The Many Faces of Diabetic Eye Disease: The Ocular Media
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).
Keratopathy
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
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.
Vitreous
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.
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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 http://www.diabeticeyes.com. |
