Diabetic retinopathy

Diabetic retinopathy is a caused by the diabetes diabetes mellitus disease of the retina of the eye. The progressive damage to small blood vessels ( microangiopathy ) caused an initially undetected damage to the retina. It can lead to blindness. Current therapies can only delay the disease progresses, stopping at best. The prevention is to optimize the therapy of diabetes mellitus.

• 5.1 Retinal Laser Therapy
• 5.2 injection therapies
• 5.3 operation

Occurrence

Diabetic retinopathy is in Europe and North America, the leading cause of blindness in people between 20 and 65 years. After 20 years of disease duration show up at 90 % of diabetics sign of the disease in the fundus. In type I diabetics appear first changes in the middle after 10-13 years. For optimum control and treatment, the disease leads only in 5 % of cases of severe loss of vision. On average, this blind 2% of all diabetics retinopathy. Type I diabetics suffer with 40 % approximately twice as often as type II diabetics. However, 5% of all diabetics show age at diagnosis of diabetes already retinopathy changes.

Causes

The cause for the development of diabetic retinal disease, several risk factors are known. Main factor is the duration of the diabetes. A poor control of blood sugar levels is another major risk factor. A rigorous control of blood glucose, the development or progression of diabetic retinopathy can be prevented or at least delayed. During the phases of hormonal change, the risk is also increased. Therefore, pubescent adolescents and pregnant women are at increased risk for development and progression of the disease. Within pregnancy, the risk is amplified by poor blood sugar control, a too rapid glycemic control in early pregnancy, as well as pre-eclampsia on. Another independent risk factor is hypertension. Similarly, a diabetic renal injury increases the risk of developing also on the eye. Another risk factor is an increase in blood fats.

Forms and pathogenesis

Nonproliferative retinopathy

The nonproliferative retinopathy is characterized in that at her still occur no vascular neoplasms. It divides the nonproliferative retinopathy in a mild, moderate and severe retinopathy.

In the mild form (also Background retinopathy ) to aneurysms of the capillaries show ( microaneurysms ).

By further damage to the vascular endothelium, the vessels are leaky, it comes to the stage of moderate retinopathy. It caused deposits of fats from the blood plasma ( so-called " hard exudates "). By closures of capillaries there is point-like and / or sheet-like bleeding in the retina. The retinal veins can be thickened beaded.

In the severe form, these changes are more advanced: it show up frequent hemorrhages, cotton - wool spots ( retinal infarction ), segmentation, thickening and loop formation of the veins and zones of the retina, which are no longer supplied with blood vessels. It comes at a retinal edema, initially focal, then diffuse. There are increasingly growth factors released which stimulate neovascularization. Around 50% of patients with severe non-proliferative retinopathy proliferative retinopathy develop within a year.

Proliferative retinopathy

This heavy, visusbedrohende form of diabetic retinopathy is characterized by formation of abnormal blood vessels in the retina and in the vitreous. This stage of disease is shown in the non-proliferative diabetic retinopathy: In the not -perfused areas of the retina ( ischemic zones ) messengers are formed, which stimulate vascular growth. This retina districts call for help, so to speak. Through these messengers (eg VEGF ) leads to the formation of new blood vessels that grow from the retinal level in the interior of the eye, the vitreous. The neoplasms arise preferably from the papilla of the optic nerve and from large vessels of the retina. These vessels have only a weak wall so that it can be used in particular in sudden increase in blood pressure, bleeding. Bleeding it into the vitreous body, this results in a sudden and drastic deterioration of the visual acuity. In a later stage, thus resulting vessel trees can shrink to the retina scarred and so the retina from the background stand ( tractional retinal detachment ), which can lead to blindness or even loss of the eye. The effects of vasoactive mediators are also visible in other places in mind, so it can in serious cases, to neovascularization on the iris (Iris ), the so-called rubeosis iridis come. This can in turn by switching the outflow pathways of aqueous humor to a (sometimes painful ) increase in intraocular pressure lead ( rubeotisches secondary glaucoma).

Proliferative retinopathy occurs in type 1 diabetic patients more frequently than in type 2 diabetic patients. So suffer after 15-20 years of disease 50 % of type 1 diabetics and 15-30 % of type 2 diabetics at this stage of the disease. It develops most rapidly during periods of hormonal change such as puberty or pregnancy.

Diabetic maculopathy

In maculopathy, the point of sharpest vision in the center of the retina ( macula) is damaged, leading to progressive loss of central vision and thus frequently eg leads to the loss of reading performance and the loss of car driving ability. This is due to fatty deposits ( Lipidexsudate ) and edematous swelling of the retina in the macula ( macular edema ) due to the damage to the small vessels. It can also be damaged early in the course by a lack of blood supply to the macula. The maculopathy is the most common reason for a strong visual loss in patients. It can occur at any stage of the disease.

Investigation

In addition to the reflection of the fundus (ophthalmoscopy ) are depending on the stage of the disease process such as fluorescence angiography, which may represent the blood vessels of the retina, and diagnostics. In particular, before laser treatment, this is obligatory. For several years, optical coherence tomography (OCT) is used, with a cross-sectional imaging of the macula is possible. This method is particularly well suited for the detection and evaluation of progression of diabetic macular edema. All forms of retinopathy remain for the patient usually very long time without symptoms. It was only in the late stage by participating in the macular or vitreous hemorrhage, the patient noticed a decrease in vision. This can be slow progressing, but are also symptomatic of a sudden blindness in a vitreous hemorrhage of the eye.

Treatment

For the treatment of diabetic retinopathy, there are, depending on the stage, different approaches. Common to all, however, is that a sufficient treatment success can only be achieved if the diabetes is treated as underlying disease correctly and consistently.

A real "cure" of diabetic retinal disease is, as a cure of diabetes itself, at present not yet possible. However, it can often through various treatment measures and good control of diabetes is an improvement of vascular damage, or at least stop the disease reach. In general, the earlier the diabetic retinal disease is detected and the sooner treatment is started, the better the chances of success. The later start the treatment of a derailed metabolism, the higher the risk of diabetic retinopathy.

The patient plays the most important role in therapy: through consistent implementation of the diabetes therapy with adequate diet, avoiding smoking and excessive alcohol consumption. The durable good attitude of blood glucose levels is a basic requirement to protect against diabetic retinopathy ( and all the other complications of diabetes). As a patient, you should be well informed about the quality of blood glucose control. These are, inter alia, of diabetics and pass the knowledge of the so-called long -term blood glucose value ( HbA1c ), which provides as " blood sugar memory " information about the average blood glucose levels over the past three months.

Arterial hypertension must be treated equally consistent; Notes to the advantage of certain groups of substances of antihypertensives not be found.

Retinal laser therapy

An indication for laser therapy is as soon as neovascularization or vitreous hemorrhage have trained. It there are different methods available:

• Panretinal laser photocoagulation: Here, the retina at around 1,000 to 2,000 bodies are scarred by a lattice lasering. The macula as a place of sharpest vision is spared. The scarred areas remain sehfähig usually because the laser only the outer portions, but not destroy the photoreceptors. The laser treatment reduces the oxygen consumption of scarred retina shares, so that the supply situation of the macula improved. Possible side effects of the therapy are disturbances of color vision and adaptation to darkness. In large-scale scarring it can also lead to a restriction of the visual field. As a long-term consequence may, in particular for large-scale interventions, an overgrowth of the retina with membranes ( macular pucker ) occur which damages the eyesight.
• Focal laser photocoagulation: This method is the method of choice for macular edema occurs. The responsible for the edema leaky neovasculature be scarred. Characterized both the edema and the Lipidexsudate are reversible. The treatment generally leads only to a stabilization of the visual acuity, rarely improved. A panretinal laser treatment is not displayed when macular edema, because it can lead to deterioration.

Injection therapies

In the treatment of diabetic macular edema by the introduction of new treatments and medications lately new treatment opportunities have become available. Injections of drugs directly into the vitreous humor of the eye ( intravitreal injections) have been established in recent years as a method of therapy, even if they are still no absolute standard procedures in the field of diabetic Makulo / retinopathy. Two groups of active substances are available:

• Kortikosteroidpräparat the dexamethasone can affect a positive diabetic macular edema, but must be repeated injection into the vitreous. However, it is an off- label use, what the patient must be informed. The triamcinolone previously used more frequently than dexamethasone caused an increase in intraocular pressure and cataracts.

• Anti -angiogenic drugs. These substances block the vascular growth -promoting substances directly in the eye and can lead to a swelling of the central retina. Often they are repeatedly injected at intervals of a few weeks in the eye. ( Utilized drugs are Bevacizumab, which was borrowed from cancer therapy, ranibizumab and pegaptanib. Ruboxistaurin is a PKC -beta inhibitor, which is taken as a tablet.

Operation

If persistent bleeding into the vitreous or retinal detachment with membrane formation, a removal of the vitreous ( vitrectomy ) is displayed with enucleation of the blood. The vitreous is replaced with gas or silicone oil, in order to secure the retina, since it is held only by the pressure of the glass body in its position. During the operation, a laser treatment is carried out in general.

Provision

The successful treatment of diabetic retinopathy depends on the early diagnosis of diabetes mellitus, the early diagnosis of retinopathy and consequent therapy. With timely treatment progression and thus a loss of vision can be prevented. As the diabetic retinopathy can progress long, without causing significant discomfort, the diabetic should always go once a year to the ophthalmologist. Should show signs of diabetic eye disease studies ( every 3-6 months usually ) should be repeated at shorter intervals.

In acute deterioration of vision, new problems arise when reading, the color perception or appearances as Rußregen an immediate ophthalmologic examination should be performed.

In diabetic women who are planning a pregnancy, the blood sugar should be optimized before pregnancy and monitored intensively during pregnancy (see also gestational diabetes ). Before the start of pregnancy, or as early as possible after admission, an ophthalmological examination should be performed, because the hormonal changes can lead to a deterioration of the eye findings. In 10-26 % of patients in whom no or only presented to a small retinopathy before pregnancy, there is a deterioration of the findings.

Studies (FIELD 2007 ACCORD 2008) showed for the lipid-lowering agent fenofibrate independent of lipid levels slowing the progression of diabetic retinopathy, and reduced the need for laser photocoagulation. In Australia, fenofibrate was approved drug legally for this indication.