This article originally posted 02 July, 2004 and appeared in
The Many Faces of Glaucoma
Paul Chous, M.A., O.D.
Doctor of Optometry
Type 1 diabetic since 1968
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Glaucoma is the term used to describe a group of eye diseases that share the
following characteristics: progressive structural damage to the optic nerve, often
(but not always) associated with an increase in intraocular pressure (IOP), resulting
in a progressive and characteristic pattern of visual field loss and, if left
untreated, blindness. Glaucoma is broadly classified as either open angle or narrow
angle (this refers to the “angle” formed by the posterior cornea and
the iris root, the main route of passage for aqueous humor out of the eye), and
as either primary or secondary (the latter caused by preexisting ocular pathologies,
including intraocular inflammation and iris neovascularization.) The majority
of persons with glaucoma, including diabetics, have primary open angle glaucoma
(POAG).
The optic nerve consists of about one million individual nerve fibers that
transmit visual signals from distinct regions (fields) of vision. If enough
nerve fibers are damaged, permanent scotomata develop. Seminal research done
at Harvard University demonstrated that up to 50% of nerve fibers may be destroyed
before measurable visual field loss results. It also must be emphasized that
most patients are unaware of field loss until it is substantial. Glaucoma is
the second leading cause of blindness in the US, with 1-2% of the population
affected, and approximately 120,000 Americans were blind from the disease in
2002. It is believed that close to 400,000 Americans with diabetes have glaucoma.
Risk factors for developing open angle glaucoma include: African American ancestry
(5-6 fold increase in relative risk); family history, particularly in siblings
(2-3 fold increase); age (most persons with glaucoma are past age 50); ocular
hypertension (defined as intraocular pressure above 21 mm Hg – the higher
the IOP, the higher the risk); and diabetes (2-3 fold increase in relative risk).The
recently completed Ocular Hypertension Treatment Study (OHTS) revealed another
suspected but previously unsubstantiated risk factor, corneal thickness; study
participants with ocular hypertension and thinner corneas (<550 microns)
were three times as likely to develop glaucoma than were ocular hypertensives
with thicker corneas (>588 microns), as intraocular pressure measurements
are falsely low and falsely high for thin and thick corneas, respectively.
The etiology of increased susceptibility to POAG in diabetics remains somewhat
obscure. One hypothesis is that metabolic defects associated with diabetes alter
the biochemical and structural integrity of collagen that comprises the trabecular
meshwork through which circulating aqueous humor re-enters the vasculature,
and which gives mechanical support to optic nerve fibers as they exit through
the optic disc and sclera. Another view is that chronic hyperglycemia and concomitant
dyslipidemia adversely affect optic nerve microvasculature, resulting in a compromised
optic nerve ill-equipped to tolerate even modestly elevated IOP. Recent glaucoma
research has focused on malfunctioning programmed cell death (apoptosis) occurring
among proximal nerve fiber axons, and it may be that diabetic metabolism exacerbates
such genetic susceptibilities. Secondary, neovascular glaucoma is a direct consequence
of iris ischemia and neovascular closure of the anterior chamber angle, and
is a common sequelae of proliferative diabetic retinopathy (PDR) and ischemic
retinal vein occlusion (also more common in diabetes).
Intraocular pressure is a very important but often misunderstood element in
the diagnosis of glaucoma. Although most cases of glaucoma are associated with
elevated IOP, many are not. Studies show that between 5% and 20% of patients
with definitive glaucomatous optic atrophy and repeatable visual field defects
have IOPs consistently below 21mm Hg (so-called “normotensive” or
“low tension” glaucoma). Furthermore, most ocular hypertensives
do not develop glaucoma. Although elevated IOP is a definite risk factor, and
the primary factor amenable to medical and/or surgical intervention, it is neither
a necessary nor a sufficient cause of glaucoma.
Current treatment strategies are aimed at reducing intraocular pressure (even
in low tension glaucoma), as this has been shown conclusively to slow disease
progression. A variety of topical hypotensive agents are available, including
medicines which enhance outflow of aqueous humor (including miotics like pilocarpine,
and the newer prostaglandin analogs like latanoprost, travaprost and bimatoprost),
and those which inhibit formation of aqueous humor by the ciliary body (including
topical beta blockers, alpha agonists, and carbonic anhydrase inhibitors). Laser
trabeculoplasty and various glaucoma filtering surgeries typically are used
when medical therapy fails to achieve target IOP or is poorly tolerated by the
patient. The Collaborative Initial Glaucoma Treatment Study (CIGTS) demonstrated
similar outcomes (preservation of optic nerve and visual field) for medical
and surgical therapies over a four year period. Future treatments will likely
focus on neuroprotection of optic nerve fibers, and a host of claims have been
made for the neuroprotective effects of current ocular hypotensives.
Diabetics can reduce their risk of developing and/or losing vision to glaucoma
by achieving and maintaining good blood glucose control, and by getting regular
aerobic exercise when not contraindicated; in fact, several studies show that
aerobic exercise lowers IOP and improves ocular circulation. An annual dilated,
stereoscopic optic nerve evaluation in tandem with evaluation of risk factors
is critical in early diagnosis and preservation of vision. Computerized retinal
nerve fiber layer analysis and topographic optic nerve imaging now are commonly
used in clinical practice, and allow detection of subtle changes in optic nerve
architecture, but such changes are not necessarily pathognomonic of glaucoma.
The real key to preventing vision loss from glaucoma is patient compliance with
examination and treatment regimens, factors which depend, ultimately, upon excellent
patient education; in this respect, glaucoma management is quite analogous to
systemic management of diabetes.
In my next segment, we will consider diabetic eye diseases that affect the
transparent ocular media (pre-corneal tear film, cornea, lens and vitreous),
including diabetic keratopathy and cataract.
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 http://www.diabeticeyes.com.
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