests can be helpful in “uncovering” occult involutional entropion. Asking the patient to squeeze their eyes tightly (voluntarily, or by instilling topical anaesthetic drops) is the commonest such test. Sometimes, patients will be more prone to develop entropion when lying supine, so this can also be worth checking.
The anatomical features which cause lid margin instability are horizontal lower lid laxity, lower lid retractor disinsertion and, less commonly, overriding of the lower lid orbicularis muscle. Surgical repair addresses all these factors, but several “first aid” solutions may also help. Taping of the lower lid can reduce lid laxity if the tape is tightened horizontally and not pulling the lid down, as might seem tempting. Botox injections into the inferior orbicularis reduce the effect of orbicularis override but can increase laxity. Temporary everting sutures may also be used while awaiting definitive surgical repair. There is nothing to be gained by epilation in cases of involutional entropion as the lower lid skin will still be rubbing the cornea and doing at least as much damage as the lashes would have.
Fig 2. Entropion: the unstable lid margin has rotated onto the ocular surface
Cicatricial entropion is when conjunctival and/or lid margin scarring has distorted the normal anatomy, causing posterior migration of lid margin structures. This will give rise to symptoms once it causes lash-globe contact, but much more damage occurs if the keratinised epithelium of the lower lid skin comes into contact with the cornea. The classic example of blinding cicatricial entropion is trachoma. Stevens-Johnson syndrome can be equally dramatic. Chemical injuries, and even severe adenoviral conjunctivitis can cause cicatricial entropion, but as with trichiasis, the commonest cause we see tends to be from chronic lid margin inflammation and meibomian gland dysfunction.
Epilation is a reasonable acute measure, unless there is already skin-cornea contact, and some patients will be happy to have epilation performed on a regular, ongoing basis. Lashes usually regrow over about 6-8 weeks, but epilation may need to be more frequent if there are multiple “crops” of lashes. Treatment of the underlying inflammation should be started as early as possible to reduce long-term scarring.
If one or more aberrant lashes consistently regrow in the same position, then permanent lash ablation is indicated. Electrolysis or laser treatment is useful for small numbers of lashes. Lash excision or a lid wedge excision can be useful if there are many aberrant lashes in a localised area of lid. If lash ablation is planned, the patient should be instructed not to have lash epilation performed for 4-6 weeks prior. Many patients arrive for electrolysis having had all the offending lashes carefully removed a couple of days previously, making it impossible to know where to treat!
Epiblepharon is a fold of skin and orbicularis muscle that can override the medial lower lid margin and push the lashes against the globe. It is more common in infants, and much more common in some Asian populations. It is remarkably well-tolerated in the early stages, as only the softer shaft of the lashes rubs the eye, and because infants’ tear films are usually very protective. Again, epilation will make the situation considerably worse, particularly if the lashes are broken in the attempt. There is a strong tendency towards spontaneous resolution in the first decade of life, so supportive measures and reassurance are all that is usually required.
Fig 3. Epiblepharon: the skin/muscle fold is pushing lashes onto the globe, but the eye is quiet
Lashes may be abnormally long (trichomegaly) or abnormally abundant (hypertrichosis), most commonly caused by prostaglandin analogues (PGA), or other proprietary cosmetic treatments. Such lashes may be cosmetically unsightly but are usually not otherwise troublesome. However, these findings should be regarded as an indicator for potential prostaglandin periorbitopathy in patients receiving PGA glaucoma treatment. Other features of prostaglandin periorbitopathy include severe meibomian gland dysfunction and orbital fat atrophy and can be severe enough to warrant cessation of treatment.
Lashes may also be reduced in number (madarosis), in either a localised or generalised pattern. Generalised lash loss is seen in aging, and with chronic lid margin inflammation. Local lash loss may be due to trauma or may be a sign of lid margin malignancy. Finally, there is the distinctive picture of trichotillomania, which is obsessive self-epilation: the finding of widespread broken lashes of varying lengths is pathognomonic for this rare condition.
Fig 4. Hypertrichosis: abnormally dense lashes. Note the deep upper lid sulcus, characteristic of prostaglandin periorbitopathy
Dr Brian Sloan is a consultant ophthalmologist specialising in oculoplastic surgery, currently working at Greenlane Clinical Centre and in private practice.