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