Secondary Logo

Journal Logo

ARTICLE

Laser in situ keratomileusis in patients with diabetes

Halkiadakis, Ioannis MD; Belfair, Nadav MD; Gimbel, Howard V. MD, MPH

Author Information
Journal of Cataract & Refractive Surgery: October 2005 - Volume 31 - Issue 10 - p 1895-1898
doi: 10.1016/j.jcrs.2005.03.075
  • Free

Abstract

Diabetes is among the major health problems in the Western world. In the United States, 8.3% of persons older than 20 years has diagnosed or undiagnosed diabetes.1 Unfortunately, the incidence of diabetes will continue to grow, as indicated by high rates of impaired fasting glucose levels, increasing rates of obesity, and a trend toward more sedentary lifestyles. Retinopathy, neuropathy, and nephropathy are the most recognized complications caused by the disease. Apart from causing retinopathy, diabetes mellitus affects the eyes in many ways; diabetic papillopathy, neovascular glaucoma, cataract, ptosis, oculomotor nerve palsies, inflammation of eyelids, and orbital infections are well-recognized ocular complications of diabetes mellitus.2 A significant percentage of diabetic patients develop corneal lesions during their lifetime; dry eye, superficial punctuate keratopathy, recurrent corneal erosions, persistent epithelial defects, filamentary keratitis, decreased corneal sensitivity, neurotrophic corneal ulceration, and corneal endothelial dysfunction constitute the spectrum of diabetic keratopathy.3–10

Given the increased risk for corneal complications, the safety of refractive surgery in patients with diabetes mellitus is in question.11 The only study on this subject reported poor refractive results and a significant (47%) risk for postoperative epithelial complications after laser in situ keratomileusis (LASIK) in patients with diabetes.12 More data are needed, however, before recommendations about the safety of LASIK in patients with diabetes can be made.

The purpose of this study was to review the refractive outcomes and complications in the patients with diabetes who had LASIK at our refractive centers.

PATIENTS AND METHODS

The database of all LASIK surgeries (35 200) performed between July 1996 and January 2004 in Gimbel Eye Centres (Calgary and Edmonton) was searched. Twenty-four patients (46 eyes) with diabetes were identified, and their clinical records were reviewed.

The data collection included demographic information, type and duration of diabetes when available, medical treatment, preoperative uncorrected visual acuity (UCVA), preoperative best spectacle-corrected visual acuity (BSCVA), preoperative refractive error, postoperative UCVA, postoperative BSCVA, postoperative refractive error, enhancement procedures, length of follow-up, and complications.

A complete ocular and medical history was obtained of all patients who received the following tests preoperatively: autorefractometry, auto and manual keratometry, UCVA, BSCVA, slitlamp examination, Goldmann applanation tonometry, fundus biomicroscopy, and indirect ophthalmoscopy. Corneal topography and ultrasound pachymetry were also performed before LASIK.

Patients included in the study fulfilled general candidacy criteria for LASIK surgery: no history of eye disease including severe dry eye and corneal epitheliopathy, no previous eye trauma, BSCVA >20/30, stable refraction for at least 1 year, spherical equivalent (SE) <10.0 diopters (D) in patients with myopia and <4.0 D in those with hyperopia, corneal thickness >500 μm, and intraocular pressure <21 mm Hg. Furthermore, diabetes was well controlled with medication and patients were in good physical condition without diabetic neuropathy, nephropathy, significant retinopathy, or macular edema.

All surgeries were done with the Nidek EC-5000 excimer laser by different experienced surgeons. The suction ring was applied, adequate suction was generated, and a Hansatome microkeratome (Bausch & Lomb Surgical) was used to create an 8.5 mm or a 9.5 mm flap. A depth plate of 160 μm or 180 μm was used. In 1 patient, an Automated Corneal Shaper (Chiron) microkeratome was used. The flap was reflected and excimer laser ablation of the stromal bed performed. The flap was repositioned on the stromal bed, followed by interface irrigation with a balanced salt solution. Postoperatively, patients were given instructions to wear a moisture chamber (NITEYE Xomed Surgical Products) over the operated eyes for the first few hours. Antibiotic and steroid drops were administered for 1 week postoperatively. All patients were examined on day 1 and after 1 week, 1 month, and 4 months by surgeons at the centers or by referring ophthalmologists. When necessary, further appointments were made.

RESULTS

Table 1 shows the clinical profiles of the patients. Seven patients had type I diabetes, and 17 patients had type II diabetes. Duration of diabetes was indicated in the patient's record in 13 cases. Mild nonproliferative diabetic retinopathy marked by a small number of hemorrhages and microaneurysms was present in 2 cases (2 eyes). No other significant retinal lesion or abnormality associated with diabetes was present.

Table 1
Table 1:
Clinical profiles of patients.

All eyes had a BSCVA of 20/20 preoperatively. Mean preoperative SE was −4.88 ± 2.13 D (range +1.625 to −9.00 D), and mean preoperative cylinder was −1.18 ± 0.9 D (range −0.25 to −3.75 D). No eye lost BSCVA at the last follow-up visit. Mean UCVA after first surgery was 20/25 (logarithm of the minimum angle of resolution [logMAR] 0.11 ± 0.16) improved to 20/23 (logMAR 0.05 ± 0.11) after enhancement. Forty-one eyes (89.1%) achieved UCVA 20/40 or better, and 29 eyes (63%) achieved UCVA 20/25 or better after the first surgery. Enhancement surgery was performed in 13 eyes (28.3%) of 8 patients. Forty eyes (87%) achieved UCVA 20/25 or better after 1 enhancement surgery.

Forty (87%) eyes were within ±1.0 D of targeted SE after first surgery, 31 (67%) eyes were within ±0.5 D of targeted SE after first surgery, and 43 (93.5%) were within ±0.5 D of targeted SE after enhancement.

Complications occurred in 3 eyes (6.5%) of 3 patients; 1 patient had type I diabetes and 2 had type II diabetes. None of these patients had diabetic retinopathy. Two eyes developed epithelial defects and subsequently epithelial ingrowths. The flap was lifted, and removal of epithelium was performed. No relapse of the ingrowth was observed, and BSCVA remained 20/20 at the last follow-up visit 5 months after the procedure. One eye developed an epithelial defect after enhancement surgery. A bandage contact lens was placed for 2 days. The defect healed without further complications. Using Pearson correlation between independent variables, epithelial defects were correlated to age and separately to duration of diabetes. No statistically significant correlations were found.

At the last follow-up visit, no development or progress of diabetic retinopathy or macular edema was noted in any eye.

DISCUSSION

Results of this study indicate the short-term safety of LASIK for well-controlled diabetic patients. No significant epithelial complications were encountered after 46 primary surgeries and 13 enhancements. These results are in contrast to those in a study by Fraunfelder and Rich.12 They reported that after LASIK in 30 eyes of patients with diabetes, 9 eyes developed punctuate epithelial erosions and 6 eyes developed persistent epithelial defects. Several explanations might account for the different results.

Epithelial complications after LASIK may occur during surgery as a result of preexisting clinical or subclinical epithelial basement membrane dystrophy13–15 and the shearing force of microkeratome to the epithelium16 or after surgery as result of the damage to corneal nerves, causing dry eye17 and neurotrophic epitheliopathy.18 Fraunfelder and Rich12 attributed the epithelial complications in their case series to preexistence of diabetic keratopathy, which was exacerbated by LASIK. It has been thought that diabetic keratopathy represents a form of diabetic neuropathy4 and that impairment of corneal sensitivity in people with diabetes is in direct correlation to degree of polyneuropathy,4,10,19 duration of diabetes,19,20 and stage of diabetic retinopathy.7,21,22 In our case series, all patients had well-controlled diabetes mellitus without neuropathy, and only 2 had minimal retinopathy. Unfortunately, Fraunfelder and Rich12 did not include data on the severity of diabetes in between the 2 series their case series. It is possible that the differing results represent differences in the duration and severity of disease.

It has been suggested that intraoperative epithelial defects significantly increased with older age.16 In our study, the average age of the diabetic patients was 42 years, whereas in the Fraunfelder and Rich study, the average age was 10 years older.

Different microkeratomes were used in the 2 studies. In the Fraunfelder and Rich study, the Nidek microkeratome was used. In our study, the Hansatome was the microkeratome of choice. Previous studies indicated the Nidek microkeratome is safe, predictable, and reliable for LASIK,23–25 and no significant differences with the Hansatome were found. It is of note, however, that the zero-compression head reduced the occurrence of Hansatome-induced epithelial defects.26

Differences in the technique may also play a role in the prevention of epithelial complications in predisposed eyes. As a routine, we avoid using drops, specifically topical anesthetic agents, 1 week preoperatively because they may increase epithelial fragility.13 Also, excessive irrigation of the stromal bed was avoided, and in some cases sodium hyaluronate (Eyestil) was instilled after the flap repositioning.

Our study indicated a favorable refractive outcome after LASIK in patients with diabetes. However, 28% of the eyes required enhancement surgery. Enhancement rates in our centers were 10%, which is close to those reported in the literature.27,28 The reason for the higher enhancement rates in diabetic eyes is not clear. It is possible that ultrastructural changes occurring in corneas of diabetic patients,29 together with different stromal hydration because of the dysfunction of the endothelium,5,30 made the eyes respond differently to the laser energy. Thus, usual nomograms may not be accurate in diabetic patients.

Epithelial ingrowth developed in 2 eyes (4.3%) of 2 patients (1 with type I diabetes and 1 with type II diabetes) in this case series. Epithelial ingrowth occurred in 0.5% of eyes of nondiabetic patients in our center,31 and this rate is close to the rate reported in the literature.32,33 The rate of epithelial ingrowth in patients with diabetes is higher than expected.31–34 Recently, Jabbur and coauthors34 reported that type I diabetes mellitus may increase the risk for epithelial ingrowth because of its effects on corneal epithelium. They cautioned all refractive surgeons not to perform any lamellar surgery on patients with type I diabetes or with uncontrolled diabetes. Although we agree with their second recommendation, we did not find any significant differences in refractive outcomes and complications between patients with type I and those with type II diabetes.

In the short term of follow-up, we did not observe presentation of retinopathy in eyes without retinopathy or aggravation of retinopathy in the 2 eyes with background retinopathy. Recently, Ghanbari and Ahmadieh35 reported aggravation of proliferative diabetic retinopathy after LASIK. They attributed the progression of retinopathy to the increase of retinal ischemia during suction. Although we did not note any progress in retinopathy in our patients, this study did not provide clues about the safety of performing LASIK in patients with significant diabetic retinopathy.

One major limitation of this study was the limited follow-up of the patients. It is of note, however, that in our referral-based practice, most patients are referred back to us if significant complications occur after surgery. Thus, even if the reported follow-up is limited, we have every reason to support the long-term safety of LASIK in our patients. We cannot comment on long-term refractive stability, however.

In conclusion, this retrospective study presents the largest number of patients with diabetes who had LASIK to date. Our results support the safety of performing LASIK surgery in well-controlled diabetic patients without systemic or ocular complications. Caution is advised, however, in performing LASIK surgery in patients not fulfilling the criteria described herein.

REFERENCES

1. Centers for Disease Control and Prevention (CDC), Prevalence of diabetes and impaired fasting glucose in adults United States 1999–2000. MMWR Morb Mortal Wkly Rep 2003; 52:833-837
2. Niffenegger JH, Fong D, Cavallerano J, Aiello LM. Diabetes mellitus. In: Albert DM, Jakobiec FA, eds, Principles and Practice of Ophthalmology. Philadelphia, PA, Saunders, 1994; 2925-2936
3. Hyndiuk RA, Kazarian EL, Schultz RO, Seideman S. Neurotrophic corneal ulcers in diabetes mellitus. Arch Ophthalmol 1977; 95:2193-2196
4. Schultz RO, Peters MA, Sobocinski K, et al. Diabetic keratopathy as a manifestation of peripheral neuropathy. Am J Ophthalmol 1983; 96:368-371
5. Schultz RO, Matsuda M, Yee RW, et al. Corneal endothelial changes in type I and type II diabetes mellitus. Am J Ophthalmol 1984; 98:401-410
6. Herse PR. A review of manifestations of diabetes mellitus in the anterior eye and cornea. Am J Optom Physiol Opt 1988; 65:224-230
7. Saini JS, Khandalavla B. Corneal epithelial fragility in diabetes mellitus. Can J Ophthalmol 1995; 30:142-146
8. Sánchez-Thorin JC. The cornea in diabetes mellitus. Int Ophthalmol Clin 1998; 38(2):19-36
9. Goebbels M. Tear secretion and tear film function in insulin dependent diabetics. Br J Ophthalmol 2000; 84:19-21
10. Dogru M, Katakami C, Inoue M. Tear function and ocular surface changes in noninsulin-dependent diabetes mellitus. Ophthalmology 2001; 108:586-592
11. Costin JA. Is laser vision correction safe in patients with diabetes? Cleve Clin J Med 2001; 68:385
12. Fraunfelder FW, Rich LF. Laser-assisted in situ keratomileusis complications in diabetes mellitus. Cornea 2002; 21:246-248
13. Dastgheib KA, Clinch TE, Manche EE, et al. Sloughing of corneal epithelium and wound healing complications associated with laser in situ keratomileusis in patients with epithelial basement membrane dystrophy. Am J Ophthalmol 2000; 130:297-303
14. Rezende RA, Uchoa UC, Cohen EJ, et al. Complications associated with anterior basement membrane dystrophy after laser in situ keratomileusis. J Cataract Refract Surg 2004; 30:2328-2331
15. Kenyon KR, Paz H, Greiner JV, Gipson IK. Corneal epithelial adhesion abnormalities associated with LASIK. Ophthalmology 2004; 111:11-17
16. Tekwani NH, Huang D. Risk factors for intraoperative epithelial defect in laser in-situ keratomileusis. Am J Ophthalmol 2002; 134:311-316
17. Toda I, Asano-Kato N, Komai-Hori Y, Tsubota K. Dry eye after laser in situ keratomileusis. Am J Ophthalmol 2001; 132:1-7
18. Wilson SE. Laser in situ keratomileusis-induced (presumed) neurotrophic epitheliopathy. Ophthalmology 2001; 108:1082-1087
19. Nielsen NV, Lund FS. Diabetic polyneuropathy; corneal sensitivity, vibratory perception and Achilles tendon reflex in diabetics. Acta Neurol Scand 1979; 59:15-22
20. Rosenberg ME, Tervo TMT, Immonen IJ, et al. Corneal structure and sensitivity in type 1 diabetes mellitus. Invest Ophthalmol Vis Sci 2000; 41:2915-2921
21. Saito J, Enoki M, Hara M, et al. Correlation of corneal sensation, but not of basal or reflex tear secretion, with the stage of diabetic retinopathy. Cornea 2003; 22:15-18
22. Ozdemir M, Buyukbese MA, Cetinkaya A, Ozdemir G. Risk factors for ocular surface disorders in patients with diabetes mellitus. Diabetes Res Clin Pract 2003; 59:195-199
23. Schumer DJ, Bains HS. The Nidek MK-2000 microkeratome system. J Refract Surg 2001; 17:S250-S251
24. Sarkisian KA, Petrov AA. Experience with the Nidek MK-2000 microkeratome in 1220 cases. J Refract Surg 2001; 17:S252-S254
25. Nakano K, Nakano E, Oliveira M, et al. Intraoperative microkeratome complications in 47,094 laser in situ keratomileusis surgeries. J Refract Surg 2004; 20:S723-S726
26. Kohnen T, Terzi E, Mirshahi A, Buhren J. Intraindividual comparison of epithelial defects during laser in situ keratomeileusis using standard and zero compression Hansatome microkeratome heads. J Cataract Refract Surg 2004; 30:123-126
27. Hersh PS, Fry KL, Bishop DS. Incidence and associations of retreatment after LASIK. Ophthalmology 2003; 110:748-754
28. Netto MV, Wilson SE. Flap lift for LASIK retreatment in eyes with myopia. Ophthalmology 2004; 111:1362-1367
29. Rehany U, Ishii Y, Lahav M, Rumelt S. Ultrastructural changes in corneas of diabetic patients; an electron-microscopy study. Cornea 2000; 19:534-538
30. Saini JS, Mittal S. In vivo assessment of corneal endothelial function in diabetes mellitus. Arch Ophthalmol 1996; 114:649-653
31. Gimbel HV, van Westenbrugge JA, Anderson Penno EE, et al. Simultaneous bilateral laser in situ keratomileusis: safety and efficacy. Ophthalmology 1999; 106:1461-1467; discussion by RJ Maloney, 1467–1468
32. Wang MY, Maloney RK. Epithelial ingrowth after laser in situ keratomileusis. Am J Ophthalmol 2000; 129:746-751
33. Stulting RD, Carr JD, Thompson KP, et al. Complications of laser in situ keratomileusis for the correction in myopia. Ophthalmology 1999; 106:13-20
34. Jabbur NS, Chicani CF, Kuo IC, O'Brien TP. Risk factors in interface epithelialization after laser in situ keratomileusis. J Refract Surg 2004; 20:343-348
35. Ghanbari H, Ahmadieh H. Aggravation of proliferative diabetic retinopathy after laser in situ keratomileusis. J Cataract Refract Surg 2003; 29:2232-2233
© 2005 by Lippincott Williams & Wilkins, Inc.