January 01, 2001
5 min read
Save

LASIK-induced dry eye can be managed

Patients with existing dry eye may find signs and symptoms exacerbated by LASIK.

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Editor’s note:
A well-selected patient who undergoes uncomplicated laser in situ keratomileusis (LASIK) may experience postoperative complications. It is felt that some patients who develop symptoms and signs of dryness following LASIK do so as a result of LASIK-induced neurotrophic epitheliopathy (LNE) secondary to disruption of the normal corneal innervation.

Drs. Choi and Wilson present such a case felt to be attributed to LNE. Findings, presumed etiology and management are presented. This article is well worth reading and reminds us that LASIK is an invasive procedure to the cornea.

Stephen M. Soll, MD, FACS

[bar]

A 48-year-old female with no significant ocular history presented for LASIK in April 1999. Preoperative examination revealed uncorrected visual acuity of 20/160 in the right eye and 20/160 in the left eye. Best spectacle-corrected vision was 20/20 in both eyes. Cycloplegic refraction was –2.75 +0.75 ×180° in the right eye and –3.00 +1.00 ×180° in the left eye.

Slit-lamp examination was unremarkable. Specifically there was no punctate epithelial erosion (PEE) or punctate epithelial keratopathy (PEK) in either eye. Corneal pachymetry measurements were 521 mm in the right eye and 532 mm in the left eye. Humphrey topography corneal irregularity measurements (CIM) were 0.67 in the right eye and 0.47 in the left eye, with normal being less than 1.0 to 1.5.

The patient underwent LASIK surgery in both eyes. A 9.5 to 10 mm diameter corneal flap approximately 180 mm in thickness was created with the Hansatome microkeratome and a 6 mm laser ablation zone was applied with the Visx S2 excimer laser. The flap was allowed to adhere for approximately 1 minute and a Soflens 66 F/M contact lens (Bausch & Lomb, Rochester, N.Y.) was applied until the next morning.

Follow-up examinations at 1 day and 1 week were unremarkable for visual complaints or corneal surface irregularities.

At the 1-month follow-up examination, however, the patient complained of blurred and variable vision along with a sensation of dryness of both eyes. Uncorrected visual acuity was 20/40 in the right eye and 20/20 in the left eye. Manifest refraction was –1.50 +1.25 ×87° in the right eye and –0.75 sphere in the left eye, which provided best spectacle-corrected vision of 20/15. Slit lamp examination showed +2 PEE of the inferior third of the cornea in both eyes (see figure) with rose bengal staining of this area of the cornea. Schirmer’s test without anesthetic was 10 in the right eye and 11 in the left eye. The Humphrey CIM values were 0.93 in the right eye and 1.00 in the left eye.

At the 3-month follow-up visit the patient continued to have the sensation of dryness. Uncorrected visual acuity was 20/25+ in the right eye and 20/25+ in the left eye with a manifest refraction of –1.00 +0.75 ×85° and –0.50 +0.25 ×75° respectively, resulting in best spectacle-corrected visual acuity of 20/15. The Humphrey CIM values were 1.26 in the right eye and 1.29 in the left eye. Values of Schirmer’s test without anesthesia were 12 in the right eye and 10 in the left eye.

Enhancement performed

--- The right cornea developed PEE, PEK, and rose bengal staining consistent with LASIK-induced neurotrophic epitheliopathy (LNE) at 1 month after LASIK. Similar ocular surface abnormalities developed in the fellow eye. There were no signs of dry eye disease in either eye prior to LASIK.

The patient underwent enhancement of the right eye 3 months after the initial myopic laser treatment. At 1 day and 1 week post-enhancement of the right eye, the patient was without complaints and the slit-lamp examination was unremarkable for surface irregularities.

At 1 month post-LASIK enhancement of the right eye and 8 months post-LASIK for the left eye, the patient reported good vision quality with no symptom of dryness. Uncorrected visual acuity was 20/20– in the right eye and 20/20– in the left eye. Manifest refraction of the left eye was –0.50 D with best spectacle corrected vision of 20/15. Slit-lamp examination revealed PEE of the inferior third of the cornea in the right eye with rose bengal staining over the inferior third of the cornea. The left eye had a clear cornea with no PEE, PEK, or rose bengal staining. The Humphrey topography CIM value was 1.49 for the right eye.

At 3 months following enhancement of the right eye and 11 months following LASIK treatment of the left eye, the patient noted that the vision and dryness symptoms appeared to be improving, especially in the left eye. Uncorrected visual acuity was 20/20 in the right eye and 20/25 in the left eye. Manifest refraction was –0.50 D in the right eye and –0.75 D in the left eye with best spectacle corrected visual acuity of 20/15. Slit-lamp examination revealed PEE of the inferior third of the right cornea. The left cornea was normal. Humphrey CIM values were 1.17 in the right eye and 1.25 in the left eye.

Sensory nerves severed

Many patients who have LASIK develop symptoms of dryness in the months following surgery even though they had no prior history of dry eye. We believe that many of these patients develop LASIK-induced neurotrophic epithiopathy (LNE) associated with a sensation of dryness of the eyes and the presence of corneal surface irregularities that include PEE and PEK with rose bengal or lissamine green corneal staining. This condition is triggered by the loss of neurotrophic influence for the corneal sensory nerves that are severed during formation of the flap. Patients who have pre-existing dry eye symptoms and signs can also develop superimposed LNE, and it tends to produce more severe symptoms and signs in these patients. In cases where the visual axis is affected by the corneal surface abnormalities, blurred or fluctuating vision may be noted. Some patients are totally asymptomatic. Signs and symptoms appear as early as one day after surgery, but more commonly are noted a few weeks after surgery. The PEE, PEK, and rose bengal staining tend to be confined to the flap; the zone around the hinge is typically spared since nerves in this region remain intact. The Schirmer’s test without anesthesia tends to be normal unless the patient had pre-existing dry eye.

Treatment options

Treatment consists of lubrication with nonpreserved artificial tears scheduled at least six times a day and a nonpreserved lubricating ointment at bedtime. Punctal occlusion, bandaged soft contact lenses (only if Schirmer’s test without anesthesia is relatively normal: 8 mm or greater of wetting in 5 minutes) and improved humidity levels (avoidance of dry climates, use of humidifiers and use of moisture chamber goggles at bedtime) may be of benefit in more difficult cases of LNE. Underlying meibomian gland dysfunction or blepharitis should be treated. Signs and symptoms of LNE usually resolve 6 to 8 months after surgery with or without treatment, which is the length of time required for the flap to be re-innervated.

As this case demonstrates, LNE tends to recur with enhancement because the corneal nerves in the flap are again interrupted. Thus it may be best to enhance one eye at a time in patients who develop LNE after the primary procedure. Eyes that have PRK do not usually develop an LNE-like syndrome even though the nerve endings are ablated with the excimer laser. This could be because only the nerve terminals are affected and corneal sensation is restored more quickly. Thus, PRK could be a better choice for patients with low myopia or low hyperopia who have dry eyes and are therefore at high risk for developing significant LNE.

For Your Information:
  • Stephen M. Soll, MD, FACS, is associate clinical professor of surgery/ophthalmology, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Camden, NJ. He can be reached at Soll Eye Associates, 5001 Frankford Ave., Philadelphia, PA 19124; (215) 288-2500; Fax: (215) 288-5601.
  • Rosan Y. Choi, MD, and Steven E. Wilson, MD, can be reached at the Department of Ophthalmology, Box 356485, University of Washington, Seattle, WA 98195; (206) 543-7250; fax: (206) 543-4414.
References:
  • Linna TU, Perez-Sanonja JJ et al. Recovery of corneal nerve morphology following laser in situ keratomileusis. Exp Eye Res. 1998;66:755-763.
  • Perez-Santonja, JJ, Sakla HF et al. Corneal sensitivity after photorefractive keratectomy and laser in situ keratomileusis for low myopia. Am J Ophthalmol. 1999;127:497-504.
  • Latvala T, Barraquer-Coll C et al. Corneal wound healing and nerve morphology after excimer laser in situ keratomileusis in human eyes. J Refract Surg. 1996;12:677-83.
  • Linna T, Tervo T. Real-time confocal microscopic observations on human corneal nerves and wound healing after excimer laser photorefractive keratectomy. Curr Eye Res. 1997;16:640-9.