Dry eye and refractive surgery

Four candidates in ten already have dry eyes

A multicentre study conducted across thirteen eye hospitals assessed the ocular surface of 1,849 refractive surgery candidates. Dry eye disease was diagnosed in 766 of them, or 41.4%.

In detail, 44.6% had a tear film break-up time under 5 seconds and 23.2% a Schirmer test under 5 mm.^[1]

Contact lens wear accounts for part of that gap: dry eye affected 54.1% of wearers against 35.2% of non-wearers.^[1] In the same series, 44.9% of candidates had worn contact lenses, or 830 patients out of 1,849.^[1]

Dry eye is therefore part of the usual picture in a patient who comes in wanting to be rid of contact lenses. It calls for methodical assessment, and its treatment is organised before the procedure.

What the term covers

The reference definition, established by the Tear Film and Ocular Surface Society, describes a multifactorial disease of the ocular surface characterised by a loss of tear film homeostasis, accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, inflammation and neurosensory abnormalities play a part.^[2]

That definition has a practical translation at the preoperative exam: dry eye is measured along several axes, and two patients describing the same discomfort sometimes have different underlying mechanisms. A deficit in tear production and excessive evaporation from meibomian gland dysfunction call for distinct treatments.

What each technique does to the tear film

Creating the flap in Femto-LASIK transects part of the superficial corneal nerves. Corneal sensitivity drops, the reflex tear secretion weakens, and any existing dryness worsens during the reinnervation phase. Subbasal nerve density rebuilds gradually, over several years.^[7]

PRK treats the surface and preserves the deeper nerve architecture. In exchange, epithelial healing takes longer and initial discomfort is more marked.

A prospective study measured corneal sensitivity with an aesthesiometer after both techniques, in 17 eyes treated with LASIK and 18 with PRK. Sensitivity returned to baseline at 1 month after PRK, against 6 months after LASIK.

The direct comparison between the two groups shows sensitivity significantly more depressed after LASIK over the first three months.^[9]

A systematic review of 18 studies on dry eye after refractive surgery reaches the same hierarchy: it ranks the use of LASIK over surface ablation among the factors that worsen the picture, alongside female sex, meibomian gland dysfunction and greater ablation depths.

The mechanism identified is the neurotrophic deficiency that follows nerve transection.^[10]

When dryness settles in

LASIK has a neurotrophic effect on the cornea. Cutting the nerves lowers corneal sensitivity, and that drop in turn reduces the blink reflex and reflex tear secretion. The epithelium ends up less well nourished and less well protected.

The reference review on this mechanism reports dry eye symptoms in more than 50% of patients after LASIK. The more troublesome pictures, combining visual fluctuations, reduced best corrected acuity and marked discomfort, affect roughly 10% of patients.^[11]

Intense symptoms with a normal examination

Some patients describe severe discomfort while examination of the ocular surface comes back normal. This mismatch between what the patient feels and what can be observed is well documented, to the point of having its own name in the literature, pain without stain.

The explanation now put forward involves the central nervous system. In a subgroup of patients, the pain signal is amplified and poorly regulated centrally, a mechanism termed nociplastic pain.^[12]

This mechanism sheds light on a puzzling clinical fact: in these patients, treatments aimed at the ocular surface have little or no effect, since the surface has stopped being the seat of the problem.^[12]

Corneal neuralgia

The most severe form remains rare. It combines pain persisting beyond three months, which patients compare to shards of glass in the eye, with an often unremarkable clinical examination.

A Yale team studied 21 patients from 20 unrelated families, all with persistent pain after refractive surgery: twenty after LASIK, one after PRK. Whole-exome sequencing revealed rare variants in genes coding for ion channels.^[13]

One of these variants was then characterised in the laboratory. The p.V527M mutation of the TRPV1 channel was found in a 49-year-old woman whose ocular discomfort score reached 100 out of 100 after LASIK and a subsequent PRK enhancement. The mutated channel responds more strongly to acidification.^[14]

This work points to a lead: an individual susceptibility, partly genetic, would explain why the same procedure leaves the great majority of patients unaffected and leaves a few in lasting pain.

Options for refractory forms

Preservative-free artificial tears, treatment of the meibomian glands and anti-inflammatory drops form the first line. Autologous serum drops come next, on the principle of supplying the growth factors that artificial tears lack.

The scleral lens offers a mechanical answer: it holds a reservoir of fluid in permanent contact with the cornea. A French team evaluated it in 19 patients, 35 eyes, with irregular corneas after refractive surgery who had failed conventional lens fitting.^[15]

Best corrected visual acuity improved from 0.33 to 0.08 LogMAR, with a significant drop in the ocular discomfort score.^[15] The series is small, and these lenses require specialised fitting.

When the neuropathic component dominates, management moves closer to that of chronic pain and beyond the strictly ophthalmic field.

The case of ICL implants

The ICL implant slides between the iris and the natural lens. The cornea keeps its thickness, its curvature and its innervation. A prospective series of 117 eyes nonetheless observed a deterioration in surface parameters at 1 month, with partial recovery at 3 months.

Patients who already had symptoms before the procedure had the poorest results.^[8]

In the long run the picture clearly favours it. One study compared 94 laser-treated patients, 80 ICL patients and 83 controls, 5 to 15 years after surgery. Tear hyperosmolarity affected 73% of the laser group against 50% of controls.

The ICL group sat at the level of the controls.^[6]

That same study brings a nuance worth having in consultation: reported symptoms were somewhat less frequent in the laser group than among controls, 19% against 31%.^[6] Measurable signs and the patient's experience therefore follow distinct paths.