Diabetic retinopathy (DR), damage of the blood vessels in the retina, is one of the health care professionals interested in diabetic eye disease this book is an. The Silver Book®: Diabetic Retinopathy. Diabetic retinopathy (DR) is a serious, irreversible eye disease that can occur in people with diabetes, and is a leading. This book addresses diabetic retinopathy, an eye disease that remains one of the main causes of vision loss if not diagnosed and managed properly. It aims to.
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retinopathy, you are encouraged to review the sections on diabetes in any of the major Another excellent resource is the book Diabetic Retinopathy. Book. Diabetic Retinopathy for the comprehensive ophthalmologist. Walker J. This book will be available in electronic format on the new. Diabetic retinopathy is a significant life-altering complication affecting patients with diabetes. Understanding its pathogenesis, prevention, and.
Also included is a discussion of emerging concepts relating to the management and treatment of DR. Informative and highly-practical, Diabetic Retinopathy provides ophthalmologists, diabetologists, endocrinologists, and internists with a highly readable guide not only to understanding diabetic retinopathy, but also to its optimal clinical management.
This can be identified clinically as an enlargement of the normal foveal avascular zone on fluorescein angiography Figure 5. Capillary dropout around the fovea white arrow and in the temporal macula black arrow.
Macular edema may be present at all the stages of diabetic retinopathy and is the most common cause of vision loss in nonproliferative diabetic retinopathy. Because of the increased vascular permeability and breakdown of the blood-retinal barrier, fluid and lipids leak into the retina and cause it to swell.
This causes photoreceptor dysfunction, leading to vision loss when the center of the macula, the fovea, is affected. Clinically significant macular edema with hard exudates in the fovea. Cotton-wool spots are present near the major vessels.
Although the cause of the microvascular changes in diabetes is not fully understood, the deficient oxygenation of the retina may induce an overexpression of vascular endothelial growth factor VEGF , with a consequent increase in vascular leakage and retinal edema. In fact, elevated levels of extracellular carbonic anhydrase have been discovered in the vitreous of patients with diabetic retinopathy. Optical Coherence Tomography OCT is a widely used imaging technique that provides high-resolution imaging of the retina Figure 7.
Most patients with DME have diffuse retinal thickening or cystoid macular edema presence of intraretinal cystoid-like spaces. In some patients, DME may be associated with posterior hyaloidal traction, serous retinal detachment or traction retinal detachment.
In proliferative diabetic retinopathy, many of the changes seen in NPDR are present in addition to neovascularization that extends along the surface of the retina or into the vitreous cavity Figure 8. These vessels are in loops that may form a network of radiating spokes or may appear disorganized. In many cases the vessels are first noted on the surface of the optic disc, although they can be easily missed due to their fine calibur.
Active neovascularization in PDR. Fibrovascular proliferation overlies the optic disc white arrow. Loops of new vessels are especially prominent superior to the disc and extending into the macula, where leakage of fluid has led to deposition of a ring of hard exudate around the neovascular net black arrow.
New vessels can also appear on the iris, a condition known as rubeosis iridis Figure 9. When this occurs, careful inspection of the anterior chamber angle is essential, as growth of neovascularization in this location can obstruct aqueous fluid outflow and cause neovascular glaucoma. Rubeosis iridis in a case of PDR. Abnormal new vessels are growing along the surface of the iris arrows.
UCSF Dept. Neovascularization can remain relatively stable or it can grow rapidly; progression can be noted ophthalmoscopically over a period of weeks. Preretinal new vessels often develop an associated white, fibrous tissue component that can increase in size as the vessels regress. The resulting fibrovascular membrane may then develop new vessels at its edges. This cycle of growth and fibrous transformation of diabetic neovascularization is typical. Fibrous proliferation takes place on the posterior vitreous surface; when the vitreous detaches, the vessels can be pulled forward and the thickened posterior vitreous surface can be seen ophthalmoscopically, highlighted by areas of fibrovascular proliferation.
The severity of PDR can be classified as to the presence or absence of high-risk characteristics. As determined in the Diabetic Retinopathy Study, eyes are classified as high-risk if they have 3 of the following 4 characteristics: Vision loss in proliferative diabetic retinopathy results from three main causes. First, vitreous hemorrhage occurs because the neovascular tissue is subject to vitreous traction.
Coughing or vomiting may also trigger a hemorrhage. Hemorrhage may remain in the preretinal space between the retina and the posterior vitreous surface, in which case it may not cause much vision loss if located away from the macula Figure In other cases, though, hemorrhage can spread throughout the entire vitreous cavity, causing a diffuse opacification of the visual media with marked vision loss Figure 11 , Preretinal hemorrhage: Visual acuity is unaffected.
Dense vitreous hemorrhage almost completely obscuring the view of the fundus. Another cause of severe vision loss in PDR is retinal detachment.
As the fibrovascular membranes and vitreous contract, their attachments to the retina can cause focal elevations of the retina, resulting in a traction retinal detachment Figure In other cases the retinal vessels can be avulsed or retinal holes may be created by this traction, leading to a combined traction-rhegmatogenous retinal detachment Figure Marked fibrosis with traction exerted on the retina outside the central macula arrows.
The macula does not appear to be elevated centrally. Traction retinal detachment outside the macula.
Note elevation of retinal vessel out of the plane of focus white arrow. Scatter photocoagulation scars are seen peripherally black arrow. Finally, patients with PDR may have macular nonperfusion or coexisting diabetic macular edema that causes vision loss through photoreceptor dysfunction. Tight glucose and blood pressure control are critical systemic factors in controlling the progression of diabetic retinopathy. Ocular complications of diabetes are addressed directly through treatment with laser photocoagulation, intravitreal injections or surgery.
Laser treatment has been the primary approach to vision-threatening diabetic retinopathy for decades. Recent randomized clinical trials demonstrated that intravitreal anti-VEGF agents are more effective than laser under certain conditions.
Diabetic macular edema is believed to result from fluid and lipid transudation from microaneurysms and telangiectatic capillaries. Focal laser photocoagulation is used to heat and close the microaneurysms, causing them to stop leaking Figure Macular edema often improves following this form of treatment. Some clinicians apply laser burns in a grid pattern overlying areas of retinal edema without directing treatment to specific microaneurysms; this method can also be effective in reducing retinal thickening.
The mechanism by which grid laser treatment achieves these results is not known. Side effects of laser treatment can include scotomata, noticeable immediately after the procedure, if treatment is performed too close to the fovea. Late enlargement of laser scars can also occur, causing delayed visual loss. Inadvertent photocoagulation of the fovea is a risk of the procedure.
In the ETDRS study, only a very small percentage of eyes improved with focal laser treatment, highlighting the fact that the goal of laser treatment is not to improve vision, but rather to stabilize it and prevent worsening. For this reason, it has been argued that the study enrolled patients with excellent visual acuity, making it difficult to demonstrate small improvements in vision after laser treatment.
Due to the recent evidence on the efficacy and safety of anti-VEGF therapy for diabetic macular edema, different modalities of laser therapy have been proposed. Laser may be able to stabilize macular edema and reduce the need for multiple anti-VEGF injections.
Modified ETDRS laser techniques include lower intensity laser burns, and they take particular care in maintaining a greater space from the center of the fovea. Focal laser scars in the macula following treatment for macular edema arrow.
Edema has resolved. Although the treatment destroys normal retina, the central vision is unaffected since all spots are placed outside the macula.
The theory underlying this treatment is that photocoagulation of the ischemic peripheral retina decreases the elaboration of vasoproliferative factors contributing to PDR. Indeed, VEGF levels in the vitreous are increased in eyes with neovascularization, and they are lower after scatter photocoagulation. Side effects of scatter photocoagulation can include decreased night vision and dark adaptation, and visual field loss. The procedure can be painful, so treatment may be divided into several sessions, and either topical or retrobulbar anesthesia may be used.
Scatter photocoagulation scars in an eye with active PDR. Note that all scatter laser scars are located outside the macula.
View of laser scars superior to the macula in the same eye. Spots are approximately one-half burn width apart.
In the treated area, the retinal vessels are sclerotic arrows. Patients had one eye randomized to treatment and one eye to observation. Panretinal photocoagulation may induce or aggravate diabetic macular edema, reduce contrast sensitivity and affect the peripheral visual field. However, it is not recommended to delay panretinal photocoagulation in high-risk PDR. Recently, the DRCR. Mean peripheral visual field sensitivity loss was worse, vitrectomy was more frequent, and DME development was more common in the PRP group.
Further studies are needed in order to evaluate the long-term implications of using anti-VEGF agents alone. Ranibizumab may be a reasonable treatment alternative to consider for patients with severe NPDR or non-high-risk PDR who can follow-up regularly. It has been demonstrated that corticosteroids stabilize the blood-retinal barrier, inhibiting leukostasis and modulating the expression of VEGF receptor. It should be remembered that any of these different methods to deliver corticosteroids to the macula carry a potential risk of increasing the intraocular pressure glaucoma and inducing cataract.
The use of intravitreal triamcinolone acetonide has become accepted as a treatment option for diabetic macular edema. Several formulations are available: Kenalog, which has a black box warning against intraocular use, and the preservative-free Triesence.
Preliminary data from a randomized clinical trial showed that intravitreal corticosteroids induced a noticeable improvement of visual acuity and foveal thickness in patients with severe, refractory DME. A peribulbar corticosteroid injection is of particular interest for eyes with DME that have good visual acuity where the risks of an intravitreal injection may not be justified. Any intravitreal injection through the pars plana, in fact, may directly damage the crystalline lens or cause a severe, sight-threatening infection of the eye bacterial endophthalmitis.
Unfortunately, in a randomized clinical trial showed that peribulbar triamcinolone, with or without focal photocoagulation, is not effective in cases of mild DME with good visual acuity.
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