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Elevated IOP induces late-onset haze in some LASIK patients
The development of refractive surgery has enabled many patients to see more clearly than ever seemed possible without spectacle correction. Moreover, refractive surgery has created a whole new ophthalmic industry that will continue to expand as new techniques and devices receive approval to come to market.
However, with these new and exciting procedures, the postoperative management may create more challenging problems that accompany any new surgery. Some of these unknown complications, such as diffuse lamellar keratitis (DLK), are already plaguing the ophthalmic community. This case represents a new type of complication that has been seen in our clinic following laser in situ keratomileusis (LASIK) surgery.
Postop vision decreases
---Interface haze in the central cornea: Several patients have been diagnosed with late-onset diffuse lamellar keratitis, which did not appear until the 3-week postoperative visit. DG, a 38-year-old, white male, underwent bilateral LASIK surgery on Aug. 20, 1999, with a surgical goal of plano. DG’s preoperative refraction was –7.00 +2.25 × 012 20/20 OD and –7.75 +1.50 × 175 20/20 OS. At his 1-day postoperative visit, DG’s acuity was 20/25 OD and 20/20 OS. The corneal flap was centered, smooth and clear OU. Ciprofloxacin HCl 0.3% was prescribed four times a day for 1 week, and fluorometholone acetate 0.1% was prescribed four times a day on a tapering schedule for 4 weeks.
At the 3-week postoperative visit, DG reported a bilateral decrease in his vision. His uncorrected acuity was 20/40 OD and 20/30 OS, with a refraction of –0.75 +1.25 × 160 20/25 OD and –0.75 +0.50 × 050 20/25 OS. The corneas now presented with an acute grade 1 to 2+ diffuse lamellar keratitis that extended beyond the flap. All other aspects of the adnexa were normal. DG was diagnosed with late-onset “sands of the Sahara,” or DLK, and was prescribed prednisolone acetate 1.0% every hour, with the ciprofloxacin resumed at four times a day. The fluorometholone was discontinued.
Haze does not resolve
Following a 2-day regimen of prednisolone and ciprofloxacin, the corneal haze did not seem to be resolving. Therefore, DG underwent an irrigation of both flaps, with some light scraping of the underside of the flap to remove the inflammatory debris. The DLK now appeared to be resolving, and DG was instructed to use prednisolone every hour and ciprofloxacin four times a day and return in 5 days.
However, DG called the office 2 days later with complaints of significant irritation and decreased vision. At this visit, he had grade 2+ conjunctival injection and his corneas were swollen, demonstrating grade 1 to 2+ diffuse interface and whitish reticular haze, which was now confined to the flap. The appearance was different than the previously diagnosed DLK, which had been irrigated. Believing this was an allergic response to the prednisolone, DG was switched from the prednisolone to dexamethasone sodium phosphate 0.01% every hour OU and was scheduled to return 1 day later.
At the next visit, DG’s symptoms were significantly improved; however, visual acuity was now 20/100 uncorrected OU, with grade 1+ corneal diffuse reticular haze OU. DG continued with the dexamethasone every 2 hours OU, and the ciprofloxacin was discontinued.
IOP elevated
Returning 2 days later, DG had 20/70 and 20/50 uncorrected visual acuity, but described his vision as “milky.” The haze seemed to be resolving slowly, yet still was present 0.5+ OU. DG’s pressures were measured, using a Goldmann tonometer, to be 39 mm Hg OD and 40 mm Hg OS. DG continued using dexamethasone four times a day OU and was prescribed Cosopt (dorzolamide HCl-timolol maleate, Merck) twice a day OU.
DG returned 2 days later with marked improvement to the uncorrected visual acuity, 20/40 OD and 20/25 OS. The cornea showed faint haze, and the IOPs were measured to be 14 mm Hg OU. At subsequent follow-up visits, within 2 weeks of the initial presentation, his vision continued to improve with the continued use of Cosopt twice daily and the tapering of the dexamethasone. Three weeks after the diagnosis of elevated IOP, DG’s visual acuity remained at 20/25 OD and OS with pressure of 14 mm Hg on no medications.
Other similar cases
Since this initial presentation of IOP-induced lamellar haze, two other patients have been seen with a similar appearance — one patient using fluorometholone 0.1% at a twice-daily dosage and the other using Flarex (fluorometholone acetate 0.1%, Alcon) on a tapering schedule. These patients also presented at approximately 1 month postop with a complaint of sudden decreased visual acuity. The eyes had some mild conjunctival injection, but were essentially quiet. The corneas were examined and were found to have the same lamellar haze seen in DG.
This whitish reticular haze differed from previously seen DLK, because there seemed to be no shifting appearance of the haze. Additionally, the zone of the inflammation seemed to be limited to the central 6-mm zone of the cornea. This is in contrast to DLK, which, in our experience, has inflammation that starts peripherally, usually superiorly outside the flap at about 10 mm, and gravitates centrally. The IOPs of all these patients were recorded to be above 40 mm Hg and Cosopt was prescribed twice daily to both patients. As in DG’s case, the patients noticed immediate improvement in the vision when the IOPs were stabilized below 20 mm Hg.
These cases demonstrate another complication that can arise following LASIK surgery. Because it is predicted that there will be more than 1.5 million LASIK surgeries performed this year, it is reasonable to assume that there will also be more cases of DLK and other complications.
All three of our patients were experiencing a normal postoperative course until the 1-month visit. In contrast, most cases of DLK occur in the first 24 to 48 hours postoperatively. Unless a corneal incident occurs, it is very rare to have such a late latency period for the appearance of this inflammatory keratitis.
Sands of the Sahara
DLK, as described by Robert Maddox, MD, in 1997, as the “shifting sands of the Sahara” syndrome, is a cellular infiltrate that has been seen to develop overnight as late as day 3 following surgery. However, it is believed to be present since day 1, but in a quiescent state.
The appearance has been described as opaque, wavy and with fine lines of intervening clear areas. Treatment consists of aggressive use of steroids or irrigation under the flap. If this condition goes untreated, the cellular infiltrate may develop into a focal pattern and cause a stromal melt. The exact etiology of this condition is still unknown; however, some hypothesize that it is caused by exotoxins from contaminated solutions or a bacterial infection, although none has ever been cultured. Still others theorize that rust on the microkeratome, chemicals on the blade, motor residue, autoclave biofilm, ethylene oxide gas residue, Merocel sponges, meibomian gland secretions or thermal injury from the laser may lead to the inflammatory corneal presentation (Gimbel HV, Anderson EE. LASIK Complications, Prevention, and Management. Thorofare, NJ: Slack Inc., 1999; 30-36).
Whatever the cause, the appearance can vary from patient to patient and needs immediate treatment to reduce any chance of permanent vision loss. The condition described in these three patients did not present as an opaque or wavy appearance, as in DLK, but rather as a whitish, lattice appearance, which was aggregated to the central cornea.
The only consistent factor of the three patients is that they all had LASIK, were approximately 1-month postop and had pressures at least 40 mm Hg. Moreover, because the postoperative thinning of the central cornea induces a false low, the IOP was actually higher than recorded. Because the pressures were elevated and the patients were all using a form of steroid, we diagnosed these patients as a variant of steroid responders.
Steroid response
In the general population, the incidence of response to topical steroids is between 6% and 30%; it is more than 30% in those with a family history of glaucoma and 75% to 90% in patients with glaucoma (Becker B. Intraocular pressure response to topical corticosteroids. Invest Ophthalmol. 1965; 4:198).
The rise in the IOP is believed to be related to changes in the mucopolysaccharides in the trabeculum from damage to the lysosomal membranes of the goniocytes found in the trabecular meshwork. The typical clinical picture resembles that of primary open-angle glaucoma, with an open, normal-appearing anterior chamber angle and absence of symptoms. Topical corticosteroid therapy is more associated with an IOP rise than is the case with systemic administration.
This may occur not only with drops or ointment applied directly to the eye but also with steroid preparations used in treating the skin of the eyelids (Vie R. Glaucoma and amaurosis associated with long-term application of topical corticosteroids to the eyelids. Acta Derm Venereol. 1980; 60:541; Cubey RB. Glaucoma following the application of corticosteroid to the skin of the eyelids. Br J Dermatol. 1976; 95:207; Zugerman C, Saunders D, Levit F. Glaucoma from topically applied steroids. Arch Dermatol. 1976; 112:1326). Studies have also shown that a patient’s response to earlier topical steroid therapy does not always predict how an individual will respond to other steroid treatments (Herschler J. Increased intraocular pressure induced by repository corticosteroids. Am J Ophthal. 1976; 82:90).
Although the onset of this pressure elevation seemed to take a month to be induced, it is not uncommon to have an acute presentation, in which the pressure rises within hours after the administration of topical steroids (Francois J. Corticosteroid glaucoma. Ann Ophthal. 1977; 9:1075; Weinreb RN, Polansky JR, Kramer SG, Baxter JD. Acute effects of dexamethasone on intraocular pressure in glaucoma. Invest Ophthal Vis Sci. 1985; 26:170). We can only speculate that the increase in pressure created the unusual reticular haze present in these corneas.
Outflow patterns altered by LASIK?
The fact that these patients were using relatively low dosages of mild steroids leads to the question of whether LASIK surgery can alter the outflow patterns of the trabeculum. The etiology of the increase in the pressure and the corneal appearance of these patients need further investigation. It does demonstrate that the variability in the appearance of DLK most likely is associated with an elevated pressure. This IOP-induced haze needs to be differentiated from true DLK. Therefore, IOP needs to be evaluated in any unusual looking lamellar haze or if any patient is on long-term steroid use postoperatively.
Because the flap is a crucial component in the success of LASIK, it is important to be careful to not displace it when using Goldmann tonometry. Our patients responded to Cosopt, and no other treatment was needed. This case illustrates the perplexities and variability in treating the postoperative LASIK patient.
For Your Information:
- Marc R. Bloomenstein, OD, FAAO, is director of refractive services at the Barnet Dulaney Eye Center. He is also president of the Arizona Optometric Association. He can be reached at the Barnet Dulaney Eye Center, 4800 North 22nd Street, Phoenix, AZ 85016; (602) 955.1000; fax: (602) 508-4700; e-mail: marc.bloomenstein@barnetdulaney.com. Dr. Bloomenstein has no direct financial interest in the products mentioned in this article, nor is he a paid consultant for any companies mentioned.
- David D. Dulaney, MD, has been in practice for 25 years. He is a diplomate of the American Board of Ophthalmology and a fellow in the American Academy of Ophthalmology. He can also be reached at the Barnet Dulaney Eye Center.
Primary Care Optometry News could not confirm whether or not Dr. Dulaney has a direct financial interest in any of the products mentioned in this article or if he is a paid consultant for any companies mentioned.