LASIK in Patients With Diabetes Mellitus

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 by Amy Lin, MD on May 4, 2023.

Diabetes is a relatively common disease, affecting more than 9% of adults in US population[1], and its prevalence is expected to increase in correlation with rising obesity rates[2]. As this segment of the population continues to grow, more diabetic patients are requesting laser vision correction.

The US FDA considers diabetes a relative contraindication to LASIK surgery; however when this recommendation was issued, there was very limited data on the safety and efficacy of LASIK in these patients. The recommendation was therefore based on theoretical, rather than actual, risk.

The link between diabetes and ocular complications is well established, and there was concern that the corneal abnormalities often seen in diabetic patients may increase operative and postoperative complications, and limit successful outcomes[3]. There was also concern that diabetic patients might be at a higher risk for postoperative infections.

Recent research on the outcomes of LASIK in this patient population is mixed; however there is a growing body of evidence that indicates LASIK may be safely performed in diabetic patients with tight glycemic control and no systemic or ocular complications.

Ocular Complications of Diabetes Mellitus

The complications of diabetes affect almost every organ system in the body, and the eye is no exception.

Retinal Complications

Diabetic retinopathy is the most common ocular complication of diabetes. Etiology is multifactorial, but is most likely caused by chronic hyperglycemia[4] via several proposed mechanisms. These mechanisms include impaired regulation of retinal blood flow, leading to increased shear stress on the retinal vessels[5], accumulation of sorbitol within the retina, which can cause cellular swelling and damage[6], and buildup of advanced glycosylation end products, which leads to retinal inflammation[7].

The result of these processes is diseased retinal tissue. As the disease progresses, retinal tissue becomes ischemic. This leads to the release of vascular endothelial growth factor (VEGF) from neighboring retinal tissue[8], which induces new vessel growth, at which point the disease process is classified as proliferative. The end result is vision compromise, and if untreated, blindness.

Corneal Complications

The corneal changes in diabetic patients, while perhaps less recognized than retinal complications, are equally important[9].

Epithelial Changes

There are a vast number of changes experienced by the corneal epithelium in patients with diabetes. Epithelial basement membrane thickening and multilayering is common[10], and a number of abnormalities in the basement membrane anchoring complex have also been described[11]. These abnormalities are likely responsible for the delayed epithelial healing rate observed in diabetic eyes postoperatively[12]. These changes may also explain the compromised epithelial barrier function that is observed in the eyes of many diabetic patients[13],[14].

Corneal epithelial complications are thought to be common (60-80%) among diabetic patients, especially in those with other ocular and systemic complications of the disease[15],[16].

Diabetic Corneal Neuropathy

Corneal neuropathy occurs within the setting of systemic diabetic neuropathy, and manifests clinically as reduced corneal sensation[17]. The sequelae of reduced corneal sensation include impaired cellular adhesion, decreased mitosis, and impaired healing[18],[19].

Endothelial Changes

Morphological abnormalities of the corneal endothelium are often seen in diabetic patients. These abnormalities include a decrease in the percentage of hexagonal cells, a higher rate of cell loss and decreased cell density[20]. As a result, intracellular interdigitation occurs, allowing excess fluid to leak into the corneal stroma[21],[22]. Because corneal transparency and thickness depend on a healthy, hydrophilic stroma, disturbances within the stroma can cause significant problems.

Primary prevention

Other corneal complications of diabetes include dry eye, superficial punctate keratopathy, recurrent corneal erosions, and neutrophilic corneal ulcerations[18],[23],[24].

Diabetes and Infection Risk

The link between diabetes and increased infection risk is widely accepted. The pathophysiology behind this phenomenon is multifactorial. Research has clearly demonstrated neutrophil chemotaxis, phagocytosis and intracellular bactericidal activity are all impaired in diabetic patients with hyperglycemia[25],[26]. The impaired immune response in diabetic patients is often exacerbated by vascular insufficiency, which is common in these patients[27].

Diabetes and Surgical Site Infection

As a result of the impaired immune response in diabetic patients, they are at increased risk for post-surgical infections. The link between diabetes and surgical site infections (SSI) is very well established and documented in the literature[28]. There are no large-scale studies to determine if the well-established link between SSI and diabetes extends to surgical incisions involving the eye; however there are many anecdotal case reports of postoperative infections in these patients.

LASIK in Diabetic Patients

Given the large number of corneal complications and depressed immune activity seen in diabetic patients, there are questions regarding the safety and efficacy of LASIK in this patient population.

Preoperative Assessment

Although limited data exists, good outcomes have been reported in diabetic patients with consistently good glucose control, stable refractive error, no evidence of neuropathy or nephropathy, and without significant retinopathy or keratopathy[2].

Type I vs. Type II

There is no data to support any difference in outcomes between type I and type II diabetic patients[2][3][25].

Glucose Control

In two studies that eliminated patients with poor glucose control, the complication rate was not significantly higher than the complication rate in the control group[2][26]. The only study reporting a significantly high rate of postoperative complications (47%) did not report glucose control among their patients[3]. Additionally, the lone case report of post-LASIK exacerbation of proliferative diabetic retinopathy was in a patient with markedly elevated fasting glucose and glycosylated hemoglobin levels (glucose 250 mg/dL and HgA1C 13%)[26].

Systemic Disease

Patients with evidence of systemic complications of diabetes were excluded from consideration in both studies finding no increase of postoperative complications. The reasoning for this is most likely related to strong evidence indicating patients with diabetic neuropathy are very likely to have comorbid ocular disease; at minimum corneal neuropathy[17]. Fraunfelder and Rich did not provide information on systemic disease in their patient population[3].

Ocular Disease

The two studies documenting favorable post-LASIK outcomes in diabetic patients included some patients with mild nonproliferative diabetic retinopathy. Those with moderate or severe retinopathy were excluded, as were those with evidence of proliferation. There was no greater incidence of complications in the patients with mild retinopathy than in those without. In a case report detailing post-LASIK aggravation of proliferative diabetic retinopathy, the patient had a long history of significant diabetic ocular complications and prior laser photocoagulation.

Postoperative Complications and Infection

There is contradicting data regarding the rate and nature of postoperative complications in diabetic patients.

Fraunfelder and Rich found a significant elevation in post-LASIK complications among diabetic patients (47% compared to 6.9% in the control population) in a retrospective study of 30 eyes. The most frequent complication seen was punctate epithelial erosions and persistent epithelial defects; they did not report an increased incidence of postoperative infections[3]. This study did not provide any information on glycemic control, presence of systemic complications such as neuropathy or nephropathy, or ocular involvement.

In a slightly larger study (46 eyes) of diabetic patients with a history of stable, optimum glucose control, no systemic complications, and minimal retinopathy, the complication rate was 6.5%, which was not statistically different than the complication rate in the control eye population. Observed complications were all epithelial defects, and there were no reported infections[2].

A third study of similar size (44 eyes) and patient characteristics (well controlled diabetes without systemic complications) reported a complication rate of 9.1%, which did not differ significantly from the control population. Reported complications were postoperative punctate keratopathy, mild epithelial ingrowth and a peripheral interface reaction, all resolved without sequelae[29].

There is an isolated case report of worsening proliferative diabetic retinopathy in a patient who recently underwent LASIK; this patient had poorly controlled diabetes and a long history of proliferative diabetic retinopathy. There are several opinions on why LASIK aggravated proliferative diabetic retinopathy in this patient. Proposed theories include ischemia induced by increased intraocular pressure during the procedure[30] or increased inflammatory response related to the patient’s uncontrolled hyperglycemia[31].


Data regarding post-LASIK refractive outcomes is conflicting. Fraunfelder and Rich reported a significant rate of suboptimal refractive results; with spherical correction, UCVA and astigmatism magnitude all significantly better in the control population[3]. These results have not been supported by additional studies. Both Halkiadakis and Cobo-Soriano reported refractive outcomes that were not statistically significant when compared to control eyes[3][23].

Delayed Wound Healing

Historical data shows diabetic patients do experience delayed healing after ocular surgery, excluding LASIK[12]. Fraufelder, Halkiadakis and Cobo-Soriano all reported a small, but statistically significant incidence of delayed would healing in their diabetic patients during the initial postoperative window; however at three months there was no difference between diabetic patients and the control population[2][3][23].


There is limited data available regarding the safety and efficacy of LASIK in patients with diabetes mellitus, however given the prevalence of the disease, and the popularity of LASIK, it is reasonable to assume a significant and growing number of diabetic patients are receiving this procedure. The fact that there is not a mounting quantity of case reports and case studies detailing significant complications leads many to the conclusion that despite a risk of delayed healing, LASIK can be safely performed in a select group of diabetic patients.

Therefore, when considering LASIK in a diabetic patient, it is critical to assess the following factors in addition to the standard preoperative evaluation.

Glucose Control

Patient should have a documented history of stable, well-controlled fasting glucose and glycosylated hemoglobin levels less than 9.

Systemic Disease

Patients with evidence of systemic complications of diabetes, such as peripheral neuropathy or nephropathy, should not be considered candidates for LASIK.

Ocular Disease

Evidence indicates patients with mild DR may be considered for LASIK on a case-by-case basis, however, patients with significant retinopathy or a history of diabetic eye complications should be excluded.

Additional Resources


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  2. 2.0 2.1 2.2 2.3 2.4 2.5 Halkiadakis I, Belfair N, Gimbel HV. Laser in situ keratomileusis in patients with diabetes. J Cataract Refract Surg 2005;31: 1895-1898.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Fraunfelder FW, Rich LF. Laser-assisted in situ keratomileusis complications in diabetes mellitus. Cornea;21:246-248.
  4. Frank RN. Diabetic retinopathy. N Engl J Med. 2004;350:48.
  5. Kohner EM, Patel V, Rassam SM. Role of blood flow and impaired autoregulation in the pathogenesis of diabetic retinopathy. Diabetes. 1995;44:603
  6. Ko BC, Lam KS, Wat NM, Chung SS. An (A-C)n dinucleotide repeat polymorphic marker at the 5’ end of the aldose reductase gene is associated with early-onset diabetic retinopathy in NIDDM patients. Diatebes 1995; 44:727
  7. Yeh PT, Yang CM, Huang JS, et al. Vitreous levels of reactive oxygen species in proliferative diabetic retinopathy. Ophthalmol 2008; 115:734
  8. Boulton M, Foreman D, Williams G, et al. VEGF localization in diabetic retinopathy. Br J Ophthalmol 1998; 82:561
  9. Sanchez-Thorin JC. The Cornea in Diabetes Mellitus. Int Ophthalmol Clin. 1998 Spring; 38:19-36
  10. Kenyon K, Wafai Z, Michels R, et al. Corneal basement membrane abnormality in diabetes mellitus [ARVO abstract]. Invest Ophthalmol Vis Sci 1978; (suppl)17:245
  11. Gipson IK, Spurr-Mirchaud SJ, Tisdale AS. Anchoring fibrils form a complex network in human and rabbit corneas. Invest Ophthalmol Vis Sci 1987; 289:212-221
  12. 12.0 12.1 Chen WL, Lin CT, Ko PS, et al. In vivo confocal microscopic findings of corneal wound healing after corneal epithelial debridement in diabetic vitrectomy. Ophthalmol 2001; 116:1038-47
  13. Goebbels M, Spitznas M, Oldendoerp J. Impairment of corneal epithelial barrier function in diabetics. Graefes Arch Exp Ophthalmol 1989: 227:142-144
  14. Stolwijk TR, VanBest JA, Boot JP, et al. Corneal epithelial barrier function after oxybuprocaine provocation in diaetes. Invest Ophthalmol Vis Sci 1990;31:436-439
  15. Schultz RO, Peters MA, Sobocinski K, et al. Diabetic corneal neuropathy. Trans Am Ophthalmol Soc 1983; 81:107-124
  16. Saini JS, Khandalavia B. Corneal epithelial fragility in diabetes mellitus. Can J Ophthalmol 1995; 30:142-146
  17. 17.0 17.1 Scullica L, Proto R. Rilievi clinici e statistici sulla sensibilita corneale nei diabetic. Bull Ocul 1965; 44:944-954
  18. 18.0 18.1 Parrish GM. The cornea in diabetes mellitus. In:Ferman SS, ed. Ocular problems in diabetes mellitus. Boston:Blackwell Scientific, 1992:179-205
  19. Sigelman S, Friedenwald J. Mitotic and wound healing activities of the corneal epithelium. Effect of sensory denervation. Arch Ophthalmol 1954; 52:46-57
  20. Schultz RO, Matsuda M, Yee RW, et al. Coreal endothelial changes in type I and type II diabetes mellitus. Am J Ophthalmol 184; 98:401-410
  21. Rao GN, Lohman LE. Cell size-shape relationships in corneal endothelium.Invest Ophthalmol Vis Sci 1982; 22:271-274
  22. Shaw EL, Rao GN, Arthur EJ, et al. Endothelial cell morphology and corneal deturgescence. Ann Ophthamol 1979; 11:885-899
  23. 23.0 23.1 23.2 Hyndiuk RA, Kazarian EL, Schultz RO, Seideman S. Neutrophilic corneal ulcers in diabetes mellitus. Arch Ophthalmol 1977; 95:2193-2196
  24. Herse PR. A Review of manifestations of diabetes mellitus in the anterior eye and cornea. Am J Optom Physiol Opt 1988; 224-230
  25. 25.0 25.1 Delamaire M, Maugendre D, Moreno M, et al. Impaired leucocyte functions in diabetic patients. Diabet Med 1997; 14: 29
  26. 26.0 26.1 26.2 Llorente L, De La Fuente H, Richaud-Patin, Y, et al. Innate immune response mechanisms in non-insulin dependent diabetes mellitus patients assessed by flow cytoenzymology. Immunol Lett 2000; 74: 239
  27. Weintrob AC, Sexton DJ. Susceptibility to infections in persons with diabetes mellitus. UpToDate. Updated 2012
  28. Ata A, Lee J, Bestle SL, et al. Postoperative hyperglycemia and surgical site infection in general surgery patients. Arch Surg 2010; 145: 858
  29. Cobo-Soriano R, Beltran J, Bavaria J. LASIK outcomes in patients with underlying systemic contraindications
  30. Ghanbari H, Ahmadieh H. Aggravation of proliferative diabetic retinopathy after laser in situ keratomileusis. J Cataract Refract Surg 2003; 29:2232-2233
  31. Ersanli D, Akin T, Karadayi K. Aggravation of proliferative diabetic retinopathy after LASIK (letter). J Cataract Refract Surg 2005; 31:1086-1087
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