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12 The Cornea in Diabetes Mellitus

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neovascularization, corneal touch with silicone oil, absence of fluid–gas exchange, additional surgery, and anterior chamber inflammation.92

Laser photocoagulation is commonly used to treat proliferative diabetic retinopathy and has been associated with corneal decompensation in some diabetics. Argon laser photocoagulation can result in decreased corneal sensitivity.61,93 This decreased sensitivity coupled with fundus contact lens-induced hypoxia can traumatize an already compromised cornea resulting in worsening of keratopathy. Lastly, corneal burns have been reported stemming from intraoperative laser indirect ophthalmoscope treatment.94

The emergence of refractive surgery as a widely accepted and popular procedure has raised questions regarding its use in the diabetic patient. Diabetes is a relative contraindication to refractive surgery. Studies have demonstrated its safety and efficacy in the well-controlled diabetic patient.95,96 Nevertheless, patients with diabetes who undergo LASIK are at a significantly higher risk of developing postoperative epithelial complications and are more likely to require additional laser treatment to achieve emmetropia.96,97 In this setting, a surface ablation, photorefractive keratectomy (PRK) may be a safer alternative. The diabetic patient should be carefully counseled and well informed regarding the disease-specific risks of refractive surgery.

12.6Treatment of Corneal Disease in Diabetes Mellitus

Protecting and preserving the ocular surface limits the impact of diabetic keratopathy in altering vision and comfort. As diabetes affects all components of the tear film, the role of artificial tears and lubricants is valuable.50–57 Use of preservative-free lubricants is particularly important in the postoperative period as the cornea is a greater risk of epithelial break- down.76–80 Recalcitrant keratopathy may require the use of anti-inflammatory as well. There is increasing evidence that decreased tear secretion and epithelial injury promote inflammation on the ocular surface, resulting in an increase in cytokines and proteases in the tear fluid.98 Moreover, T-cell infiltration of the conjunctiva has been observed. The use of cyclosporine A, corticosteroids, and doxycycline

in keratopathy has been demonstrated to be effica-

cious in curbing inflammation and improving signs and symptoms of ocular surface disease.99–101 Addi-

tional therapy for severe keratopathy such as erosions and persistent epithelial defects with neurotrophic keratopathy includes bandage contact lens, amniotic membrane grafts, and tarsorrhaphy.102–104 A stepwise approach to managing keratopathy with timely referral to a cornea specialist can avoid corneal stromal scarring and possible thinning with subsequent compromise of vision. Early recognition and prompt treatment of diabetic corneal disease is vital.

12.7 Conclusion

Diabetes has a significant impact on the cornea. Recognizing the pathophysiological and morphological changes in the diabetic cornea provides greater insight into the clinical manifestations and implications of ocular surgery. An altered tear film and greater epithelial fragility in conjunction with decreased corneal sensitivity leave the diabetic cornea more prone to trauma and injury that may result in complications such as infectious keratitis, neurotrophic ulcers, and stromal scarring. Endothelial cell dysfunction may place the cornea at risk for decompensation following stress. This unique constellation of properties of the diabetic cornea warrants careful understanding as diabetic retinopathy is one of the primary indications for pars plana vitrectomy and surgery can further traumatize a compromised cornea. Identifying the signs and symptoms of diabetic keratopathy is essential in establishing the appropriate treatment plan, thereby preventing further complications and minimizing visual loss.

12.8 Summary of Key Points

The diabetic cornea may appear normal, but it is not. The abnormalities correlate with the severity of diabetic retinopathy.

Accumulation of advanced glycation end products in the corneal epithelial basement membrane may be the basis of poor healing of diabetic corneal epithelial defects.

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Corneal neuropathy leads to reduced blink frequency, reduced tear secretion, and hypoesthesia.

In pars plana vitrectomy for advanced diabetic retinopathy, the use of noncontact lens systems reduces the incidence of intraoperative and postoperative problems with corneal epitheliopathy.

If silicone oil is used in surgery for advanced diabetic retinopathy, special care is warranted to avoid contact between the corneal endothelium and the silicone oil.

A low threshold for consultation with a corneal specialist is warranted for retinal specialists managing patients with advanced diabetic retinopathy having concomitant diabetic keratopathy.

Diabetes is a relative contraindication for refractive surgery. In the situation of a well-controlled diabetic being considered for a refractive procedure, photorefractive keratectomy may be the preferred option.

12.9 Future Directions

Improved understanding of the molecular abnormalities underlying diabetes mellitus should improve our ability to treat diabetic keratopathy in concert with other end-organ abnormalities. In particular, improved treatment of tear insufficiency and corneal neuropathy will be valuable in themselves, but also as aids in the management of advanced diabetic retinopathy in which corneal and retinal challenges often intersect.

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