Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Diabetic retinopathy Jon P. Tierney MD To cite this article: Jon P. Tierney MD (1992) Diabetic retinopathy, Postgraduate Medicine, 91:5, 141-158, DOI: 10.1080/00325481.1992.11701286 To link to this article: http://dx.doi.org/10.1080/00325481.1992.11701286
Published online: 17 May 2016.
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Third of three articles on eye disorders
Diabetic retinopathy The primary care physician's role in management
Preview Diabetic retinopathy is a treatable condition currently managed with aggressive therapy. Early recognition of the condition and its causes can protect the patient against blindness and sometimes restore visual acuity. From the first funduscopic examination and visual-acuity evaluation, the primary care physician starts the patient on a program of watchful follow-up, treatment, and referral to an ophthalmologist.
Jon P. Tiemey, MD •:• Diabetes is a disease that affects about 3% of the population in the United States and is the leading cause of blindness between the ages of20 and 74. There may be 5 million known cases in this country and an equal or greater number of undiagnosed ones. While not all diabetic patients fit neatly into the categories, a convenient classification divides diabetes into two groups: juvenileonset (type I) and adult-onset (type 11). The adult-onset group is by far the larger.
Diabetes can affect vision in multiple ways: (1) Cataracts are more common in the diabetic than in the nondiabetic population; (2) glaucoma is more common in the diabetic population, and this group is particularly prone to a difficult-to-control form of neovascular glaucoma; (3) diabetic circulatory changes can produce optic neuropathy; and (4) circulatory changes in the retina can affect visual function. Of the four, the retinal manifestations of diabetes are the most important cause of visual loss. This article concerns itself largely
with the causes of retinal changes in diabetes, the evaluation and referral of patients, and the treatment options.
The primary care evaluation of diabetic patients A funduscopic examination should be a part of the assessment of every diabetic patient in the primary care office. The use of 1% tropicarnide sterile ophthalmic solution or similar eyedrops to dilate the pupils facilitates examination of the retina, particularly the periphery. The presence of retinopathy with decreased central vision should prompt the primary care physician to do a complete ophthalmic evaluation. Visualization of new vessels on the disk or retina or of vitreous hemorrhage is an indication for prompt referral to an ophthalmologist. Diabetic retinopathy is progressive, and regular follow-up examinations are imperative; the interval between examinations depends on the severity of the retinopathy present at the initial examination. Calor fundus photographs are useful to record progression of retinopathy, and fluorescein angiography can show vascular changes not apparent to the examiner. Keeping simple
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Keeping simple drawings of the fundus in a diabetic patient's record is helpful in recording and remembering retinal changes.
drawings of the fundus in the patient's record is helpful in recording and remembering retinal changes. Measurement of visual acuity during the physical examination can provide a due to the presence of macular edema. Patients with juvenile-onset diabetes should undergo evaluation for retinopathy annually after 5 years' duration of disease. An estimated 72% of patients with juvenile-onset diabetes eventually progress to proliferative retinopathy, and 42% ultimately have clinically significant macular edema. Patients with adult-onset diabetes should be referred for ophthalmologic evaluation at the time of diagnosis, since 5% of these patients have a substantial amount of macular edema at that point.
Causes of visual loss in diabetic retinopathy The major factors responsible for visual loss in diabetic retinopathy are retinal edema, retinal ischemia, and retinal or preretinal hemorrhage. Retinal vascular dilatation and diffuse mild retinal edema may be the earliest funduscopic findings in diabetic retinopathy. The healthy retina is protected from the accumulation of fluid within its layers by two barrier systems: (I) the blood-retinal
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barrier, which is maintained by the integrity of the vascular endothelial cells, and (2) the tight junctions of the single-layer pigment epithelial cell layer between the retina and the peripheral choroidal circulation. Both of these barriers can fail in diabetes; when they do, the retina becomes edematous and its function is compromised. Retinal ischemia develops when the retinal arterioles and microcirculation become occluded. The retinal arterioles are all end-vessels, ie, they lack collateral circulation. Closure of retinal vessels leads to ischemic retinal damage peripheral to the site of occlusion. If the occlusion involves the circulation to the macula, central vision is affected and the visual loss will be permanent. Hemorrhage within the retina may be subtle and may go unnoticed by the patient. Preretinal or vitreous hemorrhage is usually a dramatic event, significantly affecting vision in the involved eye. Vitreous hemorrhage usually dears over a period of weeks but tends to recur if not treated. The duration of diabetes before retinopathy is visible to the examiner varies considerably. Age at onset of diabetes, severity of diabetes, and the patient's overall
medical status, as well as the adequacy of diabetic control, play a role in determining the onset of diabetic changes. Heredity may contribute, as may such personal risk factors as hypertension and smoking. Pregnancy may also aggravate diabetic retinopathy. In general, the incidence of diabetic retinopathy increases with the duration of the disease and probably with its severity. In juvenile-onset diabetes the incidence of retinopathy is 50% at 10 years' duration and about 75% at 20 years' duration. Overall in diabetes, retinopathy seldom appears before 5 years' duration, but about 25% of the juvenile-onset group have some changes by that time. In adult-onset diabetes, retinopathy may be present at the time of diagnosis, perhaps because many of these individuals have had covert diabetes for years. The chance discovery of retinal changes causing visual loss may be the precipitating factor in establishing the diagnosis of diabetes. In adult-onset diabetes, 5% of patients already have established retinopathy at the time of diagnosis.
Types of diabetic retinopathy Diabetic retinopathy may be conveniently divided into two
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In adult-onset diabetes, retinopathy may be present at the time of diagnosis.
general groups, background (nonproliferative) retinopathy and proliferative retinopathy. Ninety percent of diabetics with retinopathy have the background type.
Figure 1. Cotton-wool spots around disk in 23-year-old patient with juvenile-onset diabetes. Diffuse retinal edema is also present, along with arteriolar narrowing, flame-shaped hemorrhages, and venous irregularities. The patient is also hypertensive.
BACKGROUND RETINOPATIIY-
Ocular findings of this non proliferative type include edema, microaneurysms, retinal hemorrhages, cotton-wool spots, lipid deposits, and intraretinal vascular abnormalities. RETINAL EDEMA-This is the earliest funduscopic finding in diabetic retinopathy. However, it may be subtle, particularly if the edema is diffuse, giving the retina a uniformly grayish appearance. The leakage is often due to general dilatation of the capillary bed but can also occur through defects in the underlying pigment epithelium. Hypertension and renal disease can aggravate diffuse retinal edema. With prolonged retinal edema, cystic changes occur in the involved retina, and permanent visual damage may result. MICROANEURYSMS-The first readily visible funduscopic finding, microaneurysms are reddish focal dilatations of capillaries, up to 50 1-Lm in diameter. They usually occur in areas of poor retinal perfusion and are most likely to be found initially in the
region temporal to the macula, perhaps because this area has marginal circulation. Microaneurysms tend to leak fluid into the retina, so they often appear close to areas of retinal edema. They sometimes regress spontaneously. RETINAL HEMORRHAGES-
When they occur in the outer retinal layers, these hemorrhages have a blodike appearance, typically '!i to 1/3 disk-diameter in size. Flame-shaped hemorrhages localize in the inner retinal layers and orient themselves along the distribution of the nerve fiber layers in which they lie. Flameshaped hemorrhages are common with hypertension but can occur in nonhypertensive diabetic patients. All retinal hemorrhages are
transient in nature, usually resolving in a month or two. COTION-WOOL SPOTs-These soft exudates (figure 1) occur in areas of localized ischemia. They have irregular borders and range up to 1 disk-diameter in size, obscuring the underlying retinal detail. They represent ischemic damage to the nerve fiber layer and clear in 3 to 6 months, more slowly than retinal hemorrhage clears. Actual anatomic closure of vessels does not appear to be necessary for their development. They may not always produce visual loss, but they are damaging to retinal function. LIPID DEPOSITs-As retinal edema occurs from damaged and dilated retinal vessels, healthier vessels and the underlying pig-
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Microaneurysms are the first readily visible funduscopic finding in diabetic retinopathy.
Figure 2. Three loop or shunt vessels visible along superotemporal vein in left eye of 44-year-old patient with juvenile-onset diabetes. These intraretinal vascular changes are precursors to proliferative retinopathy. Microaneurysms, lipid, and dot -blot hemorrhages are also present.
ment epithelium attempt to reabsorb and recirculate the accumulated fluid. In localized areas the proteinaceous residues of such leakage may linger as irregular yellowish deposits known as lipid, or hard, exudates. Lipid tends to accumulate in a circinate pattern around leaking microaneurysms. While the fluid portion of retinal edema clears in a matter of weeks with elimination of the cause of the leakage, the lipid portion takes many months to clear. INTRARETINAL VASCULAR CHANGES-Shunt vessels (figure 2) are collateral venous channels that develop in conjunction with areas of retinal infarction. Venous beading, an irregular constriction and dilatation, gives the retinal veins a sausagelike appearance.
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Venous beading is generally found near areas of poor perfusion in the retina. PROLIFERATIVE RETINOPATHY
-The dividing line between background and proliferative retinopathy is reached with the development of new vessels on the surface of the retina or extending into the vitreous cavity. NEOVASCULARIZATION-Two thirds of new vessels develop either on the optic nerve head or in close proximity to it. Through a direct ophthalmoscope they are visible as fine, delicate vascular loops without supporting fibrous tissue. The use of the redfree light on the direct ophthalmoscope facilitates recognition at an earlier stage of development.
In about 25% of patients with new vessel formation, the new vessels develop in the peripheral retina and may be difficult to appreciate unless the pupil is dilated. Retinal ischemia appears to stimulate their development, and peripheral new vessels are usually found at the proximal edge of an area of significant retinal nonperfusion. In the case of new vessels on the disk, extensive diffuse retinal ischemia may provide the stimulus for their development. New vessels grow on the surface of the retina, along the vitreoretinal interface, or into the vitreous itself. Occasionally the new vessels regress spontaneously, although those on the disk are less likely to do so. The rate of growth of new vessels varies; some change little over a period of months, while others progress rapidly in weeks. NEW VESSEL HEMORRHAGEEventually, new vessels are prone to hemorrhage, and the agent of hemorrhage appears to be traction on the fragile new structures by the vitreous body. The vitreous separates from the retina as a part of the aging process, usually in the sixth decade of life. Posterior vitreous separation occurs earlier in the diabetic patient than in the nondiabetic. Traction on the new vessels by the detachcontinued
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Through a direct ophthalmoscope, new vessels are visible as fine, delicate vascular loops without supporting fibrous tissue.
ing vitreous produces hemorrhage, either at the vitreoretinal interface or into the vitreous itse!£ The hemorrhage appears to stimulate further vitreous contraction, so a self-accelerating process is created with a recurrent cycle of hemorrhage and clearing. TRACTIONAL RETINAL DETACHMENT-Ultimately, fibrous tissue develops in conjunction with the new vessels, and fibrous tissue traction on the new vessels may provoke further bleeding. In addition, pull on the retina itself may produce retinal detachment. Continued visual decline is the usual result. The proximity of disk new vessels to the macula makes them a particular threat to central vision, owing to the danger of tractional retinal detachment of the macula. About 50% of diabetic patients with significant new vessels on the disk progress to legal blindness over a 5-year period.
Treatment of diabetic retinopathy A great deal of what we have learned about the treatment of diabetic retinopathy has come to us through controlled prospective studies done at collaborating centers over the past 20 years. It is tempting to believe that strict
control of diabetes may prevent the development of retinopathy; some evidence indicates that strict control in the early years may delay the appearance of the first retinal manifestations. Once established, the retinal lesions advance at a varying rate that does not correlate well with diabetic control. Paradoxically, the sudden normalization of the blood glucose level (as in patients who are undergoing renal or pancreatic transplantation), the use of continuous-insulin-infusion devices, or a stepped-up regimen of insulin injections may worsen the retinopathy already present, at least over the short term. Similarly, the use of systemic agents, such as cholesterol-lowering drugs, has failed to demonstrate any improvement in vision in established diabetic retinopathy, although some objective improvement in its appearance has been noted. Nor has the use of anti platelet agents such as aspirin been shown to have any effect on established diabetic retinopathy. PH~COAGVLKnON-The
early lasers-the xenon photocoagulator and the ruby and the blue-green argon lasers-were ineffective in permanently sealing new vessels off the surface of the retina, and treatment to disk new
vessels resulted in serious side effects, including laser-induced optic neuritis and large visualfield defects related to nerve fiber damage. Interest turned to scatter treatment of the retina. In this method, termed panretinal photocoagulation, regularly spaced burns are delivered to the periphery of the retina. The disk, macula, and immediately adjacent areas are not treated. USE IN PROLIFERATIVE RETINOPATHY-In 1971 the Diabetic Retinopathy Study (DRS), a multicenter project to study the efficacy of laser photocoagulation in the treatment of proliferative diabetic retinopathy, identified high-risk characteristics for the development of severe visual loss: (1) the presence of new vessels on the retina; (2) the presence of new vessels on or in close proximity to the disk; (3) the severity of the new vessels present, as compared with a standard photograph; and (4) the presence of vitreous hemorrhage. More than 1,500 patients with high-risk characteristics were assigned randomly either to treatment with panretinal photocoagulation or to observation. Within 2 years it was apparent that the treated patients were at a statistically significant lower risk of severe visual loss than were untreat-
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Once established, retinal lesions advance at a varying rate that does not correlate well with diabetic control.
Figure 3. Left eye of 33-yearold patient with asymptomatic juvenile-onset diabetes and 20/20 vision. a. Extensive fine new vessels off surface of disk. b. Six months after panretinal photocoagulation, disk new vessels have regressed, leaving fibrous stalk that extends off the disk and along the superotemporal arcade.
a
b
ed controls. At completion of the DRS in 1979, investigators concluded that in patients with three of the high-risk characteristics, panretinal photocoagulation could decrease the incidence of severe visual loss by 50% to 65% (figure 3). Panretinal photocoagulation did have some undesirable side effects. Patients lost some periph-
eral vision. In addition, a small percentage had permanent loss of central vision (ie, one or more lines on the Snellen eye chart). This was attributed to exacerbation of preexisting macular edema by the peripheral photocoagulation. Investigators found that exacerbation could be lessened by dividing the laser treatment into two or more sessions or by pro-
viding simultaneous focal laser treatment to the leaking microaneurysms in the perimacular area. As a result of the DRS findings, prompt panretinal photocoagulation is now generally regarded as the treatment of choice for patients with well-established neovascularization of the retina, with or without vitreous hemorrhage. This procedure significantly reduces, but does not eliminate, the likelihood of severe visual loss in proliferative retinopathy. The exact mechanism by which peripheral laser therapy induces regression of disk new vessels is not known, but ablation of poorly perfused tissue in the peripheral retina may lessen the ischemic stimulus to new vessel formation on the disk. Longterm preservation of vision in patients receiving panretinal photocoagulation has been reported, and patients can be successfully re-treated if new vessels recur after the initial photocoagulation treatment. USE IN BACKGROUND RETINOP-
ATHY-The DRS did not answer questions about the efficacy of laser treatment in patients with background diabetic retinopathy and its associated macular edema. Macular edema can cause visual
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Panretinal photocoagulation is now generally regarded as the treatment of choice for patients with well-established neovascularization of the retina, with or without vitreous hemorrhage.
loss in juvenile-onset diabetes bur is an even greater threat in the adult-onset type. Neovascularization of the retina does occur in adult-onset diabetes, but macular edema is estimated to be three to five times more prevalent as a cause of visual loss in adult-onset diabetes. The question remained: Does laser photocoagulation aid in the prevention of visual loss in back- a ground diabetic retinopathy, and at what stage in the disease should patients receive laser therapy? To answer this question, the Early Treatment Diabetic Retinopathy Study (ETDRS) was begun in 1980, and the results of this prospective, randomized study were reported in 1985. Patients with "clinically significant macular edema" were recruited and assigned either to treatment b with laser or to observation. Clinically significant macular edema was defined as the presence of normal and were re-treated if significant amounts (>I diskretinal edema or lipid deposits rediameter in extent) of edematous curred near the macula during retinal thickening within 1 diskdiameter of the macula or the follow-up. Laser treatment conpresence of retinal lipid within sisted either of focal burns to leaking microaneurysms (figure 1 disk-diameter of the center of 4) in the perimacular area or of the macula. grid-style laser treatment to areas Patients with clinically signifiof diffuse retinal edema or capilcant macular edema assigned to lary nonperfusion, as identified laser treatment were treated even though central vision was still with fluorescein angiography.
Figure 4. Fundus of left eye of 61-year-old patient with adultonset diabetes. a. Heavy background diabetic retinopathy with retinal microaneurysms, hemorrhage, early macular lipid deposits, and diffuse retinal edema (vision, 20/200). b. Six months after heavy focal laser burns to leaking microaneurysms that avoided treatment to the immediate macular area. Patient had unexpectedly good improvement in vision to the 20/30 level.
Laser burns of 50 to 200 f.Lm were utilized to minimize visualfield changes; the macula itself was not treated. The ETDRS demonstrated that eyes with clinically significant macular edema and mild to moderate background diabetic retinopathy benefited from focal laser photocoagulation. The incidence of significant visual loss (ie,
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Macular edema can cause visual loss in juvenile-onset diabetes but is an even greater threat in adult-onset diabetes.
Jon P. Tierney, MD Or Tierney is a specialist in diseases of the vitreous and retina, Minneapolis.
two or more lines on the Snellen eye chart) over 3-year follow-up was 12% in the treated group but 24% in the untreated controls. Subtle changes in visual fields were noted after focal treatment, but the incidence was not statistically different from that of similar changes in the nontreated controls_ A relatively small percentage of treated patients with visual loss due to macular edema showed statistically significant improvement in central vision after laser therapy. In about 35% of this group, central vision improved by two or more lines on the Snellen eye chart. Since the ETDRS treated patients with clinically significant macular edema even if they had
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normal vision and since relatively few patients with visual loss due to macular edema experienced significant improvement in vision after laser therapy, the conclusion might be drawn that diabetic patients with clinically significant macular edema and normal vision should receive laser treatment focally before visual loss occurs. The ETDRS recommended that they be considered for treatment. If it is elected not to treat before visual loss, the ETDRS recommended observation at closer intervals for the development of any visual decline, at which time treatment should be instituted promptly. Diffuse retinal edema presents a more difficult problem than focal edema. Treatment for the dif-
fuse form consists of grid-style placement of 50- to 200-J..Lm laser burns to the posterior pole around the macular area, avoiding the macula itsel£ The mechanism of action for this treatment is not known. It probably does not affect the retinal capillaries, since the burn is to the outer retinal layers and adjacent pigment epithelium. Laser treatment in this situation may serve to decrease the metabolic needs of the retina by destroying photoreceptors and thus decreasing retinal metabolic needs and blood flow. Alternatively, the laser may affect the pigment epithelium, perhaps decreasing its permeability or stimulating it to reabsorb fluid from the edematous retina. VITRECIOMY-This surgical procedure removes intraocular hemorrhage and fibrous tissue from the eye to allow treatment of the underlying disease. In the diabetic patient, it is generally accompanied by the delivery of laser beams through a fiberoptic cannula to treat the retinopathy and facilitate reattachment of a retina undergoing tractional detachment. Vitrectomy is usually reserved for diabetic patients with advanced retinopathy when refracting-media opacities or vitreous hemorrhage prevents use of
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Vitrectomy is usually reserved for use in advanced retinopathy when refracting-media opacities or vitreous hemorrhage prevents use of conventional laser therapy or interferes with vision.
conventional laser therapy or interferes with vision. While it can often preserve vision in advanced diabetic retinopathy, it carries a statistically significant rate of complications (induced cataract, retinal tears) and is somewhat less effective than laser photocoagulation delivered at an earlier stage in the diabetic process. The Diabetic Retinopathy Vitrectomy Study (DRVS) researched the role of early vitrectomy in treating vitreous hemorrhage severe enough to preclude the use of laser photocoagulation. The DRVS demonstrated that prompt vitrectomy in juvenile-onset diabetes with severe vitreous hemorrhage could decrease the incidence of severe visual loss from 35% to 11%. Early vitrectomy cleared the refracting media and allowed prompt laser photocoagulation to the underlying retinopathy (figure 5). In a comparison of adultonset and juvenile-onset diabetic patients with severe vitreous hemorrhage who were observed for clearing of the hemorrhage, the DRVS found that the adultonset group was somewhat less prone to development of severe visual loss and more likely to have spontaneous clearing, prob-
Figure 5. Right fundus of 28year-old patient with juvenileonset diabetes. a. Extensive new vessels and fibrosis off the disk, obscuring retinal detail and preventing laser photocoagulation. Optic nerve is barely visible at 3-o'clock position. Vision was limited to hand movements. b. After pars plana vitrectomy to clear refracting media and allow laser photocoagulation to retinopathic areas. Laser scars are visible temporal to optic nerve. Visual recovery was limited to 20/400 because of poor retinal circulation.
ably because their underlying retinopathy was not apt to be as severe. The DRVS concluded that patients with adult-onset diabetes could safely be observed for spontaneous clearing for a longer period than those in the juvenile-onset group; in the latter, prompt vitrectomy is beneficial.
Comment Through the use of funduscopic examinations and visualacuity measurement, primary care physicians play an important role in obtaining timely therapy for their diabetic patients. The number of these pa-
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tients is impressive and increasing. A great many of them are not being seen by an ophthalmologist; many have no eye care of any type. When finally referred, many already have significant retinopathy; treatment might have been more effective if it had been instituted earlier in the course of their disease. Laser photocoagulation cannot prevent all visual loss in all diabetic patients but can sub-
stantially reduce the amount and severity in many. A recent socioeconomic study investigated the cost of screening all diabetic patients for significant retinopathy and for treating the expected incidence of visionthreatening retinopathy. Using a cost-accounting basis, investigators determined that the cost of effective treatment was appreciably less than the cost to society in Social Security dis-
ability payments. Proposals have been made to institute such a program. Rl't'l
-®
Earn credit on this article. See CME Quiz.
Address for correspondence: Jon P. Tierney, MD, Park Avenue Medical Building, 710 E 24th St, Suite 406, Minneapolis, MN 55404.
Bibliography Blakenship GW. Proliferative diabetic retinopathy: principles and techniques of surgical treatment. In: Ryan SJ, ed. Retina. St Louis: Mosby-Year Book, 1989:515-39 Bresnick GH. Background diabetic retinopathy. In: Ryan SJ, ed. Retina. St Louis: Mosby-Year Book, 1989:327-66 Cantrill HL. The Diabetic Retinopathy Study and the Early Treatment Diabetic Retinopathy Study. Int Ophthalmol Clin 1984;24(4): 13-29 Davis MD. Diabetes mellitus. In: Gold DH, Weingeist TA, eds. The eye in systemic disease. Philadelphia: JB Lippincott, 1990:79-85 The DCCT Research Group. The Diabetes Control and Complications Trial (DCCT): design and methodologic considerations for the feasibility phase. Diabetes 1986;35(5):530-45 The Diabetic Retinopathy Vitrectomy Srudy Research Group. Early vitrectomy for severe proliferative diabetic retinopathy in eyes with useful vision: results of a randomized trial. Diabetic Retinopathy Vitrectomy Study Report 3. Ophthalmology 1988;95(10):1307-20 Early Trearment Diabetic Retinopathy Srudy
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Research Group. Photocoagulation for diabetic macular edema: Early Treatment Diabetic Retinopathy Study report number 1. Arch Ophthalmol 1985; 103(12): 1796-806 Garcia CA, Ruiz RS. Diabetes and the eye. Clin Symp 1984;36(4):2-32 Harris MI, Hadden WC, Knowler WC, et al. Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in US population aged 20-74 yr. Diabetes 1987;36(4):523-34 JavittJC, Canner JK, Sommer A. Cost effectiveness of current approaches to the control of retinopathy in type I diabetics. Ophthalmology 1989;96(2):255-64 Kahn HA, Hiller R. Blindness caused by diabetic retinopathy. Am J Ophthalmol 1974; 78(1):58-67 Klein R, Klein BE, Moss SE. Visual impairment in diabetes. Ophthalmology 1984;91(1): 1-9 Klein R, Klein BE, Moss SE, et al. The Wisconsin Epidemiologic Srudy of Diabetic Retinopathy. II. Prevalence and risk of diabetic retinopathy when age at diagnosis is less than
30 years. Arch Ophthalmol1984;102(4):520-6 Klein R, Klein BE, Moss SE, et al. The Wisconsin Epidemiologic Study of Diabetic Retinopathy. Ill. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Arch Ophthalmol 1984; 102(4):527 -32 Mensher JH. Laser in diabetic retinopathy. Ophthalmol Clin North Am 1989;2(Dec) :58396 Olk RJ. Modified grid argon (blue-green) laser photocoagulation for diffuse diabetic macular edema. Ophthalmology 1986;93(7):938-50 Rand U, Prud'homme GJ, Ederer F, et al. Factors influencing the development of visual loss in advanced diabetic retinopathy: Diabetic Retinopathy Study (DRS) Report No. 10. Invest Ophthalmol Vis Sci 1985;26(7):983-91 Skyler J. Relation of metabolic control of diabetes mellitus to chronic complications. In: Rifkin H, ParteD, eds. Diabetes mellitus. 4th ed. New York: Elsevier Science Publishing, 1990:856-68
DIABETIC RETINOPATHY • VOL 91/NO 5/APRIL 1992/POSTGRADUATE MEDICINE
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Diabetic retinopathy Jon P. Tierney MD To cite this article: Jon P. Tierney MD (1992) Diabetic retinopathy, Postgraduate Medicine, 91:5, 141-158, DOI: 10.1080/00325481.1992.11701286 To link to this article: http://dx.doi.org/10.1080/00325481.1992.11701286
Published online: 17 May 2016.
Submit your article to this journal
View related articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [University of Technology Sydney]
Date: 23 July 2016, At: 00:55
Symposium
Downloaded by [University of Technology Sydney] at 00:55 23 July 2016
Third of three articles on eye disorders
Diabetic retinopathy The primary care physician's role in management
Preview Diabetic retinopathy is a treatable condition currently managed with aggressive therapy. Early recognition of the condition and its causes can protect the patient against blindness and sometimes restore visual acuity. From the first funduscopic examination and visual-acuity evaluation, the primary care physician starts the patient on a program of watchful follow-up, treatment, and referral to an ophthalmologist.
Jon P. Tiemey, MD •:• Diabetes is a disease that affects about 3% of the population in the United States and is the leading cause of blindness between the ages of20 and 74. There may be 5 million known cases in this country and an equal or greater number of undiagnosed ones. While not all diabetic patients fit neatly into the categories, a convenient classification divides diabetes into two groups: juvenileonset (type I) and adult-onset (type 11). The adult-onset group is by far the larger.
Diabetes can affect vision in multiple ways: (1) Cataracts are more common in the diabetic than in the nondiabetic population; (2) glaucoma is more common in the diabetic population, and this group is particularly prone to a difficult-to-control form of neovascular glaucoma; (3) diabetic circulatory changes can produce optic neuropathy; and (4) circulatory changes in the retina can affect visual function. Of the four, the retinal manifestations of diabetes are the most important cause of visual loss. This article concerns itself largely
with the causes of retinal changes in diabetes, the evaluation and referral of patients, and the treatment options.
The primary care evaluation of diabetic patients A funduscopic examination should be a part of the assessment of every diabetic patient in the primary care office. The use of 1% tropicarnide sterile ophthalmic solution or similar eyedrops to dilate the pupils facilitates examination of the retina, particularly the periphery. The presence of retinopathy with decreased central vision should prompt the primary care physician to do a complete ophthalmic evaluation. Visualization of new vessels on the disk or retina or of vitreous hemorrhage is an indication for prompt referral to an ophthalmologist. Diabetic retinopathy is progressive, and regular follow-up examinations are imperative; the interval between examinations depends on the severity of the retinopathy present at the initial examination. Calor fundus photographs are useful to record progression of retinopathy, and fluorescein angiography can show vascular changes not apparent to the examiner. Keeping simple
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Keeping simple drawings of the fundus in a diabetic patient's record is helpful in recording and remembering retinal changes.
drawings of the fundus in the patient's record is helpful in recording and remembering retinal changes. Measurement of visual acuity during the physical examination can provide a due to the presence of macular edema. Patients with juvenile-onset diabetes should undergo evaluation for retinopathy annually after 5 years' duration of disease. An estimated 72% of patients with juvenile-onset diabetes eventually progress to proliferative retinopathy, and 42% ultimately have clinically significant macular edema. Patients with adult-onset diabetes should be referred for ophthalmologic evaluation at the time of diagnosis, since 5% of these patients have a substantial amount of macular edema at that point.
Causes of visual loss in diabetic retinopathy The major factors responsible for visual loss in diabetic retinopathy are retinal edema, retinal ischemia, and retinal or preretinal hemorrhage. Retinal vascular dilatation and diffuse mild retinal edema may be the earliest funduscopic findings in diabetic retinopathy. The healthy retina is protected from the accumulation of fluid within its layers by two barrier systems: (I) the blood-retinal
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barrier, which is maintained by the integrity of the vascular endothelial cells, and (2) the tight junctions of the single-layer pigment epithelial cell layer between the retina and the peripheral choroidal circulation. Both of these barriers can fail in diabetes; when they do, the retina becomes edematous and its function is compromised. Retinal ischemia develops when the retinal arterioles and microcirculation become occluded. The retinal arterioles are all end-vessels, ie, they lack collateral circulation. Closure of retinal vessels leads to ischemic retinal damage peripheral to the site of occlusion. If the occlusion involves the circulation to the macula, central vision is affected and the visual loss will be permanent. Hemorrhage within the retina may be subtle and may go unnoticed by the patient. Preretinal or vitreous hemorrhage is usually a dramatic event, significantly affecting vision in the involved eye. Vitreous hemorrhage usually dears over a period of weeks but tends to recur if not treated. The duration of diabetes before retinopathy is visible to the examiner varies considerably. Age at onset of diabetes, severity of diabetes, and the patient's overall
medical status, as well as the adequacy of diabetic control, play a role in determining the onset of diabetic changes. Heredity may contribute, as may such personal risk factors as hypertension and smoking. Pregnancy may also aggravate diabetic retinopathy. In general, the incidence of diabetic retinopathy increases with the duration of the disease and probably with its severity. In juvenile-onset diabetes the incidence of retinopathy is 50% at 10 years' duration and about 75% at 20 years' duration. Overall in diabetes, retinopathy seldom appears before 5 years' duration, but about 25% of the juvenile-onset group have some changes by that time. In adult-onset diabetes, retinopathy may be present at the time of diagnosis, perhaps because many of these individuals have had covert diabetes for years. The chance discovery of retinal changes causing visual loss may be the precipitating factor in establishing the diagnosis of diabetes. In adult-onset diabetes, 5% of patients already have established retinopathy at the time of diagnosis.
Types of diabetic retinopathy Diabetic retinopathy may be conveniently divided into two
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In adult-onset diabetes, retinopathy may be present at the time of diagnosis.
general groups, background (nonproliferative) retinopathy and proliferative retinopathy. Ninety percent of diabetics with retinopathy have the background type.
Figure 1. Cotton-wool spots around disk in 23-year-old patient with juvenile-onset diabetes. Diffuse retinal edema is also present, along with arteriolar narrowing, flame-shaped hemorrhages, and venous irregularities. The patient is also hypertensive.
BACKGROUND RETINOPATIIY-
Ocular findings of this non proliferative type include edema, microaneurysms, retinal hemorrhages, cotton-wool spots, lipid deposits, and intraretinal vascular abnormalities. RETINAL EDEMA-This is the earliest funduscopic finding in diabetic retinopathy. However, it may be subtle, particularly if the edema is diffuse, giving the retina a uniformly grayish appearance. The leakage is often due to general dilatation of the capillary bed but can also occur through defects in the underlying pigment epithelium. Hypertension and renal disease can aggravate diffuse retinal edema. With prolonged retinal edema, cystic changes occur in the involved retina, and permanent visual damage may result. MICROANEURYSMS-The first readily visible funduscopic finding, microaneurysms are reddish focal dilatations of capillaries, up to 50 1-Lm in diameter. They usually occur in areas of poor retinal perfusion and are most likely to be found initially in the
region temporal to the macula, perhaps because this area has marginal circulation. Microaneurysms tend to leak fluid into the retina, so they often appear close to areas of retinal edema. They sometimes regress spontaneously. RETINAL HEMORRHAGES-
When they occur in the outer retinal layers, these hemorrhages have a blodike appearance, typically '!i to 1/3 disk-diameter in size. Flame-shaped hemorrhages localize in the inner retinal layers and orient themselves along the distribution of the nerve fiber layers in which they lie. Flameshaped hemorrhages are common with hypertension but can occur in nonhypertensive diabetic patients. All retinal hemorrhages are
transient in nature, usually resolving in a month or two. COTION-WOOL SPOTs-These soft exudates (figure 1) occur in areas of localized ischemia. They have irregular borders and range up to 1 disk-diameter in size, obscuring the underlying retinal detail. They represent ischemic damage to the nerve fiber layer and clear in 3 to 6 months, more slowly than retinal hemorrhage clears. Actual anatomic closure of vessels does not appear to be necessary for their development. They may not always produce visual loss, but they are damaging to retinal function. LIPID DEPOSITs-As retinal edema occurs from damaged and dilated retinal vessels, healthier vessels and the underlying pig-
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Microaneurysms are the first readily visible funduscopic finding in diabetic retinopathy.
Figure 2. Three loop or shunt vessels visible along superotemporal vein in left eye of 44-year-old patient with juvenile-onset diabetes. These intraretinal vascular changes are precursors to proliferative retinopathy. Microaneurysms, lipid, and dot -blot hemorrhages are also present.
ment epithelium attempt to reabsorb and recirculate the accumulated fluid. In localized areas the proteinaceous residues of such leakage may linger as irregular yellowish deposits known as lipid, or hard, exudates. Lipid tends to accumulate in a circinate pattern around leaking microaneurysms. While the fluid portion of retinal edema clears in a matter of weeks with elimination of the cause of the leakage, the lipid portion takes many months to clear. INTRARETINAL VASCULAR CHANGES-Shunt vessels (figure 2) are collateral venous channels that develop in conjunction with areas of retinal infarction. Venous beading, an irregular constriction and dilatation, gives the retinal veins a sausagelike appearance.
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Venous beading is generally found near areas of poor perfusion in the retina. PROLIFERATIVE RETINOPATHY
-The dividing line between background and proliferative retinopathy is reached with the development of new vessels on the surface of the retina or extending into the vitreous cavity. NEOVASCULARIZATION-Two thirds of new vessels develop either on the optic nerve head or in close proximity to it. Through a direct ophthalmoscope they are visible as fine, delicate vascular loops without supporting fibrous tissue. The use of the redfree light on the direct ophthalmoscope facilitates recognition at an earlier stage of development.
In about 25% of patients with new vessel formation, the new vessels develop in the peripheral retina and may be difficult to appreciate unless the pupil is dilated. Retinal ischemia appears to stimulate their development, and peripheral new vessels are usually found at the proximal edge of an area of significant retinal nonperfusion. In the case of new vessels on the disk, extensive diffuse retinal ischemia may provide the stimulus for their development. New vessels grow on the surface of the retina, along the vitreoretinal interface, or into the vitreous itself. Occasionally the new vessels regress spontaneously, although those on the disk are less likely to do so. The rate of growth of new vessels varies; some change little over a period of months, while others progress rapidly in weeks. NEW VESSEL HEMORRHAGEEventually, new vessels are prone to hemorrhage, and the agent of hemorrhage appears to be traction on the fragile new structures by the vitreous body. The vitreous separates from the retina as a part of the aging process, usually in the sixth decade of life. Posterior vitreous separation occurs earlier in the diabetic patient than in the nondiabetic. Traction on the new vessels by the detachcontinued
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Through a direct ophthalmoscope, new vessels are visible as fine, delicate vascular loops without supporting fibrous tissue.
ing vitreous produces hemorrhage, either at the vitreoretinal interface or into the vitreous itse!£ The hemorrhage appears to stimulate further vitreous contraction, so a self-accelerating process is created with a recurrent cycle of hemorrhage and clearing. TRACTIONAL RETINAL DETACHMENT-Ultimately, fibrous tissue develops in conjunction with the new vessels, and fibrous tissue traction on the new vessels may provoke further bleeding. In addition, pull on the retina itself may produce retinal detachment. Continued visual decline is the usual result. The proximity of disk new vessels to the macula makes them a particular threat to central vision, owing to the danger of tractional retinal detachment of the macula. About 50% of diabetic patients with significant new vessels on the disk progress to legal blindness over a 5-year period.
Treatment of diabetic retinopathy A great deal of what we have learned about the treatment of diabetic retinopathy has come to us through controlled prospective studies done at collaborating centers over the past 20 years. It is tempting to believe that strict
control of diabetes may prevent the development of retinopathy; some evidence indicates that strict control in the early years may delay the appearance of the first retinal manifestations. Once established, the retinal lesions advance at a varying rate that does not correlate well with diabetic control. Paradoxically, the sudden normalization of the blood glucose level (as in patients who are undergoing renal or pancreatic transplantation), the use of continuous-insulin-infusion devices, or a stepped-up regimen of insulin injections may worsen the retinopathy already present, at least over the short term. Similarly, the use of systemic agents, such as cholesterol-lowering drugs, has failed to demonstrate any improvement in vision in established diabetic retinopathy, although some objective improvement in its appearance has been noted. Nor has the use of anti platelet agents such as aspirin been shown to have any effect on established diabetic retinopathy. PH~COAGVLKnON-The
early lasers-the xenon photocoagulator and the ruby and the blue-green argon lasers-were ineffective in permanently sealing new vessels off the surface of the retina, and treatment to disk new
vessels resulted in serious side effects, including laser-induced optic neuritis and large visualfield defects related to nerve fiber damage. Interest turned to scatter treatment of the retina. In this method, termed panretinal photocoagulation, regularly spaced burns are delivered to the periphery of the retina. The disk, macula, and immediately adjacent areas are not treated. USE IN PROLIFERATIVE RETINOPATHY-In 1971 the Diabetic Retinopathy Study (DRS), a multicenter project to study the efficacy of laser photocoagulation in the treatment of proliferative diabetic retinopathy, identified high-risk characteristics for the development of severe visual loss: (1) the presence of new vessels on the retina; (2) the presence of new vessels on or in close proximity to the disk; (3) the severity of the new vessels present, as compared with a standard photograph; and (4) the presence of vitreous hemorrhage. More than 1,500 patients with high-risk characteristics were assigned randomly either to treatment with panretinal photocoagulation or to observation. Within 2 years it was apparent that the treated patients were at a statistically significant lower risk of severe visual loss than were untreat-
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Once established, retinal lesions advance at a varying rate that does not correlate well with diabetic control.
Figure 3. Left eye of 33-yearold patient with asymptomatic juvenile-onset diabetes and 20/20 vision. a. Extensive fine new vessels off surface of disk. b. Six months after panretinal photocoagulation, disk new vessels have regressed, leaving fibrous stalk that extends off the disk and along the superotemporal arcade.
a
b
ed controls. At completion of the DRS in 1979, investigators concluded that in patients with three of the high-risk characteristics, panretinal photocoagulation could decrease the incidence of severe visual loss by 50% to 65% (figure 3). Panretinal photocoagulation did have some undesirable side effects. Patients lost some periph-
eral vision. In addition, a small percentage had permanent loss of central vision (ie, one or more lines on the Snellen eye chart). This was attributed to exacerbation of preexisting macular edema by the peripheral photocoagulation. Investigators found that exacerbation could be lessened by dividing the laser treatment into two or more sessions or by pro-
viding simultaneous focal laser treatment to the leaking microaneurysms in the perimacular area. As a result of the DRS findings, prompt panretinal photocoagulation is now generally regarded as the treatment of choice for patients with well-established neovascularization of the retina, with or without vitreous hemorrhage. This procedure significantly reduces, but does not eliminate, the likelihood of severe visual loss in proliferative retinopathy. The exact mechanism by which peripheral laser therapy induces regression of disk new vessels is not known, but ablation of poorly perfused tissue in the peripheral retina may lessen the ischemic stimulus to new vessel formation on the disk. Longterm preservation of vision in patients receiving panretinal photocoagulation has been reported, and patients can be successfully re-treated if new vessels recur after the initial photocoagulation treatment. USE IN BACKGROUND RETINOP-
ATHY-The DRS did not answer questions about the efficacy of laser treatment in patients with background diabetic retinopathy and its associated macular edema. Macular edema can cause visual
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Panretinal photocoagulation is now generally regarded as the treatment of choice for patients with well-established neovascularization of the retina, with or without vitreous hemorrhage.
loss in juvenile-onset diabetes bur is an even greater threat in the adult-onset type. Neovascularization of the retina does occur in adult-onset diabetes, but macular edema is estimated to be three to five times more prevalent as a cause of visual loss in adult-onset diabetes. The question remained: Does laser photocoagulation aid in the prevention of visual loss in back- a ground diabetic retinopathy, and at what stage in the disease should patients receive laser therapy? To answer this question, the Early Treatment Diabetic Retinopathy Study (ETDRS) was begun in 1980, and the results of this prospective, randomized study were reported in 1985. Patients with "clinically significant macular edema" were recruited and assigned either to treatment b with laser or to observation. Clinically significant macular edema was defined as the presence of normal and were re-treated if significant amounts (>I diskretinal edema or lipid deposits rediameter in extent) of edematous curred near the macula during retinal thickening within 1 diskdiameter of the macula or the follow-up. Laser treatment conpresence of retinal lipid within sisted either of focal burns to leaking microaneurysms (figure 1 disk-diameter of the center of 4) in the perimacular area or of the macula. grid-style laser treatment to areas Patients with clinically signifiof diffuse retinal edema or capilcant macular edema assigned to lary nonperfusion, as identified laser treatment were treated even though central vision was still with fluorescein angiography.
Figure 4. Fundus of left eye of 61-year-old patient with adultonset diabetes. a. Heavy background diabetic retinopathy with retinal microaneurysms, hemorrhage, early macular lipid deposits, and diffuse retinal edema (vision, 20/200). b. Six months after heavy focal laser burns to leaking microaneurysms that avoided treatment to the immediate macular area. Patient had unexpectedly good improvement in vision to the 20/30 level.
Laser burns of 50 to 200 f.Lm were utilized to minimize visualfield changes; the macula itself was not treated. The ETDRS demonstrated that eyes with clinically significant macular edema and mild to moderate background diabetic retinopathy benefited from focal laser photocoagulation. The incidence of significant visual loss (ie,
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Macular edema can cause visual loss in juvenile-onset diabetes but is an even greater threat in adult-onset diabetes.
Jon P. Tierney, MD Or Tierney is a specialist in diseases of the vitreous and retina, Minneapolis.
two or more lines on the Snellen eye chart) over 3-year follow-up was 12% in the treated group but 24% in the untreated controls. Subtle changes in visual fields were noted after focal treatment, but the incidence was not statistically different from that of similar changes in the nontreated controls_ A relatively small percentage of treated patients with visual loss due to macular edema showed statistically significant improvement in central vision after laser therapy. In about 35% of this group, central vision improved by two or more lines on the Snellen eye chart. Since the ETDRS treated patients with clinically significant macular edema even if they had
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normal vision and since relatively few patients with visual loss due to macular edema experienced significant improvement in vision after laser therapy, the conclusion might be drawn that diabetic patients with clinically significant macular edema and normal vision should receive laser treatment focally before visual loss occurs. The ETDRS recommended that they be considered for treatment. If it is elected not to treat before visual loss, the ETDRS recommended observation at closer intervals for the development of any visual decline, at which time treatment should be instituted promptly. Diffuse retinal edema presents a more difficult problem than focal edema. Treatment for the dif-
fuse form consists of grid-style placement of 50- to 200-J..Lm laser burns to the posterior pole around the macular area, avoiding the macula itsel£ The mechanism of action for this treatment is not known. It probably does not affect the retinal capillaries, since the burn is to the outer retinal layers and adjacent pigment epithelium. Laser treatment in this situation may serve to decrease the metabolic needs of the retina by destroying photoreceptors and thus decreasing retinal metabolic needs and blood flow. Alternatively, the laser may affect the pigment epithelium, perhaps decreasing its permeability or stimulating it to reabsorb fluid from the edematous retina. VITRECIOMY-This surgical procedure removes intraocular hemorrhage and fibrous tissue from the eye to allow treatment of the underlying disease. In the diabetic patient, it is generally accompanied by the delivery of laser beams through a fiberoptic cannula to treat the retinopathy and facilitate reattachment of a retina undergoing tractional detachment. Vitrectomy is usually reserved for diabetic patients with advanced retinopathy when refracting-media opacities or vitreous hemorrhage prevents use of
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Vitrectomy is usually reserved for use in advanced retinopathy when refracting-media opacities or vitreous hemorrhage prevents use of conventional laser therapy or interferes with vision.
conventional laser therapy or interferes with vision. While it can often preserve vision in advanced diabetic retinopathy, it carries a statistically significant rate of complications (induced cataract, retinal tears) and is somewhat less effective than laser photocoagulation delivered at an earlier stage in the diabetic process. The Diabetic Retinopathy Vitrectomy Study (DRVS) researched the role of early vitrectomy in treating vitreous hemorrhage severe enough to preclude the use of laser photocoagulation. The DRVS demonstrated that prompt vitrectomy in juvenile-onset diabetes with severe vitreous hemorrhage could decrease the incidence of severe visual loss from 35% to 11%. Early vitrectomy cleared the refracting media and allowed prompt laser photocoagulation to the underlying retinopathy (figure 5). In a comparison of adultonset and juvenile-onset diabetic patients with severe vitreous hemorrhage who were observed for clearing of the hemorrhage, the DRVS found that the adultonset group was somewhat less prone to development of severe visual loss and more likely to have spontaneous clearing, prob-
Figure 5. Right fundus of 28year-old patient with juvenileonset diabetes. a. Extensive new vessels and fibrosis off the disk, obscuring retinal detail and preventing laser photocoagulation. Optic nerve is barely visible at 3-o'clock position. Vision was limited to hand movements. b. After pars plana vitrectomy to clear refracting media and allow laser photocoagulation to retinopathic areas. Laser scars are visible temporal to optic nerve. Visual recovery was limited to 20/400 because of poor retinal circulation.
ably because their underlying retinopathy was not apt to be as severe. The DRVS concluded that patients with adult-onset diabetes could safely be observed for spontaneous clearing for a longer period than those in the juvenile-onset group; in the latter, prompt vitrectomy is beneficial.
Comment Through the use of funduscopic examinations and visualacuity measurement, primary care physicians play an important role in obtaining timely therapy for their diabetic patients. The number of these pa-
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tients is impressive and increasing. A great many of them are not being seen by an ophthalmologist; many have no eye care of any type. When finally referred, many already have significant retinopathy; treatment might have been more effective if it had been instituted earlier in the course of their disease. Laser photocoagulation cannot prevent all visual loss in all diabetic patients but can sub-
stantially reduce the amount and severity in many. A recent socioeconomic study investigated the cost of screening all diabetic patients for significant retinopathy and for treating the expected incidence of visionthreatening retinopathy. Using a cost-accounting basis, investigators determined that the cost of effective treatment was appreciably less than the cost to society in Social Security dis-
ability payments. Proposals have been made to institute such a program. Rl't'l
-®
Earn credit on this article. See CME Quiz.
Address for correspondence: Jon P. Tierney, MD, Park Avenue Medical Building, 710 E 24th St, Suite 406, Minneapolis, MN 55404.
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Research Group. Photocoagulation for diabetic macular edema: Early Treatment Diabetic Retinopathy Study report number 1. Arch Ophthalmol 1985; 103(12): 1796-806 Garcia CA, Ruiz RS. Diabetes and the eye. Clin Symp 1984;36(4):2-32 Harris MI, Hadden WC, Knowler WC, et al. Prevalence of diabetes and impaired glucose tolerance and plasma glucose levels in US population aged 20-74 yr. Diabetes 1987;36(4):523-34 JavittJC, Canner JK, Sommer A. Cost effectiveness of current approaches to the control of retinopathy in type I diabetics. Ophthalmology 1989;96(2):255-64 Kahn HA, Hiller R. Blindness caused by diabetic retinopathy. Am J Ophthalmol 1974; 78(1):58-67 Klein R, Klein BE, Moss SE. Visual impairment in diabetes. Ophthalmology 1984;91(1): 1-9 Klein R, Klein BE, Moss SE, et al. The Wisconsin Epidemiologic Srudy of Diabetic Retinopathy. II. Prevalence and risk of diabetic retinopathy when age at diagnosis is less than
30 years. Arch Ophthalmol1984;102(4):520-6 Klein R, Klein BE, Moss SE, et al. The Wisconsin Epidemiologic Study of Diabetic Retinopathy. Ill. Prevalence and risk of diabetic retinopathy when age at diagnosis is 30 or more years. Arch Ophthalmol 1984; 102(4):527 -32 Mensher JH. Laser in diabetic retinopathy. Ophthalmol Clin North Am 1989;2(Dec) :58396 Olk RJ. Modified grid argon (blue-green) laser photocoagulation for diffuse diabetic macular edema. Ophthalmology 1986;93(7):938-50 Rand U, Prud'homme GJ, Ederer F, et al. Factors influencing the development of visual loss in advanced diabetic retinopathy: Diabetic Retinopathy Study (DRS) Report No. 10. Invest Ophthalmol Vis Sci 1985;26(7):983-91 Skyler J. Relation of metabolic control of diabetes mellitus to chronic complications. In: Rifkin H, ParteD, eds. Diabetes mellitus. 4th ed. New York: Elsevier Science Publishing, 1990:856-68
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