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Ординатура / Офтальмология / Английские материалы / Diabetes and Ocular Disease Past, Present, and Future Therapies 2nd edition_Scott, Flynn, Smiddy_2009

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314 Diabetes and Ocular Disease

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16

Nonretinal Ocular Abnormalities

in Diabetes

INGRID U. SCOTT, MD, MPH,

AND HARRY W. FLYNN, JR., MD

CORE MESSAGES

Corneal abnormalities associated with diabetes include decreased corneal sensitivity, bacterial keratitis, neurotrophic ulcers, persistent epithelial defects, and recurrent epithelial erosions.

There may be an association between diabetes and primary open-angle glaucoma, angle-closure glaucoma, neovascular glaucoma, and blood-associated glaucoma.

Lens abnormalities associated with diabetes include refractive changes and cataract.

Optic nerve abnormalities associated with diabetes include acute optic disc edema, Wolfram syndrome, optic nerve hypoplasia, and optic atrophy.

Diabetes is associated with cranial nerve III, IV, and IV palsies.

Diabetes is associated with an increased risk of endophthalmitis and mucormycosis.

Although diabetes-related visual impairment is most commonly due to complications of diabetic retinopathy, many nonretinal ocular abnormalities may contribute to visual loss and must be considered in the management of

patients with diabetes.

CORNEAL DISEASES

Diabetic patients may have significantly decreased corneal sensitivity, and the severity of the decreased sensitivity is usually correlated positively with the severity of retinopathy [1–3]. Diabetes has also been reported to be associated with

321

322 Diabetes and Ocular Disease

dry eyes, with the severity of dry eyes correlated positively with the severity of diabetic retinopathy [4]. Decreased corneal sensitivity and increased dry eyes may account for the increased incidence of contact lens-associated bacterial corneal ulcers [5] and neurotrophic ulcers [6] in diabetic patients compared with nondiabetic persons (Fig. 16.1).

Intrinsic abnormalities of the epithelial basement membrane complexes [7] and impaired epithelial barrier function [8] predispose to superficial punctuate keratitis, poor epithelial wound healing after trauma, and persistent epithelial defects [6]. The latter are seen frequently in diabetic patients whose corneal epithelium was removed during vitreoretinal surgery (Fig. 16.2) [9].

Diabetic patients are prone to recurrent corneal erosions, especially after photocoagulation and vitrectomy [10]. In a study of 100 vitrectomies performed for advanced diabetic retinopathy with vitreous hemorrhage, persistent epithelial defects or recurrent corneal erosions occurred in 25% of patients [11]. In another study, 55 vitreoretinal surgeons were asked to retrospectively report how many pars plana vitrectomies they performed in 1 year on diabetic eyes and in what percentage of cases the corneal epithelium was debrided [12]. The frequency of epithelial debridement was 17.4%; the use of irrigating contact lenses was associated with a significantly higher rate of debridement compared with the use of sewon or binocular indirect operating microscope (BIOM) noncontact lenses (23.5% vs. 12.1%, respectively; P < 0.001). In another study of patients who underwent pars plana vitrectomy, diabetic patients had more postoperative corneal epithelial defects if hand-held infusion lenses were used (32.1%) than if sew-on lenses (8.8%; P = 0.011) or noncontact lenses (0%; P < 0.001) were employed [13].

When the epithelium of the diabetic cornea is removed, it often comes off as an intact epithelial sheet, with the basement membrane attached to basal epithelial cells. In the nondiabetic eye, scraping of the epithelium removes only the epithelium and usually leaves the basement membrane intact and adherent to the

Figure 16.1. Neurotrophic corneal ulcer in a diabetic patient with decreased corneal sensitivity.

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323

Figure 16.2. Persistent corneal epithelial defect in a diabetic patient after vitreoretinal surgery.

stroma [9,14]. Ultrastructural abnormalities of the diabetic corneal epithelial basement membrane complex mimic findings in epithelial basement membrane dystrophies [15] and include thickening of the multilaminar basement membrane [7], decreased hemidesmosome frequency [16], and decreased penetration of anchoring fibrils [17].

The poor adhesiveness of the diabetic corneal basement membrane may be related to changes in biochemical composition induced by increased sorbitol and fructose produced by the aldose reductase pathway [9]. While topical aldose-reductase inhibitors may promote epithelial regeneration [18–20] and may prevent decreased corneal sensitivity due to diabetes [21] (and oral aldose-reductase inhibitors may improve corneal sensation in diabetic patients) [22], most studies have been performed in rats [18,19,21] and the efficacy of these agents in humans is unproven. In contrast, lubricants, limited epithelial debridement, and bandage contact lenses have proven to be effective in avoiding major ocular surface problems.

GLAUCOMA

Primary Open-Angle Glaucoma. The association between diabetes and primary openangle glaucoma (POAG) is unclear. Several studies have demonstrated a higher prevalence of elevated mean intraocular pressure (IOP) and POAG among diabetic patients compared with nondiabetic persons [23–25]. Several case-control studies support an association between diabetes and POAG, with the relative odds of having glaucoma among diabetic patients versus controls ranging from 1.6 to 4.7 [26–29]. Other studies, including population-based surveys such as the Baltimore Eye Survey, demonstrated no association between diabetes and POAG [30,31]. Although diabetes was common in participants of the Barbados Eye Survey and participants of the Baltimore Eye Survey, it was unrelated to the prevalence of openangle glaucoma [31,32]. Similarly, no significant association between diabetes and