|Year : 2017 | Volume
| Issue : 2 | Page : 35-43
Galal Mohamed Ismail
Department of Optometry, College of Health Sciences, University of Buraimi, Al Buraimi, Sultanate of Oman
|Date of Web Publication||26-Feb-2018|
Galal Mohamed Ismail
Department of Optometry, College of Health Sciences, University of Buraimi, POB 890, PC 512, Al Buraimi
Sultanate of Oman
Source of Support: None, Conflict of Interest: None
Diabetes Mellitus (DM) is an important health problem affecting wide population band globally. World Health Organization (WHO) reports showed considerable number of individuals were diagnosed with DM, however, noteworthy numbers are still undiagnosed to varied grounds. Diabetics are at risk of developing pathological complications in particular ocular complications seemed to appear early and might lead to blindness at late stages. Diabetic retinopathy and cataract are the main causes of visual loss in DM although other ocular complications certainly exist. This article meant to review mainly diabetic retinopathy and its effect on ocular structures high lighting the role of the diabetic clinicians' teams and the patients in senses of reducing the risk of the severe damaging stages. Furthermore, to list the available investigative techniques and the methods of managements.
Keywords: Antivascular endothelial growth factor intravitreal fluocinolone, diabetes mellitus, diabetic maculopathy, diabetic retinopathy, fundus photography, ocular coherence tomography, photocoagulation
|How to cite this article:|
Ismail GM. Diabetic Retinopathy. Sudanese J Ophthalmol 2017;9:35-43
| Introduction|| |
Diabetes mellitus (DM) is an important cause of visual impairment. It affects most of the ocular and visual components in different ways, structurally and functionally. Diabetic retinopathy and diabetic cataract are the main causes of visual loss in DM although other complications certainly exist. It is still widely believed that excellent blood glucose control decreases the risk of the diabetic complications.,,
Diabetic retinopathy remains one of the leading causes of vision loss and blindness in globally. Although diabetic retinopathy manifests itself as a disease of the microvasculature, the pathophysiology unquestionably reflects compromise of metabolic, endocrine, and hematological systems. The imbalance of carbohydrate metabolism that results from diabetes, characterized by hyperglycemia and hypoinsulinemia and the associated disturbances of lipid and protein synthesis impair the integrity of vasculature throughout the body. The characteristic response of the retina to diabetes is a complex pattern of events that, if analyzed individually, appear typical of tissue injury.
This article meant to review diabetic retinopathy and its effects on the ocular structures high lighting the role of the clinicians and the patients in senses of reducing the risk of the severe damaging stages. On the other hand list, the available treatment methods used to lessen the damages occur.
| Incidence of Diabetic Retinopathy|| |
Diabetic retinopathy makes blindness 25 times more frequent in diabetics than nondiabetics. Retinopathy may exist in some diabetic patients without visual impairment; however, 15% of diabetics have a level of retinopathy more likely to show market visual impairment if left untreated. For instance, in 1930 <1% of new cases of blindness in the United States were associated with diabetes, by 1960, with advanced level of diabetic care which increased life expectancy and the associated long-term complications, this figure had risen to around 15%. Sorsby reported a lower rate of 7% of 10,000 new blind registrations for the period 1958–1962 whereas in the following interval, 1963–1968, this increased to 13% of male and 18.2% of female blind registrations. Palmberg found that diabetic retinopathy to be responsible for about 10% of the new blind registrations at all ages, about 20% of who were between the ages of 45–74 years.
More recent population-based studies show that the prevalence rates of diabetic retinopathy could vary between 24% and 70% depending on the country of origin of data.,,,,
Along with the differences due to the age factor, the two main diabetic types are reported to affect the diabetic retinopathy incidences differently. There are big variations in the reported incidence of DR in different studies. In insulin-dependent DM (IDDM) patients, the incidence is about 40% whereas in noninsulin-dependent DM (NIDDM), it is 20%. Khan et al. noted some degree of retinopathy in 97% of insulin-dependent diabetic patients after 15 years of diabetic duration and in about 60% of insulin-treated diabetics. However, the prevalence of retinopathy was noted by this study to be greatest in the insulin-dependent diabetic, three to six times greater, up to 80% of all cases, and 60% of proliferative cases were noninsulin-dependent diabetic patients.
| Diabetic Retinopathy Mechanism|| |
The sequence of anatomical changes in the retina leading to blindness in diabetes is fairly well defined; however, the causes are poorly understood., Most complications of diabetic retinopathy, including endothelial proliferation, capillary closure, and preretinal neovascularizion, occur in other diseases. In contrast, the constellation of lesions, from early thickening of the basement membrane and loss of pericytes to microaneurysms to increased permeability and neovascularizion, is quite specific in DM.
Selective loss of retinal capillary pericytes (mural cells) is agreed to be the early anatomical change in diabetics. These cells are thought to control blood flow through the retinal vasculature and may also contribute to the stability of the vessel wall. Abnormalities of the integrity of blood-retinal barrier and the blood flow in retinal blood vessels may exist before any anatomical lesion is evident.
The capillary wall consists of endothelial cells and intramural pericytes surrounding the endothelial cells. Tight connections between the retinal capillary endothelial cells maintain the normal blood-retinal barrier and prevent organic anions from passing into the extravascular space. Selective loss of pericytes is agreed to be the early anatomical change in the retinal vascular that create microaneurysms. This occurs as a result of the alteration in permeability due to opening of the tight endothelial cell junctions caused by these selective pericytes. Therefore, the loss of the mural cells weakens the blood vessel wall such that out-pouching produces microaneurysms. It was also noted that there was evidence of more endothelial cell damage in the areas, which might contribute to the formation of microaneurysms.
Fluorescein angiography has allowed the breakdown of the blood-retinal barrier to be demonstrated. However, good control of glycemia has been noted to resolve the leakage seen in the retinal vessels. Early leakage of fluorescein into the vitreous was reported to be found, possibly days after the diagnoses of diabetes. This leakage has been taken as evidence of early damage to the blood-retinal barrier before any other demonstrable abnormalities are found.
The Sorbitol pathway in diabetic patients is noted to be operative in a number of tissues, lens, intramural pericytes of retinal capillaries, and Schwann cells. The rate-limiting enzyme in the sorbitol pathway, aldose reductase, has a very low affinity for glucose. Therefore, appreciable sorbitol production occurs only in the presence of a high level of glucose. Sorbitol accumulation in the lens responsible for the diabetic cataract formation and its accumulation in the blood vessel wall may well be responsible for the changes seen in diabetic retinopathy, once there is accumulation of large amount of Sorbitol within a high glucose presence. The pericytes contain aldose reductase, therefore, in hyperglycemic events; there is a possibility of polyol pathway stimulation. Basement membrane thickening and loss of mural cells in retinal capillaries are reported to be associated with an increase in aldose reductase activity in the polyol pathway of glucose metabolism. Dilatation and leakage of capillaries occur as a result of the mentioned abnormalities.
Palmberg noted that development of diabetic retinopathy, particularly of the proliferative type, is influenced by the central retinal artery perfusion pressure (blood pressure minus intra-ocular pressure). High blood pressure seems to speed up retinopathy development; however, diabetic retinopathy is rare in the events of high intraocular pressure alone.
Capillary nonperfusion causes are unclear; however, a possible relation is thought to exist as a result of an increased coagulation of the blood and endothelial cell damage due to increased blood flow that leads to intravascular clotting. This increase in retinal blood flow is associated with the autoregulatory blood vessel dilatation and further increase in blood flow, as the retinopathy develops, causes focal occlusion of the capillaries. Total nonperfusion of the retinal capillaries can only take place once the endothelial cells disappear and that is possibly due to lack of nourishment. The retinal capillaries permeability increase causing intraretinal edema and hard exudates as a preclinical stage. Oxygen diffusion rate may be reduced by the fluid accumulation; however, its removal may be difficult due to thickening of the basement membrane, which clearly acts as a greater hinder to the diffusion at the level of the pigment epithelial cell layer., Nevertheless, the diabetic red blood cell has an increased affinity for oxygen, causing an oxygen deficit in the venous part of the circulation even though a normal arterial pressure is present in the circulation. The blood seems to show a degree of hyperviscosity due to the increased amounts of plasma proteins, leading to a decreased local blood flow which increases the pressure within the capillaries and eventually leads to leakage of serum into the tissue space.
On the other hand, leakage can occur as a result of other mechanisms, i.e., decreased erythrocyte deformability, decreased fibrinolysis, increased coagulability, and increased agreeability of the platelets and red cells.,
Colwell, 1983, noted that insulin treatment seems to help partially in reversing forementioned abnormalities although they all contribute gradually toward irreversible capillary occlusion.
| Classification|| |
A group of elements are recognized as giving the clinical features of diabetic retinopathy. They are microaneurysms, venous abnormalities, hemorrhages, edema, exudates, new vessel formation, glial proliferation, and vitreoretinal traction. All of these elements appear in the different types according to the development and progression of diabetic retinopathy. The most suitable classification based on the literature survey for diabetic retinopathy is:
- Background or nonproliferative diabetic retinopathy
- Preproliferative diabetic retinopathy
- Proliferative diabetic retinopathy
- Advanced diabetic ocular disease:
- Vitreous hemorrhage
- Detachment traction
- Opaque membrane formation
- Neovascular glaucoma (NVG).
In general, the clinical feature of nonproliferative diabetic retinopathy is an alteration in the original retinal vasculature; however, proliferative retinopathy is characterized by neovascularization and fibrous tissues.
Background diabetic retinopathy
The clinical picture of background retinopathy is capillary occlusion, with characteristic lesions of microaneurysms, hemorrhages, and exudates. The most common observed changes in the diabetic fundus are in the region temporal to the center of the macular, in the inner plexiform and inner nuclear layers.
The hallmark of diabetic retinopathy is the capillary microaneurysm, an outpouching of a capillary wall when it is filled with blood; it appears as a small red dot with discrete borders. Microaneurysms arise as localized capillary dilatation of 10–100 μmm in diameter and are due to retinal hypoxia not being fully compensated for by the increased retinal blood flow. Microaneurysms of 30 μmm and above in diameter are the only ones demonstrable by fluorescein angiography as areas of capillary nonperfusion and are observable by ophthalmoscopy. At the early stage, the new microaneurysms seem to have thin walls, as time passes they tend to thicken due to deposition of basement membrane that leads to their occlusion.
It is reported that at least one microaneurysm in either eye will be seen in about 50% and over in type I diabetics who have had a diabetic duration for 5–10 years. The life of a microaneurysm varies between a few weeks up to years. Fluorescein angiogram studies had shown that the overall disappearance rate is about 3.3/month in mild conditions and 3.2% in severe ones. It was also noticed that there was no difference in the rate of appearance and disappearance among the different degrees of diabetic retinopathy.
Microaneurysms associated with diabetes occur primarily on the venous side and are limited to the smallest vessels of the microcirculation. Microaneurysms in diabetic patients' fundus seemed to appear initially at the area temporal to the macular. In contrast, microaneurysms occur in retinal vein occlusion, pernicious anemia, systemic hypertension, and other such states with associated retinal ischemia showing involvement on the arterial side of the capillary circulation and they tend to be limited to the peripheral retina.
Hemorrhages occur as a result of either leakage of red blood cells or other blood components from microaneurysms or other weakened vascular. Hemorrhages from diabetic retinopathy are typically dot and blot in shape and are deep in the retina. Superficial flame-shaped hemorrhages in the nerve fiber layer are also observed in diabetics. Small dot hemorrhages are difficult to distinguish from microaneurysms. Large numbers of blot hemorrhages may be a sign of an active stage of the disease. It has been reported that extensive intraretinal hemorrhages count as a risk factor for the development of a severe visual loss in the presence of proliferative retinopathy. Hemorrhages are possibly resolved within 6 months time.
Hard exudates or waxy exudates
These yellow-white discrete deposits occur when leaky walls allow the escape of plasma proportions in the outer plexiform layer. This leakage when reabsorbed leaves behind fatty irregular patches, consisting of protein (possibly residual serum) and fat accumulations. Both of them are left free in the tissues and within macrophages and cystoid bodies. The presence of the fluid causes retinal thickening, leading to macular oedema which is a feature of diabetic maculopathy if it involves the foveal and para-foveal areas. Hard exudates similar to microaneurysms can appear and disappear within months or years. Three basic shapes of exudates are known discrete dots, rings, and plaques. The latter takes the longest period to resolve because they are large. Most frequently exudates are found in the premacular area between the superior and inferior temporal regions.
Preproliferative diabetic retinopathy
It is diagnosed once there is arteriolar and arterial involvement within the capillaries. The clinical picture for this stage of diabetic retinopathy is characterized by:
These are typical hallmarks of widespread ischemia.
Cotton wool exudates
These indicate microinfarcts in the nerve fiber layer secondary to alteration of the axoplasmic flow. At the beginning these lesions appear grayish in color, later changing to white color giving the appearance of cotton wool. When these lesions are present, they are an indication of a rapidly deteriorating retinopathy.
Intraretinal microvascular abnormalities
These either indicate an intraretinal proliferation or a dilation of capillaries due to increased hydrostatic pressure associated with capillary leakage.
This occurs where veins are enlarged as a result of an autoregulatory mechanism in response to local hypoxia. Beading of the veins with irregularities and possible loop formations may be noticed.
The presence of a few cotton wool spots may be consistent with a relatively slow progressing retinopathy although intraretinal microvascular abnormalities and veinopathy are serious prognostic indications and deterioration leading to the proliferative stage.
Venous abnormalities seem to increase in frequency with increase of the degree of retinopathy, and it reaches a value of about 80% of cases which are seen in the proliferative retinopathy stage.
Nevertheless, an increase in the retinal vessel diameter with increased duration of juvenile diabetes or constriction of veins away from the arteriovenous crossings may also be observed.
The clinical features of diabetic maculopathy are microaneurysms, hemorrhages, hard exudates, and edema, all concentrated at the macular causing central visual impairment. It is more common in elderly type II diabetics soon after the diagnosis of diabetes. In Donovan clinical sample, out of 23% of patients with diabetic retinopathy, 6.1% were reported to have diabetic maculopathy. Aiello et al. had observed that macular edema in patients who were <50 years in age was usually associated with preproliferative and proliferative stages of diabetic retinopathy. Different types of diabetic maculopathies are noticed and each type is related to the extent of the leakage and occlusions in the retina.
Ischemic diabetic maculopathy
It is characterized by microaneurysms, hemorrhages, and a few exudates. It is frequently associated with varying degrees of edema. Fluorescein angiograms reveal a large extrafoveal area of nonperfusion. Visual acuity is very poor.
Cystoid diabetic maculopathy
It is characterized by extensive macular edema with accumulation of extracellular fluid in Henle's layer. Small cysts are also observed due to the severe macular edema; in this stage, fluorescein angiography reveals leakage in a flower petal pattern. The vision is severely affected with the persistent damage of the pigment epithelium.
Focal diabetic maculopathy
The main feature is focal dilatation of the vessels and the leakage from the dilated abnormal capillaries with evidence of exudates. It is the most common type, and the visual loss is permanent once the leakage reaches the macular. The recognition of the importance of vascular endothelial growth factor (VEGF) in both proliferative retinopathy and macular edema has led to treatment with intravitreal injection of agents which block the effects of VEGF.
Proliferative diabetic retinopathy
Proliferative changes arise as a result of a stimulus from large areas of ischemic retina. Such changes occur in 5%–6% of all diabetic retinopathy cases, and it is the most common dangerous stage of diabetic retinopathy. It occurs within 11–18 years of diabetic duration and is more commonly observed in type I diabetes., The rate of incidence of proliferative diabetic retinopathy was reported to be 67% in type I within 35 years of diabetic duration while it was 15.5% among type II diabetics with 15 years or more in duration., The incidence seems to increase as the juvenile becomes adult. Figures were suggested in the past for the proportion of diabetic juvenile patients who live to middle age will possibly show evidence of proliferative diabetic retinopathy. It had been suggested to occur in 20% by Caird et al., 25% in Fukuda study, 33% noted by L'Esperance 1981, about 50% by Knowles and the same figure by White (cited in Jarrett 1981). The typical picture of the proliferative stage is the new vessel growth, and this will occur if there are large areas of capillary nonperfusion. The new vessels are observed either on the optic disc head or along the course of the major temporal vascular arcades.
There would appear to be a three process in new vessels formation. First, the extracellular matrix breakdown by proteases, this is followed by endothelial cell migration at the apex of the new capillary formed. The final stage is that of the cell division behind the apex leading to the new vessel elongation.
The new vessels can be categorized into five groups as follows:
- Preretinal, they are along the retinal surface
- Retinovitreal, new vessels that are extending from the retinal surface along the vitreous strand into the vitreous
- Papillovitreal, these are the vessels seen proliferating into the vitreous along the highly detached posterior hyaloid vitreous face
- Peripapillary, new vessels that are growing from the optic disc along the shallow detached vitreous face
- Epipapillary, new vessels that are small twings on the optic disc center.
In general, new vessels initially consist of fine loops with no connective tissue which makes them very fragile and they indigenously bleed. Gradually, they become supported by fibrous tissue which inters through the internal limiting membrane and attaches itself to the posterior vitreous face. In an attempt to support the new vessels, some glial tissue proliferates although shrinkage of the fibrovascular membrane or the vitreous itself produces an elevation of the retina. This elevation causes breakage of the new vessels into the vitreous.
The Diabetic Research Group reported that varies factors are thought to increase the 2-year-risk of developing severe visual loss accompanying proliferative diabetic retinopathy. These factors are as follows: first, the presence of vitreous or preretinal hemorrhages; second, the presence of new vessels; third, location of the new vessels on or near the disc; and finally, the severity of the new vessels. In the event of only one or two of these forementioned risk factors, the risk is low although it rises from 8.5% to 26.7% once three risk factors are identified.
The presence of proliferative diabetic retinopathy is associated with a short survival rate. The average survival period from appearance of the retinitis proliferans was found to be 5.4 years with a mortality figure of 14%. This figure matches the figures reported by other authors for blind diabetics, the mean survival time of about 5 years, with only 21% surviving for 10 years. The poor survival rate was noted to correspond with the patient age, whether he or she was above or below 60 years. Nevertheless, the rate is also associated with the relation between the proliferative stage and the other systemic, long-term diabetic complications such as nephropathy and coronary heart disease. In addition, a significant relationship between severe retinopathy and elevated blood urea nitrogen was reported, as up to 50% of diabetic patients with elevated urea nitrogen experience proliferative retinopathy. This was compared to 25% of diabetic patients without urea nitrogen. A considerable improvement of survival rates has been noticed since 1967 as a response to the continuous improvement in diabetic care.
Advance diabetic retinopathy
The hemorrhages are boat-like with a rounded bottom and a horizontal fluid level. They affect the vision seriously, obscuring the media, or causing retinal detachment. If detachment occurs in the posterior hyaloid membrane, then this will also lift off the fibrovascular tissue, as it has attached on to this membrane. Hemorrhaging into the vitreous in conjunction with the collapse of collagen structure in the vitreous gel will cause a condensation of the vitreous strands and shrinkage of the central vitreous.
If the vitreous shrinkage increases and vitreoretinal traction become excessive, this will lead to hemorrhages and later retinal detachment. A hemorrhage may be absorbed rapidly if it is in the retinovitreal space although it will last for a long period if it breaks into the vitreous gel.
In advanced cases, vitrectomy is performed to remove blood, fibrin, and membranes and the removed substances replaced by Ringer's solution to give shape and clarity. It also helps the new vessels to regress and stop bleeding. This surgical procedure is useful in eyes with vitreous opacities only, and previous retinal ischemia, degeneration, or fibrosis tends to reduce the chance of a good prognosis, however, vision improvement with vitrectomy is present in between 68% and 80% of the cases.
It is classified as a secondary glaucoma. It has been referred to as hemorrhagic glaucoma, thrombotic glaucoma, congestive glaucoma, rubeotic glaucoma, and diabetic hemorrhagic glaucoma. Numerous secondary ocular and systemic diseases that share one common element, retinal ischemia/hypoxia, and subsequent release of an angiogenesis factor, cause new blood vessel growth (NVG). The condition depends on the progression of NVG; it can cause glaucoma either through secondary open-angle or secondary closed-angle mechanisms. This is accomplished through the growth of a fibrovascular membrane over the trabecular meshwork in the anterior chamber angle, resulting in the obstruction of the meshwork and/or associated peripheral anterior synechiae. Late diagnosis or poor management can result in complete loss of vision or, quite possibly, loss of the globe itself. Early diagnosis of the disease, followed by immediate and aggressive treatment, is necessary. In managing NVG, it is essential to treat both the elevated intraocular pressure and the underlying cause of the disease.
| Nonocular Clinical Factors Influencing Diabetic Retinopathy|| |
Diabetic retinopathy progress is influenced by a number of clinical factors such as: age of the patient at the diabetic onset, duration of diabetes, degree of control of hyperglycemia, means of control, blood pressure, and pregnancy.,
Positive correlation between diabetic retinopathy and age of the patient at diabetic onset has been reported. The presence of visual problems in younger onset patients seems to correlate with proliferative retinopathy; on the other hand, the older-onset patients are more likely to suffer from maculopathy. Jarrett et al. reported that there was no difference in the prevalence rate in both young and older-onset patients. Carid et al. postulated that adult onset diabetics develop retinopathy sooner compared to juvenile diabetics.
Diabetic duration has the highest significant relationship to retinopathy and proliferative diabetic retinopathy. Retinopathy evidence is common after 10 years of duration; however, it is rarely noticed before 5–10 years of duration. The incidence rate was noted to be 50% with possible increase to over 90% in juvenile patients with 30 years diabetic duration., The general trend tends to increase in the prevalence of retinopathy up to 15–20 years of duration; however, it reaches a level between 20 and 30 years. This long period is possibly due to the increased mortality with increased severity of retinopathy. The prevalence rate of total retinopathy was reported to be 97.5% for duration of 15 years with a 40% chance of proliferative lesions after 20 years.
Blood-retinal barrier permeability to fluorescein is reported to correlate to diabetic duration in IDDM patients who are diagnosed before the age of 30 years. Normal permeability occurs in patients with duration below 10 years and is increased for durations between 10 and 15 years and by 5–10 times the normal values for duration above 15 years. In noninsulin-taking patients, the prevalence of retinopathy tends to be not more than 65% and rarely does retinopathy develop within 10 years of duration; however, 20% of NIDDM have some evidence of diabetic retinopathy at the time they are diagnosed.
Hyperglycemia control is reported to influence diabetic retinopathy.,, Although many reports noted insignificant correlation between diabetic control and severity of retinal lesions regardless of the type of diabetes.,,, On the other hand, a positive correlation between good diabetic control and retinopathy come from animal experiments; however, it is suggested that good metabolic control in man may slow the early stages of retinopathy.
Means of control
Diabetic retinopathy seems to occur more frequently and more severely in patients using insulin therapy compared to those controlled orally or by diet only.,,
A higher level of fluorescein penetration through the blood-retinal barrier was noticed in insulin-taking patients than on those on tablets or diet. This high level was also noted by Mouton and Gill as they compared their insulin-taking group to patients on diet treatment alone.
Diabetic retinopathy in IDDM patients has been investigated over a 4-year-period; the patients using insulin by injecting two to three times per day showed a significantly slower increase in retinal microaneurysms than those on one injection a day., It is obvious that the tight control slows the progress of diabetic retinopathy.
The relationship between retinopathy and high blood pressure is a complex one, as it is also connected with nephropathy. A further complicating factor is the normal relationship between age and hypertension.
A significant prevalence between retinopathy and hypertension has been noted., They reported that the incidence of exudates was twice as high in diabetics with systolic blood pressure >145 mmHg as compared to those with levels <125 mmHg or the control group of nondiabetics. No relation was found between the appearance of microaneurysms or hemorrhages and the blood pressure. Some other authors have reported increased incidences of advanced retinopathy with diastolic hypertension (>150/90 mmHg).,,,
It is widely believed that pregnancy can adversely affect retinopathy. It has been reported that pregnant IDDM women of 15 years or more of diabetic duration have a 63%–82% chance of retinopathy of any type and an 18%–20% chance of developing proliferative retinopathy. At the Rigshospitalet in Oslo study, 40% of 234 pregnant diabetics, studied between 1970 and 1977, had evidence of diabetic retinopathy. In general, most surveys suggest a 25% prevalence in pregnancy although figure between 18% and 62% have been reported. Other factors seem to contribute in worsening retinopathy, for example, retinal state before pregnancy. Pregnant women without retinopathy do not usually develop retinopathy although some may get evidence of background changes. Those who initially have background retinopathy a 50% chance of worsening in the second trimester with some clearing in the late third trimester. A few may also develop new vessels and 50% of those who already have new vessels their retinopathy worsens.,,,
| Available Methods of Treatment|| |
Photocoagulation is a useful, however, not curative means of eliminating diabetic retinopathy. Photocoagulation should be attempted early before the development of visual symptoms and retinal traction complications.
Argon and Xenon beams are used in photocoagulation; however, each has its own particular advantages related to leakage and new vessels locations. The Argon laser makes small burns, and therefore, can be aimed accurately and causes less damage to the tissue particularly when surrounding area is adjacent to the disc and the macular. Hemoglobin and choroid pigment can absorb the argon beam and convert the laser energy into heat to destroy microaneurysms, leaking vessels, and infarcts areas. This will stop the stimulus for the new vessels formation, and the repetition of photocoagulation therapy may be needed.
The xenon laser has large burns making it difficult to use near to the fovea. It has widespread energy absorption as it is absorbed by the melanin in the retinal pigment epithelium. It used when extensive areas of the retina are involved.
Two techniques are available, focal and pan-retinal photocoagulation. Focal techniques burn isolated new vessels or leakage and are therefore not extensive. Panretinal techniques are used where there are new disc vessels, and where new vessels are seen in one quadrant of the retina only since most of the retina is ischemic. Panretinal photocoagulation is aimed at retinal area several disc diameters from the macular to the equator of the eye. Six to eight photocoagulation sessions will produce 2000–5000 burns of 500 μm in diameter. Burning of 20%–30% of the retina in such a way will decrease. The oxygen and nutrition needed by the retina leading to a decrease in new vessel formation.
Regression of the new vessels has been reported to occur in 80% of the treated cases, and 61% fewer eyes become blind in those treated as compared to those untreated.
VEGF in the pathogenesis of both types of diabetic retinopathy is targeted by intravitreally administration pharmacologic inhibitor agents. They are blocking agents offer new options of nondestructive treatment with better visual outcomes than laser. Diabetic macular oedema (DMO) may also respond to intraocular steroid therapy, and the development of slow-release delivery systems can now provide drug delivery for 3 years from a single injection. The assessment of DMO has been revolutionized by noninvasive imaging with OCT which allows microscopic visualization of macular detail and serial quantitative measurement of the structural response to treatment. These new therapeutic options are not only improving visual outcomes for DMO but are also creating enormous logistical problems for both patients and eye clinics as they are much more demanding in terms of frequent clinic visits and use of ophthalmology imaging services than conventional but less effective laser treatment.
- Triamcinolone: Corticosteroid used in the treatment of diabetic macular edema
- Bevacizumab: Monoclonal antibody that can help to reduce DMO and neovascularization of the disc or retina
- Ranibizumab: Monoclonal antibody that can help to reduce DMO and neovascularization of the disc or retina.
This procedure can be used in PDR in cases of long-standing vitreous hemorrhage (where visualization of the status of the posterior pole is too difficult), fractional retinal detachment, and combined fractional and rhegmatogenous retinal detachment.
When laser photocoagulation in PDR is precluded in the presence of an opaque media, such as in cases of cataracts or vitreous hemorrhage, cryotherapy may be applied instead.
The Diabetes Control and Complications Trial found that intensive glucose control in patients with IDDM decreased the incidence and progression of diabetic retinopathy. It may be logical to assume that the same principles apply in NIDDM.
Variety of methods are in use to manage diabetic retinopathy, however, the availability of a particular method and the cost might limit the choice of management. Others would be age, duration, means of control, blood pressure, and pregnancy. The whole treatment tightens by the availability of the treatment methods and the patients' affordability.
In conclusion, DM causes multicomplications on the human body, the eye is one of the affected organs, and in particular, diabetic retinopathy represents itself as a major complication due its nature of subtle style. The world health organization, the regional and local formal and nonformal should share the strategic plans to reduce the advance stages of the diabetic retinopathy. The clinicians who are much concerned of diabetic patients should work together sharing screening and monitoring programs as well as treating the eye complications. One more important element should be included is the task of educating and sharing with the patients the management plans and to be considered hand-to-hand with the continuous training to the staff sharing diabetic patient management.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Marble A. Insulin in treatment of diabetes. In: Marble A, Bradley LP, Christlieb FR, Soeldner AR, JS, editors. Joslin's Diabetes Mellitus. 12th
ed. Philadelphia: Lea & Febinger; 1985. p. 380-402.
Kohner EM. Diabetic retinopathy. Br Med Bull 1989;45:148-73.
L'Esperance FA, James WA. Diabetic Retinopathy: Clinical Evaluation and Management. St. Louis: C.V. Mosby Co.; 1981.
Khatcalourov V. The world organisation and problems of diabetes mellitus. In: Keen H, Pickup JC, Talwalkar CV, editors. Epidemiology of Diabetes and Its Vascular Complications. Proceedings of the Satellite Meeting of IX International Diabetes Federation Meeting, Bombay. International Diabetes Federation; 1976. p. 9-13.
Palmberg PF. Diabetic retinopathy. Diabetes 1977;26:703-11.
Mitchell P. The prevalence of diabetic retinopathy: A study of 1300 diabetics from Newcastle and the Hunter Valley. Aust J Ophthalmol 1980;8:241-6.
Klein R, Klein BE, Moss SE, Davis MD, De Mets DL. The Wisconsin epidemiologic study of diabetic retinopathy. II: Prevalence and risk of diabetic retinopathy when age at diagnosis is less than 30 years. Arch Ophthalmol 1984a; 102:520-6.
Klein R, Klein BE, Moss SE, Davis MD, De Mets DL. The Wisconsin epidemiologic study of diabetic retinopathy. II: Prevalence and risk of diabetic retinopathy when age at diagnosis is less than 30 years. Arch Ophthalmol 1984b; 102:520-6.
Constable IJ, Knuiman MW, Welborn TA, Cooper RL, Stanton KM, McCann VJ, et al.
Assessing the risk of diabetic retinopathy. Am J Ophthalmol 1984;97:53-61.
Nielsen NV. Diabetic retinopathy II. The course of retinopathy in diabetics treated with oral hypoglycaemic agents and diet regime alone. A one year epidemiological cohort study of diabetes mellitus. The Island of Falster, Denmark. Acta Ophthalmol (Copenh) 1984;62:266-73.
Kanski JJ. Clinical Ophthalmology. 2nd
ed. London: Butterworths; 1990.
Kahn HA, Hiller R. Blindness caused by diabetic retinopathy. Am J Ophthalmol 1974;78:58-67.
Green FD, Ghafour IM, Allan D, Barrie T, McClure E, Foulds WS, et al.
Colour vision of diabetics. Br J Ophthalmol 1985;69:533-6.
Kohner EM. The evolution and natural history of diabetic retinopathy. Int Ophthalmol Clin 1978;18:1-6.
Kornerup T. Studies in diabetic retinopathy: An investigation of 1,000 cases of diabetes. Acta Med Scand 1955;153:81-101.
Cogan DG, Toussaint D, Kuwabara T. Retinal vascular patterns. IV. Diabetic retinopathy. Arch Ophthalmol 1961;66:366-78.
Gabbay KH. Hyperglycaemia, polyol metabolism and complications of diabetes mellitus. Ann Rev Med 1975;26:521-35.
Kador PF. The role of aldose reductase in the development of ocular diabetic complications. In: Drazin B, Melmed S, Le Roith D, editors. Complications of Diabetes Mellitus. Vol. 3. New York: Alan Liss Inc.; 1989. p. 103-14.
Cunha-Vaz J, Faria de Abreu JR, Campos AJ. Early breakdown of the blood-retinal barrier in diabetes. Br J Ophthalmol 1975;59:649-56.
McMillan DE. Alteration of capillary basement membrane in diabetes. In: Little HL, Jack RL, Patza A, Forsham PH, editors. Diabetic Retinopathy. New York: Thieme Stratton; 1983. p. 107.
Williamson JR, Kilo R. Basement membrane in diabetes mellitus. In: Drazin B, Melmed S, Le Roith D, editors. Complications of Diabetes Mellitus. Vol. 3. New York: Alan Liss Inc.; 1989. p. 19-30.
Winocour PD. The role of platelets in the pathogenesis of diabetic vascular disease. In: Drazin B, Melmed S, Le Roith D, editors. Complications of Diabetes Mellitus. Vol. 3. New York: Alan Liss Inc.; 1989. p. 37-47.
Colwell JA. Platelets and diabetic retinopathy. In: Little HL, Jack RL, Patza A, Forsham PH, editors. Diabetic Retinopathy. New York: Thieme Stratton; 1983. p. 119.
Klein R, Klein BE, Moss SE, Cruickshanks KJ. The medical management of hyperglycemia over a 10-year period in people with diabetes. Diabetes Care 1996;19:744-50.
Bodansky HJ, Cudworth AG, Whitelocke RA, Dobree JH. Diabetic retinopathy and its relation to type of diabetes: Review of a retinal clinic population. Br J Ophthalmol 1982;66:496-9.
Donovan RJ. Prevalence of retinopathy in a diabetic clinic. Br Med J 1978;1:1441-2.
Aiello LM, Rand LI, Sebestyen JG, Weiss JN, Bradbury MJ, Wafai MZ, et al
. The eyes and diabetes. In: Marble A, Krall LP, Bradley FR, Christlieb AR, Soeldner JS, editors. Joslin's Diabetes Mellitus. 12th
ed. Philadelphia: Lea and Febinger; 1985. p. 600-34.
Whitelocke RA, Kearns M, Blach RK, Hamilton AM. The diabetic maculopathies. Trans Ophthalmol Soc U K 1979;99:314-20.
Blankenship GW. Diabetic retinopathy, present and future. Conclusion of diabetic retinopathy symposium. Ophthalmology 1981;88:658-61.
Diabetic Research Group. Four risk factors for severe visual loss in diabetic retinopathy. Arch Ophthalmol 1979;97:654-5.
Diabetic Research Group. Report 7. A modification of the Airlie House classification of diabetic retinopathy. Invest Ophthalmol Vis Sci 1981;21:210-25.
Mouton DP, Gill AJ. Prevalence of diabetic retinopathy and evaluation of risk factors. A review of 1,005 diabetic clinic patients. S Afr Med J 1988;74:399-402.
Szab AJ, Stewart AG, Joron GE. Factors associated with increased prevalence of diabetic retinopathy. J Can Med Assoc 1967;97:286-92.
Carid FI, Pirie A, Ramsell IG. Diabetes and the Eye. Oxford: Blackwell Scientific Publications; 1969.
Kloalchatourov V. The World Health Organisation and problems of diabetes mellitus. In: Keen H, Pickup JC, Talwalkar CV, editors. Epidemiology of Diabetes Mellitus and Its Vascular Complications. Proceedings of the Satellite Meeting of IX International Diabetes Federation Meeting, Bombay. International Diabetes Federation; 1976. p. 9-13.
Jerneld B, Algevere P. Prevalence of diabetic retinopathy in diabetes treated with oral anti-hyperglycaemic agents. Acta Ophthalmol 1985;63:535-40.
Jarrett RJ, Stewart T, Rogers L. Diabetes mellitus I: Diagnosis and initial management. Br Med J 1981;283:647-50.
Jerneld B, Algevere P. Relationship of duration and onset of diabetes to prevalence of diabetic retinopathy. Am J Ophthalmol 1986;102:431-7.
Jerneld B, Algvere P. Relationship of duration and onset of diabetes to prevalence of diabetic retinopathy. Am J Ophthalmol 1986;102:431-7.
Krogsaa B, Lund-Andersen H, Mehlsen J, Sestoft L. Blood-retinal barrier permeability versus diabetes duration and retinal morphology in insulin dependent diabetic patients. Acta Ophthalmol (Copenh) 1987;65:686-92.
Burditt AF, Caird FI, Draper GJ. The natural history of diabetic retinopathy. Q J Med 1968;37:121.
Jerneld B, Algvere P. Prevalence of retinopathy in diabetes treated with oral antihyperglycaemic agents. Acta Ophthalmol (Copenh) 1985;63:535-40.
Knuiman MW, Wellborn TA, McCann VJ, Stanton KG, Constable IJ. Prevalence of diabetic complications in relation to risk factors. Diabetes 1986;35:1332-9.
Job D, Eschwege E, Tchobroutsky G. Diabetic retinopathy: Duration of diabetes and risk. Acta Diabetol 1975;12:1-5.
Job D, Eschwege E, Guyot-Argenton C. Effect of multiple daily insulin injections on the course of diabetic retinopathy. Diabetes 1976;25:463-9.
Jarrett J, Stewart T, Rogers L. Diabetes mellitus I: Diagnosis and initial management. Br Med J (Clin Res Ed) 1981;283:647-50.
Jervell J, Moe N, Skjaeraasen J, Blystad W, Egge K. Diabetes mellitus and pregnancy – Management and results at Rikshospitalet, Oslo, 1970-1977. Diabetologia 1979;16:151-5.
Moloney J, Drury M. Retinopathy and retinal function in insulin-dependent diabetes mellitus. Br J Ophthalmol 1982;60:759-61.
Cassar J, Kohner EM, Hamilton AM. Diabetic retinopathy and pregnancy. Diabetologia 1978;15:105-11.
Towler HM. A new technologies and drugs in the management of diabetic retinopathy. Pract Diabetes 2014;31:275-80.
Rosenfeld PJ, Brown DM, Heier JS, Boyer DS, Kaiser PK, Chung CY, et al.
Ranibizumab for neovascular age-related macular degeneration. N Engl J Med 2006;355:1419-31.
Brown DM, Kaiser PK, Michels M, Soubrane G, Heier JS, Kim RY, et al.
Ranibizumab versus verteporfin for neovascular age-related macular degeneration. N Engl J Med 2006;355:1432-44.
Photocoagulation for diabetic macular edema. Early treatment diabetic retinopathy study report number 1. Early Treatment Diabetic Retinopathy Study Research Group. Arch Ophthalmol 1985;103:1796-806.