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The Many Faces of Diabetic Eye Disease: The Ocular Media

Jul 2, 2004

Paul Chous, M.A., O.D. Doctor of Optometry Type 1 diabetic since 1968

Thus far, we have considered two significant causes of permanent vision loss in patients with diabetes: diabetic retinopathy (particularly proliferative retinopathy and diabetic macular edema) and glaucoma. Now, we will turn our attention to manifestations of diabetic eye disease affecting the transparent ocular media (pre-corneal tear film, cornea, aqueous humor, lens, and vitreous).


Diabetic keratopathy refers to the deleterious effects of diabetes on the cornea, which can reduce vision and cause a good deal of patient discomfort, and is often under-diagnosed in my experience. Biochemical and histopathologic evidence demonstrates that chronic hyperglycemia weakens hemidesmosomal attachments between the corneal epithelium and its underlying basement membrane, making patients much more susceptible to both incidental corneal abrasions and recurrent corneal erosion syndrome; the latter condition is characterized by chronic, episodic denuding of a fragile corneal epithelium, and is typically accompanied by considerable photophobia, lacrimation (tearing) and pain (recall that the cornea contains more free nerve endings per square millimeter than any part of the body). Although corneal epithelium typically regenerates very quickly, hyperglycemia retards mitosis of the basal epithelium, which may not attach adequately due to fewer and poorly anchored hemidesmosomes, and a vicious cycle of erosions followed by healing followed by more erosions ensues; acute hyperglycemia and/or casual eye rubbing may reinitiate the cycle, even in cases where overall glycemic control is good.

Keratopathy may be compounded by the fact that many diabetics experience reduction of normal corneal sensitivity (neurotrophic keratitis). This is essentially a form of diabetic neuropathy affecting the ophthalmic division of the Vth (Trigeminal) cranial nerve, with subsequent irregular thickening of Schwann cells, axonal degeneration, and reduced ability to recover from hyopoxic stress (as incurred by prolonged lid closure during sleep and/or contact lens wear). Another effect is decreased secretion of tears (secondary to both afferent and efferent neuropathic defects), a factor which increases tear osmolarity and contributes to corneal epithelial fragility.

The pre-corneal tear film serves lubricant, immunologic, and optical functions. Both sufficient quantity and quality of this triphasic layer (consisting of lipid, water, and mucin) are required to prevent corneal desiccation and infection, and to yield stable, high-quality visual optics. An inadequately moisturized, compromised, desensitized corneal epithelium poses chronic risk of microbial infection, ulcerative keratitis and vision loss. Consequently, diabetes is a relative contraindication to contact lens wear, and should always be approached with heightened caution and meticulous follow-up by an experienced eye care professional.


Cataract, clouding of the crystalline lens sufficient to cause reduced visual acuity, is part of the normal aging process. Patients with diabetes tend to experience cataracts 10-20 years prematurely, and their cataracts tend to develop more rapidly than those found in persons without diabetes. Glucose in the aqueous humor freely enters the crystalline lens where it is metabolized by four distinct pathways; the accumulation of sorbitol, mediated by aldose reductase and the rate-limiting enzyme polyol dehydrogenase, causes true “diabetic cataract” (snowflake opacities in the lens cortex) by drawing water into the lens and disrupting the precise arrangement of collagen fibers required for lens transparency. More typical cataracts, including those more commonly seen in diabetes, are associated with glycosylation of lens proteins, accumulation of sugar alcohols, and influx of sodium ions, calcium ions and water, leading to a loss of transparency. Refractive shifts are common as cataracts develop, particularly and acutely in patients with poor glycemic control. Although cataract surgery is curative, widely available in the West, and typically very successful, diabetic patients do experience a higher rate of surgical complications, including infection, worsening of pre-existing retinopathy, and cystoid macular edema.


The vitreous humor in diabetic patients without retinopathy is typically normal, save higher concentrations of glucose. With the onset of retinopathy, however (particularly PDR), the vitreous may become the “root of all evil within the eye” (at least according to one prominent retinal specialist I encountered during my training). Hemorrhage from diabetic retinopathy is readily absorbed by the retina, but once it percolates anteriorly into the vitreous body, is slow to reabsorb and may cause moderate to profound visual impairment. Moreover, the vitreous provides necessary mechanical support for the development of fibrovascular tissue encountered in PDR, and resultant contraction of the vitreous exerts the tractional forces required for traction retinal detachment and blindness. Although vitreous hemorrhage usually resolves without intervention (in one to six months), surgical removal of vitreous and blood (vitrectomy) by a vitreoretinal subspecialist is sometimes needed. Surgical removal of vitreous that is tethered to the retina by fibrovascular proliferation is more problematic, and visual prognosis is often poorer is these cases.

Generally speaking, the risk and severity of diabetic eye disease affecting the optical media may be attenuated by tight glycemic control, by regular consultation with an optometrist or ophthalmologist experienced with and interested in diabetic eye disease, and by excellent patient education. Next time, we will consider diabetes and double vision and, in a few weeks, some “clinical pearls” for helping your patients avoid or minimize the eye complications of diabetes.

Dr. Paul Chous received his undergraduate education at Brown University and the University of California at Irvine, where he was elected to Phi Beta Kappa in 1985. He received his Masters Degree in 1986 and his Doctorate of Optometry in 1991, both with highest honors from the University of California at Berkeley. Dr. Chous was selected as the Outstanding Graduating Optometrist in 1991. He has practiced in Renton, Kent, Auburn and Tacoma, Washington for the last 12 years, emphasizing diabetic eye disease and diabetes education. Dr. Chous has been a Type 1 diabetic since 1968. He lives in Maple Valley, Washington with his wife and son.

About the Author

Dr. Paul Chous is the recent author of a critically acclaimed book for patients and health care providers on diabetes and the eye, Diabetic Eye Disease: Lessons From A Diabetic Eye Doctor – How To Avoid Blindness and Get Great Eye Care (Fairwood Press). He may be reached via his web site at