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OPHTHALMOLOGY PRACTICE
Year : 2000  |  Volume : 48  |  Issue : 4  |  Page : 321-30
 

Management of diabetic retinopathy


Department of Ophthalmology and Visual Sciences, King George's Medical College, University of Lucknow, Lucknow, India

Correspondence Address:
S Saxena
Department of Ophthalmology and Visual Sciences, King George's Medical College, University of Lucknow, Lucknow
India
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PMID: 11340894

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  Abstract 

Diabetic retinopathy remains a major cause of blindness despite increased understanding of this disease and identification of successful treatments. The Diabetic Retinopathy Study identified risk factors associated with a high risk of blindness and confirmed the benefits of panretinal photocoagulation. The Early Treatment Diabetic Retinopathy Study defined the retinal characteristics, indications of treatment and results of laser treatment of clinically significant macular oedema. The Diabetic Retinopathy Vitrectomy study established the benefits and timing of vitrectomy for non-clearing vitreous haemorrhage and severe proliferative diabetic retinopathy. The Diabetes Control and Complications Trial and the United Kingdom Prospective Diabetes Study have also demonstrated the value of tight control of blood sugar and blood pressure in diabetic retinopathy. These studies developed specific recommendations for the management of diabetic retinopathy. Optimum use of this information can minimize visual loss due to diabetic retinopathy.


Keywords: Diabetic Retinopathy, diagnosis, surgery, Humans, Laser Coagulation, methods, Prognosis, Vitrectomy, methods,


How to cite this article:
Saxena S, Jalali S, Meredith T A, Holekamp N M, Kumar D. Management of diabetic retinopathy. Indian J Ophthalmol 2000;48:321

How to cite this URL:
Saxena S, Jalali S, Meredith T A, Holekamp N M, Kumar D. Management of diabetic retinopathy. Indian J Ophthalmol [serial online] 2000 [cited 2014 Aug 20];48:321. Available from: http://www.ijo.in/text.asp?2000/48/4/321/14834


Diabetic retinopathy (DR) remains a leading cause of visual disability and blindness in the developed world, accounting for 10% of all new cases of blindness in the United States.[1] In a population-based study in South India,[2] diabetic retinopathy was detected in 1.78% of the patients screened, and was projected to become a significant cause of blindness in the coming decade. This blindness usually results from non-resolving vitreous haemorrhage, fractional retinal detachment and diabetic macular oedema. Three multi-centre, randomized, collaborative clinical trials, the Diabetic Retinopathy Study (DRS), the Early Treatment Diabetic Retinopathy Study (ETDRS) and the Diabetic Vitrectomy Study (DRVS), developed highly specific recommendations for the appropriate management of DR. These studies are briefly summarized in [Table - 1] and [Table - 2]. This article highlights some of the important management principles and guidelines for the management of patients to prevent or minimize visual loss due to diabetic retinopathy.


  Eye Examination in Diabetic Patients Top


All patients with a history of diabetes need complete eye examination. The eye examination should be scheduled at the time of diagnosis of diabetes if age of onset of diabetes is more than 31 years and after 5 years of onset of diabetes if age of onset of diabetes is less than 30 years.[3] Pregnant females with diabetes should have an eye examination early in the first trimester.[3] Evaluation of the eyes in diabetics is essential to detect not only diabetic retinopathy but also other commonly associated problems such as cataract and glaucoma. Systemic conditions that are known to increase the risk of progression of diabetic retinopathy are nephropathy, pregnancy, history of recent institution of insulin. [Figure - 1] briefly outlines the approach to a patient with diabetes. In addition to dilated fundus evaluation, eye examinations must include evaluation of visual acuity, intraocular pressure, slitlamp biomicroscopic examination of iris, pupillary reactions, anterior chamber, angles and the lens. Fundus examination also helps to detect visual loss from causes other than diabetic retinopathy such as vascular occlusions, ischaemic optic neuropathy, cerebral strokes, epiretinal membrane, etc., all of which are common in patients with diabetes. If diabetic retinopathy is detected, the next step is to classify the level of DR so as to formulate a specific and tailored management plan for treatment and follow up. If retinopathy is not detected and the visual acuity remains good, the patient is followed up regularly on yearly basis; or earlier, on appearance of any new symptoms.

A hazy ocular media could be due to cataract, and or vitreous haemorrhage. A careful ultrasonography (USG) of vitreous and retina is necessary to evaluate the state of vitreous haemorrhage or any associated tractional retinal detachment. When vitreoretinal pathology is ruled out and the degree of lens opacity is accurately ascertained, the patient can undergo extracapsular cataract extraction (ECCE) with posterior chamber intraocular lens (PC IOL) implantation. Retinal examination after dilatation, should be done one week postoperatively in such eyes to confirm the presence and measure the level of DR [Figure - 1]. Management of eyes with hazy media due to vitreous haemorrhage with or without associated cataract, is discussed later.


  Levels of Diabetic Retinopathy Top


Diabetic Retinopathy often progresses from a mild to severe risk for visual loss. The retinopathy is hence classified into two broad categories-non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR).[4] NPDR is further classified into mild, moderate and severe and each of these may be with or without involvement of the macula. PDR is classified further into PDR with or without high-risk characteristics (HRC). The maculopathy, which can occur both in NPDR and PDR, is classified into: a) non -clinically significant macular oedema, b) clinically significant macular oedema (CSME) that may be focal or diffuse, c) ischaemic maculopathy with or without associated CSME and d) cystoid macular oedema.[5]

The baseline level of retinopathy indicates the risk of retinopathy progression and visual loss. The level and severity of retinopathy is determined by detailed clinical examination of the retina using the indirect ophthalmoscope for a panretinal view, and stereoscopic slitlamp biomicroscopy of the disc and macula using +90D + 78 D handheld lens. Ancillary tests, selectively useful are systematic stereo fundus photography [Figure:1a], and fluorescein angiography.


  Non-proliferative diabetic retinopathy (NPDR): classification and management Top


NPDR is characterized by presence of retinal haemorrhages, exudates and configurational changes of veins. In some cases there is macular oedema, but characteristically there is absence of retinal or optic disc new vessels. The severity of retinopathy is further classified[4] and managed as



  1. 1. Mild NPDR [Figure - 2]: Presence of at least one retinal microaneurysm and one or more of the following: retinal haemorrhage, hard exudate, or soft exudate. These eyes need yearly retinal evaluation. They do not need other investigations such as fundus fluorescein angiography (FFA).


  2. 2. Moderate NPDR [Figure - 3]: Haemorrhages or microaneurysms or both, greater than those in standard photograph 2A of the modified Airlie House Classification of DR[4] in at least one quadrant, and one or more of the following: soft exudates, venous beading and intraretinal microvascular abnormality (IRMA). Eyes with moderate NPDR are followed up every 6-12 months. No FFA is needed and very rarely colour fundus photography may be used to classify level of DR.


  3. 3. Severe NPDR [Figure - 4]: Haemorrhages or microaneurysms or both greater than standard photograph 2A in all four quadrants, venous beading in two or more quadrants, and IRMAs greater than standard photograph 8A in at least one quadrant[4] characterize severe NPDR (4-2-1 rule). These eyes need close observation every 3-4 months to check for progression. FFA may be used occasionally along with colour fundus photographs to assess the risk for progression. Systemic risk factors are also considered while planning management in such patients. The usefulness of panretinal photocoagulation (PRP) in such eyes is uncertain and depends on the individual clinical case and the risk of progression.




The risk factors for progression of NPDR to PDR[5] on colour fundus photographs have been identified as: (1) IRMA [Figure - 4]; (2) venous beading; and (3) haemorrhages and microaneurysms. The FFA risk factors[5] are: (1) dry leakage, (2) capillary dilatation, and (3) capillary loss. Although the FFA provides additional prognostic information, the colour fundus photographic grading of retinopathy levels of both eyes also provides prognostic results.


  Diabetic maculopathy: Classification and Management: Top


Involvement of the macula in diabetes can lead to serious and often irreversible visual loss. Therefore it is essential to detect and treat all sight-threatening macular lesions at the earliest. Diabetic maculopathy is further classified into CSME which may be focal or diffuse, ischaemic (non-perfusion of capillaries around the foveal avascular zone) with or without associated CSME, cystoid macular edema, and Non-CSME.[5] The visual acuity alone is not considered an important criteria while deciding the treatment of diabetic maculopathy. The type of maculopathy and its extent are important factors. If diabetic maculopathy is treated appropriately when the visual acuity is good, it can prevent serious visual loss in a majority of the patients. Even in eyes with visual loss, treatment can prevent further visual loss.


  Clinically significant macular oedema (CSME) Top


This term was defined in the ETDRS[6] in an effort to differentiate sight threatening from non-sight threatening macular lesion and lay guidelines for laser treatment.

CSME [Figure - 5] is detected on stereoscopic binocular slitlamp biomicroscopic evaluation of the macula using a + 90 D lens (or any other similar lens) for fundus examination. FFA is not mandatory for diagnosis of CSME, but may be necessary to detect the treatable lesions. CSME includes:[6]



  1. (1) Retinal thickening involving or within 500μm of the centre of the macula;


  2. (2) Hard exudate(s) with thickening of the adjacent retina located not more than 500μm from the center of the macula; and


  3. (3) A zone of retinal thickening one disc area or larger in size, any part of which is located within one disc diameter of the centre of the macula.




Laser treatment of CSME [Figure - 5] reduces by about 50% the risk of moderate visual loss. It also increases the chance of improvement in visual acuity of one line or more. Eyes with CSME which need PRP for severe NPDR/ PDR should always undergo treatment for the macular oedema first followed by PRP after 2-4 weeks. PRP alone or, simultaneous with macular treatment, can worsen the macular oedema and lead to severe visual loss. Similarly, while treating CSME, one should be careful to treat only the treatable lesions (vide infra) and not treat beyond the macula close to the arcades as this works as a PRP and worsens the visual acuity considerably [Figure - 6]. The treatable lesions[6] are described as:



  1. 1. Focal leaks > 500μm from the centre of the macula causing retinal thickening or hard exudates


  2. 2. Focal leaks 300 to 500μm from the centre of the macula causing retinal thickening or hard exudates if the treatment is not likely to destroy the remaining perifoveal capillary network


  3. 3. Areas of diffuse leakage that have not been treated previously [Figure - 6]


  4. 4. Thickened retinal avascular zones, other than the normal foveal avascular zone, not treated previously.




Laser is not indicated for eyes with visual loss solely due to ischaemic maculopathy. If oedema and ischaemia coexist, the oedema should be treated after explaining the guarded prognosis.[5] The role of laser in visual loss due to diabetic cystoid macular oedema is also not well known. Such eyes can be rehabilitated in some cases by low-vision aids and associated rehabilitation services. Eyes with diabetic maculopathy that do not reach the criteria for CSME (non-CSME, [Figure - 2]), should not be treated with laser. This is especially required if most of the leakage is close to the fovea increasing the risk of damage to it from direct treatment or subsequent migration of treatment scars.

[TAG:2]Technique of laser treatment for diabetic maculopathy[5][/TAG:2]

The treatment technique is divided into two main categories: (i) focal direct treatment of fluorescein leaks and (ii) grid treatment of diffuse areas of leakage or non-perfused retinal thickening.

1. Focal Treatment

Focal treatment [Figure - 5] is required for focal lesions located between 500 and 3000μm from the centre of the macula, believed to be causing the hard exudates and retinal thickening. Spot size of 100 - 200μm of 0.lsecond duration is used to treat all lesions that leak the fluorescein dye; it includes microaneurysms, IRMA, or short capillary segments. The end point is a whitening or darkening of the treated lesion. Treatment is optional for focal lesions that do not fill or leak on FFA but are located beyond 3000μm from the center of the macula. Treatment of these lesions is considered if prominent leaks are present and associated with retinal thickening or hard exudates, that extend closer to the centre. Focal leaks between 300μm and 500μm from the centre are treated in exceptional cases during follow-up treatment sessions. Treatment for such leaks is indicated if other leaks have been treated, visual acuity is 6/12 or less and treatment is unlikely to destroy the remaining perifoveal capillary network.[5]

2 Grid Treatment

Grid laser is applied to areas of thickened retina that show diffuse fluorescein leakage [Figure - 6] or capillary dropout. Burns of light intensity (above threshold but less intense than PRP burns) are placed in this area using 100-200μm spots of 0.1-0.05 seconds duration. Grid treatment is not applied within 500μm of the centre of the macula or within 500μm of the disk margin, but can be placed in the papillomacular bundle. It may extend in all directions up to 2 DD from the centre of the macula, or to the border of the PRP treatment, if present. Any focal leaks within the zone of grid treatment are treated focally.[5]


  Follow-up Top


About 4-6 weeks after the treatment of the macula, the patients are reviewed, and if some obvious treatable lesions were missed, they are treated. Should CSME and treatable lesions persist beyond 4-6 months, repeat treatment is performed after FFA confirmation. The patients should be explained in detail that laser treatment of diabetic macular oedema is effective mainly in preventing further visual loss rather than restoring the lost vision.[5]


  Proliferative Diabetic Retinopathy (PDR) Top


PDR is characterized by presence of newly formed blood vessels arising from the optic disc (NVD) or elsewhere on the surface of retina (NVE).[7] These new vessels may be flat along the surface or elevated into the vitreous cavity[7] and may be with or without a component of glial cell proliferation fibrovascular proliferation (FVP/ FP). As the fibrous tissue contracts the eyes develop recurrent preretinal [Figure - 7] and vitreous haemorrhages, tractional retinal detachment and occasionally combined with rhegmatogenous retinal detachment. Rubeosis iridis is another characteristic of some eyes with PDR. All such eyes need active treatment with scatter (panretinal) laser photocoagulation, with or without additional surgery.

Eyes with PDR are further described as those with 'high-risk characteristics' (HRC) where risk of severe visual loss over two years is very high, and, those with non-high-risk characteristics which have a lesser risk of severe visual loss. The HRC (described by the DRS) is based on: (1) presence of preretinal or vitreous haemorrhage [Figure - 7] (2) presence of new vessels (3) location of new vessels on or near the disc and (4) severity of new vessels. The risk grows as the number of risk factors increases. Eyes with three or more risk factors are at a much higher risk of severe visual loss in two years than eyes with two or fewer risk factors.[8]


  Panretinal Photocoagulation (PRP) Top


PRP involves laser scatter ablation of the retina extending from the retinal vascular arcades at the posterior pole to the peripheral retina beyond the equator. The aim of PRP is to prevent the onset or induce regression of neovascularization without vitreous haemorrhage or fibrovascular proliferation.

Indications

PRP is not recommended[8] for eyes with mild or moderate NPDR or eyes with burnt out retinopathy or showing spontaneous regression of retinopathy (which is rare). PRP should not be delayed in eyes with HRC, rubeosis iridis, or angle neovascularization.

The HRC eyes are those (i) NVD >l/4-l/3 disc area (ii) vitreous or preretinal haemorrhage with any extent of NVE, observed or assured to be observed by haemorrhage [Figure - 7].

The role of PRP in eyes with tractional retinal detachment (TRD) is not well defined. The PRP may increase the extent of traction and lead to a macular detachment. However, one could consider PRP in eyes with TRD not involving the fovea as the first line of management. Care should be taken to avoid laser at the areas of vitreoretinal adhesion and traction, and areas of elevated retina. These eyes need close follow up and if the macula is threatened or gets detached, they would need early surgical intervention. In eyes where the TRD involves macula at presentation, early surgical intervention along with intraoperative PRP may give better visual results.[9]

Various factors known to worsen the retinopathy may influence the decision to initiate laser treatment in eyes with severe NPDR or early PDR without HRC.[7] They include pregnancy, nephropathy, cardiac failure, carotid artery disorders, cataract surgery, YAG capsulotomy, uncontrolled blood sugars, recent institution of insulin in a patient with NIDDM, poor patient follow up, etc ([Figure - 1]-footnote). These factors should be considered in making the decision to treat or not, besides the guidelines provided in the randomized clinical trials.[7]

Technique of PRP

The pupils are fully dilated and topical anaesthesia is usually sufficient. The most common wavelengths used are argon green (514 nm) or blue-green, (488 nm) frequency doubled green laser, (532 nm) or diode laser (810 nm). In case of hazy media due to cataract or vitreous haemorrhage, krypton red (639 nm) can be used. The slitlamp delivery system is commonly used and various types of lenses are available to visualize different areas of the retina, so as to cover as much area of the retina as possible. However in patients with poorly dilating pupils, poor cooperation, inability to sit at the slitlamp, peripheral cortical cataract, etc. the indirect ophthalmoscopic delivery system can be used with greater efficacy.

The frequently used settings of the argon laser are 500μ spot size, 0.1 second duration, 200-250 mW power to give a moderate intensity burn of grayishwhite colour. Burns are placed outside the arcades and extend peripherally up to the equator and beyond [Figure - 7]. Burns vary in number from 1600-2000 and are spaced one burn-width apart. Treatment is avoided to areas of vessels, macula, traction, pigments, previous burns etc so as to avoid large scotomas and haemorrhage.[7]

Follow up



  • There are no post-treatment physical restrictions following PRP. The patients are scheduled for follow-up examination in 4-6 weeks to assess the efficacy of laser photocoagulation [Figure - 7]. The following factors are evaluated for any repeat laser treatment.


  • change in new vessel since last visit/ photocoagulation treatment


  • appearance of new vessels


  • frequency and extent of vitreous haemmorhage since last visit/last PRP


  • status of posterior vitreous detachment


  • extent of PRP scars


  • extent of tractional retinal detachment and fibrous proliferations.




Additional laser is applied when there is no regression of new vessels after initial treatment, presence of active new vessels (tight networks, little fibrous tissue, rapid growth in size), recurrent vitreous haemorrhage, and presence of skip areas.[7] Additional laser is less urgent if: fibrous proliferation is already developed, in single episode of vitreous haemorrhage associated with posterior vitreous detachment (PVD), lack of skip areas, and near complete PVD. Areas chosen for retreatment are generally those toward which the new vessels appear to be growing or in which the photocoagulation scars appear to be less tightly spaced.[7] The number of additional burns required to cause significant reduction of retinopathy and decrease incidence of visual loss could range from 1,500 to 12,000. [10,11] The amount of initial laser treatment required for regression of retinopathy is not well known but may be considerably higher than that recommended by the DRS.[11] If recurrent haemorrhage is due to traction of partially detached posterior hyaloid on elevated new vessels, then vitrectomy may be indicated since repeated PRP may not stop recurrent vitreous haemorrhages. Early surgery has been shown to have better anatomic and visual results in such eyes.[12]


  Complications of laser treatment Top


Laser treatment for diabetic retinopathy, if carried out properly, rarely causes serious complications. Serious complications reported earlier include occurrence of choroidal neovascular membrane and cilio-choroidal detachments. [5,7] Most of these and other transient complications including photophobia, transient myopia and impaired accommodation can be reduced by dividing the treatment in multiple sessions and avoiding very heavy intensity burns.[7] Another infrequent complication is macular subretinal fibrosis following treatment for macular oedema, especially seen in eyes with pre-existing severe hard exudates.[13]


  Vitreo-retinal Surgery in Diabetic Retinopathy and the Diabetic Retinopathy Vitrectomy Study (DRVS) Top


Standard laser treatment cannot be performed in eyes with vitreous haemorrhage precluding visualization of the retina. Laser does not help in eyes with tractional retinal detachments (TRD, [Figure - 8]) and in fact can worsen pre-existing TRD.[14] The DRVS [Table - 2] was a randomized controlled clinical trial that evaluated the risks and benefits of surgical versus conventional treatment for vitreous haemorrhage and very severe PDR.[14] Results of this trial demonstrated that eyes managed by vitreoretinal surgery had better outcome than those treated conservatively, especially when the presenting vision was good. Early vitrectomy offers the chance for prompt visual recovery which is of greatest importance to patients who do not have useful vision in the fellow eye. The current indications and contraindications for vitrectomy in diabetic eye disease15 are shown in [Table - 3]. Posterior traction detachments not involving the fovea may remain stable and should be observed. However, once the fovea is detached, surgery should be performed promptly, to prevent degenerative changes in the retina and consequent poor visual recovery after retinal reattachment.[16]

The basic goals of surgery include removal of all media opacities, release of all vitreous traction and performing or completing retinal ablation, usually by laser, to prevent subsequent neovascular proliferation. Retinal tamponade may be required using either long acting gases or silicone oil depending on the extent and type of retinal pathology encountered during surgery.[16] Owing to improved techniques and instrumentation early surgery is now increasingly done. Results from recently published reports are encouraging.[16] eyes with preoperatively attached macula and recurrent vitreous haemorrhage 40%-62% cases achieved a visual acuity of 6/60. while in eyes with TRD and detached macula preoperatively, 21-58% eyes achieved 6/60. Loss of light perception was seen in 5-17% in the first group (attached macula) and in 11-19% in the second group (detached macula).[16] The visual results are generally stable for a long time. Vitrectomy with removal of the posterior hyaloid is currently evaluated for diabetic maculopathy[15] and hopefully this modality will help selected eyes with maculopathy that are not suitable for laser treatment.


  Management of Concomitant Cataract and Diabetic Retinopathy Top


All diabetics presenting with cataract should undergo a thorough anterior and posterior segment evaluation. Eyes with CSME and cataract should preferably undergo laser treatment for the maculopathy first, followed by cataract surgery after six or more weeks since cataract surgery is known to worsen the maculopathy.[17] In case the cataract is too advanced for good visualization of the macula, then there is no option but to carry out the laser treatment 3-4 weeks after the cataract surgery. In such cases the situation should be clearly explained pre-operatively to the patient.[5]

In patients, presenting with cataract and proliferative diabetic retinopathy, as much PRP as possible should be done 4-5 weeks before surgery. If adequate PRP is not possible due to media opacity, there are several management options. The options include (a) cataract extraction and IOL implantation followed by PRP (preferably laser indirect photocoagulation) in early postoperative period; (b) simultaneous IOL and vitreous surgery (preferably phacoemulsification),[18] (c) IOL surgery in first stage, and vitreous surgery in second stage at an internal of 3 to 4 weeks. Eyes with preoperative rubeosis iridis can undergo simultaneous cataract and vitreous surgery with or without IOL implantation, but the visual recovery is often poor[16] and such eyes may be a relative contraindication for surgery.[15] Cataract surgery in diabetics who have significant retinopathy must be planned in conjunction with a retinal specialist.


  Peripheral Retinal Cryoablation Top


With improvement in pars plana vitrectomy techniques (particularly use of wide angle viewing systems) and versatile laser delivery systems, cryoablation of peripheral retina, a common modality in past, is rarely used now. The main indications include media haze precluding laser PRP (even with the indirect ophthalmoscope) and repeated vitreous haemorrhages despite a complete and additional PRP or after vitrectomy.[19] The main complication is acceleration of tractional retinal detachment. This treatment should not be done in eyes with vitreous haemorrhage of unknown aetiology, eyes with TRD or with areas of strong vitreoretinal adhesions, detected clinically or with ultrasonography. The treatment is done either transconjunctivally or after a limbal peritomy. The treatment should be visually monitored with indirect ophthalmoscopy. Usually 10-15 seconds are needed at a temperature of -60 C and a total of 18-20 spots are applied, distributed over the four quadrants of the sclera, extending from ora serrata to the equator.[19]


  Medical Management Top


Besides laser and surgery to the affected eye (s) adequate attention should be paid by the treating ophthalmologist to the systemic status of the patient. Systemic risk factors [Figure - 1] are known to influence the occurence, progression and effect of treatment on DR.


  Blood sugar control Top


Several studies have shown link of hyperglycemia and strict control of blood sugar with level and progression of retinopathy. Obviously the first line of medical management should be directed to good control of blood sugar. Control of blood sugar should be carried out alongwith the appropriate laser therapy. Laser therapy should not be delayed, particularly in proliferative diabetic retinopathy, while awaiting for adequate blood sugar control. Two important studies of effect of glycemic control and diabetic retinopathy are summarized below.


  Diabetes control and complications trial (DCCT) Top


The DCCT [20,21] tested very tight control of blood glucose levels versus standard control of blood glucose levels to determine the magnitude of decrease in risk of progression of diabetic retinopathy. The DCCT showed that strict control of blood sugar could reduce the occurrence of diabetic retinopathy, slow down the progression of any retinopathy and also lead to a better response to laser therapy in causing regression of new vessels.[20] Other complications such as neuropathy and nephropathy were also reduced by strict control of the blood sugar.[21]

One recent report[22] showed that in long-standing, poor glycemic controlled diabetic patients, there is an early worsening of moderate NPDR immediately after starting insulin therapy. Ophthalmologic monitoring before initiation of intensive insulin treatment and periodical monitering at every three months upto a year thereafter seems appropriate for such a high-risk stage. In patients whose retinopathy is nearly at high-risk stage, it may be prudent to delay the initiation of intensive treatment until photocoagulation can be completed, particularly if Haemoglobin A1C is high.[21]


  United Kingdom Prospective Diabetes Study (UKPDS) Top


The United Kingdom Prospective Diabetes Study has demonstrated that tight control of blood pressure in Type 2 (NIDDM) patients achieves a clinically important reduction in the risk of deaths related to diabetes, progression of diabetic retinopathy and deterioration in visual acuity.[23] This study has also shown that DR is common in newly diagnosed cases of NIDDM and so a careful ophthalmic assessment at the time of diagnosis of diabetes is important.[24]


  Antiplatelet Therapy Top


Various antiplatelet drugs, including aspirin, have been studied for their possible role in prevention and progression of DR, due to inhibition platelet aggregation. In patients with mild-to-severe NPDR and early PDR, aspirin had no clinically important beneficial effects on the progression of DR.[25] Aspirin use did not appear to increase the occurrence of vitreous/preretinal haemorrhage or influence the rate of vitrectomy. There were no ocular contraindications to aspirin when indicated for cardiovascular disease or other medical conditions.[25]


  Lipid reduction Top


Reducing blood lipids and treating anaemia slow the progression of DR. [26,27] In patients with extensive hard exudates, the serum lipids should be checked and if found elevated, should be treated. Lipid lowering may decrease the risk of hard exudate formation and associated visual loss.[28] Agents such as Lovastatin and Pravastatin are useful in lowering the hard exudates in the macula.[29] The lipid lowering therapy is best given in consultation with an internist.

In conclusion, we have outlined the guidelines and management principles for diabetic retinopathy in this paper. When applied in clinical practice, these. Can lead to substantial reduction of visual loss. This is based on reduction the current published evidence. New information on diabetes is rapidly emerging. Ophthalmologists and primary-care physicians must keep up with these advances.



 
  References Top

1.Kahn HA, Hiller R. Blindness caused by diabetic retinopathy. Am J Ophthalmol 1974;78:58-67  Back to cited text no. 1  [PUBMED]  
2.Dandona L, Dandona R, Naduvilath TJ, McCarty CA, Rao GN. Population based assessment of diabetic retinopathy in an urban population in South India. Br J Ophthalmol 1999;83:937-940.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]
3.The American Academy of Ophthalmology. Preferred Practice pattern:Diabetic Retinopathy. 1993;l-32.  Back to cited text no. 3    
4.Early Treatment Diabetic Retinopathy Study Research Group. Grading diabetic retinopathy from stereoscopic color fundus photographs. An extension of the modified Airlie House classification. Early Treatment Diabetic Retinopathy Study report Number 10. Ophthalmology 1991;98:786-806.  Back to cited text no. 4  [PUBMED]  
5.Bresnick GH. Non-proliferative diabetic retinopathy. In, Ryan SJ, Schachat AP, Murphy RB, (editors):Retina. St. Louis:CV Mosby Co. 1994. Vol 2, pp 1290-1305.  Back to cited text no. 5    
6.Early Treatment Diabetic Retinopathy Study Research Group. Photocoagulation for diabetic macular edema. Early Treatment Diabetic Retinopathy Study Report Number 1. Arch Ophthalmol. 1985;103:1796-1806.  Back to cited text no. 6  [PUBMED]  
7.Davis MD. Proliferative diabetic retinopathy. In, Ryan SJ, Schachat AP, Murphy RB, (editors). Retina St. Louis CV Mosby Co. 1994. Vol 2, pp 1320-59.  Back to cited text no. 7    
8.Diabetic Retinopathy Study Research Group. Four risk factors for severe visual loss in diabetic retinopathy: The third report from the diabetic retinopathy study. Arch Ophthalmol. 1979;97:654-55.  Back to cited text no. 8    
9.Diabetic Retinopathy Vitrectomy Study 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;95:1307-20.  Back to cited text no. 9    
10.Jalali S, Das TP. Augumented panretinal photocoagulation for proliferative diabetic retinopathy. Afro-Asian J Ophthalmol. 1993;112:257-59.  Back to cited text no. 10    
11.Reddy VM, Zamora RL, Olk RJ. Quantitation of retinal ablation in proliferative diabetic retinopathy. Am j Ophthalmol 1995;119:760-66.  Back to cited text no. 11  [PUBMED]  
12.Diabetic Retinopathy Vitrectomy Study Research group. Early vitrectomy for severe vitreous haemorrhage:two-year results of a randomized trial. Diabetic Retinopathy Vitrectomy Study report 2. Arch Ophthalmol 1985;103:1644-52.  Back to cited text no. 12  [PUBMED]  
13.Early Treatment Diabetic Retinopathy Study Research Group. Subretinal fibrosis in diabetic macular oedema. ETDRS report 23. Arch Ophthalmol. 1997;115:873-77.  Back to cited text no. 13  [PUBMED]  
14.Diabetic Retinopathy Vitrectomy Study Research group. Early vitrectomy for severe vitreous haemorrhage in eyes with useful vision. Clinical applications of results of a randomized trial. Diabetic Retinopathy Vitrectomy Study report 4. Ophthalmology. 1988;95:1321-34.  Back to cited text no. 14    
15.Ho T, Smiddy WE, Flynn HW. Vitrectomy in the management of diabetic eye disease. Survey Ophthalmol 1992;37:190-202.  Back to cited text no. 15    
16.Gardner TW, Blankenship GW. Proliferative diabetic Retinopathy: principles and techniques of surgical treatment. In: Ryan SJ, Schachat AP, Murphy RB, (editors). Retina St. Louis: CV Mosby Co. 1994. Vol 3, pp 2407-37. 1979;97:1276-80.  Back to cited text no. 16    
17.Dowler JG, Sehmi KS, Hykin PG, Hamilton AM. The natural history of macular oedema after cataract surgery in diabetics. Ophthalmology 1999;106:663-68.  Back to cited text no. 17  [PUBMED]  
18.Honjo M. Ogura Y. Surgical results of parsplana vitrectomy combined withphacoemulsification and intraocular lens implantation for complications of proliferative diabetic retinopathy Ophth Surg Lasers 1998;29:99-105.  Back to cited text no. 18    
19.Schimek RA, Spencer R. Cryopexy treatment of proliferative diabetic retinopathy. Arch Ophthalmol 1979;97:1276-80.  Back to cited text no. 19  [PUBMED]  
20.The Diabetes Control and Complications Trial Research Group. The effect of intensive diabetes treatment on the progression of diabetic retinopathy in insulin-dependent diabetes mellitus. Arch Ophthalmol 1995;113:36-51.  Back to cited text no. 20    
21.The Diabetes Control and Complications Trial Research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in Insulin-dependent diabetes mellitus. N Engl J Med. 1993;329(14):977-86.  Back to cited text no. 21    
22.The Diabetes Control and Complications Trial Research Group. Early worsening of diabetic retinopathy in the diabetic control and complications trial. Arch Ophthalmol 1998;116:874-86.  Back to cited text no. 22    
23.United Kingdom Prospective Diabetes Study Group. Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. B M J. 1998;317:703-13.  Back to cited text no. 23    
24.Kohner EM, Aldington SJ, Stratton IM, Manley SE, Holman RR, Mathews DR et al United Kingdom Prospective Diabetes Study, 30:diabetic retinopathy at diagnosis of non-insulin dependent diabetes mellitus and associated risk factors. Arch Ophthalmol 1998;116:297-303.  Back to cited text no. 24    
25.Early Treatment Diabetic Retinopathy Study Research group. Effect of aspirin treatment on diabetic retinopathy. ETDRS report No. 8. Ophthalmology 1991;98:757-65.  Back to cited text no. 25  [PUBMED]  
26.Davis MD, Fuller MR, Gangnon RE, Barton F, Aeillo LM, Chew EY, Ferris FL 3rd et al. Risk factors for high-risk proliferative diabetic retinopathy and severe visual loss. Early Treatment Diabetic Retinopathy Study Report 18. Inrest Ophthalmol Vis Sci. 1998;39:233-52.  Back to cited text no. 26    
27.Berman DH, Friedman EA. Partial absorption of hard exudates in patients with end-stage renal disease and severe anaemia after treatment with erythropoietin. Retina 1994;14:l-5.  Back to cited text no. 27  [PUBMED]  
28.Chew EY, Klein ML, Ferris FL, Remaley NA, Murphy RP, Chantry K et al. Association of elevated serum lipid levels with retinal hard exudates in diabetic retinopathy. Early Treatment Diabetic Retinopathy Study Report 22. Arch Ophthalmol 1997;114:1079-84.  Back to cited text no. 28    
29.Gordon B, Chang S, Kavanagh M, Berrocal M, Yannuzzi Z, Robertson C, Drexler A. The effects of lipid lowering on diabetic retinopathy. Am J Ophthalmol 1991;112:385-91.  Back to cited text no. 29    


    Figures

[Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7], [Figure - 8], [Figure - 9]

    Tables

[Table - 1], [Table - 2], [Table - 3]


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2005 - Indian Journal of Ophthalmology
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Online since 1st April '05