Diabetic retinopathy

from Wikipedia, the free encyclopedia
Classification according to ICD-10
E10-E14 Diabetes mellitus
.3+

H36.0 * 		With eye complications
- diabetic retinopathy
Retinopathia diabetica
ICD-10 online (WHO version 2019)

The diabetic retinopathy (also: diabetic retinopathy ) is a due to diabetes diabetes mellitus induced disease of the retina of the eye. The increasing damage to small blood vessels ( microangiopathy ) causes initially unnoticed damage to the retina. It can lead to blindness over time. Previous therapies can only delay the further course of the disease, in the best case stop it. Prevention consists in optimal therapy for diabetes mellitus.

Occurrence

Diabetic retinopathy is the leading cause of blindness in people between the ages of 20 and 65 in Europe and North America . After 20 years of illness, 90% of diabetics show signs of the disease on the fundus. In type 1 diabetics, the first changes occur on average after 10–13 years. With optimal control and treatment, the disease only leads to severe visual impairment in 5% of cases. On average, 2% of all diabetics go blind from retinopathy. Type 1 diabetics are 40% twice as likely to develop the disease as type 2 diabetics. However, 5% of all type 2 diabetics show retinopathic changes when they are first diagnosed with diabetes.

causes

Several risk factors are known to cause the development of diabetic retinal disease. The main factor is the length of time the diabetes has persisted. Poor control of blood sugar levels is another major risk factor. Strict control of blood sugar levels can prevent or at least delay the development or progression of diabetic retinopathy. The risk is also increased during the phases of hormonal changes. Therefore have pubescent adolescents and pregnant women at increased risk of development and progression of the disease. During pregnancy, the risk is further increased by poor blood sugar control, too rapid blood sugar control in early pregnancy, and preeclampsia . Another independent risk factor is high blood pressure . Likewise, diabetic kidney damage increases the risk of developing eye diseases. Another risk factor is an increase in blood lipids .

Forms and disease origins

Non-proliferative retinopathy

The non- proliferative retinopathy is characterized by the fact that it does not yet have neovascularization. Non-proliferative retinopathy is divided into mild, moderate and severe retinopathy.

The mild form (also background retinopathy) shows vascular sagging of the capillaries (microaneurysms).

Further damage to the vascular endothelium causes the vessels to leak, leading to the stage of moderate retinopathy with the breakdown of the internal blood-retinal barrier . Deposits of fats form from the blood plasma (so-called "hard exudates"). Blockages of capillaries lead to punctiform and / or extensive bleeding into the retina. The retinal veins can be thickened like a string of pearls.

In the severe form, these changes are more advanced: there are accumulated hemorrhages in the retina, cotton-wool spots (retinal infarcts), segmentation, pearl-like thickenings in several areas of the retina and looping of the veins and zones of the retina that are no longer with Blood vessels are supplied. There are more than 20 individual microaneurysms. Retinal edema develops, initially focal, then diffuse. Increasingly growth factors are released that stimulate the formation of new blood vessels. Around 50% of patients with severe non-proliferative retinopathy develop proliferative retinopathy within one year.

Proliferative Retinopathy

Diabetic retinopathy after focal laser treatment

This severe, vision-threatening form of diabetic retinopathy is characterized by the formation of new abnormal blood vessels in the retina and vitreous humor. This stage of the disease arises from non-proliferative diabetic retinopathy: In the areas of the retina that are no longer supplied with blood (ischemia zones), messenger substances are formed that stimulate vascular growth. These areas of the retina call for help, so to speak. These messenger substances (including VEGF ) lead to the formation of new vessels that grow from the retinal level into the interior of the eye, the vitreous body . The neoplasms arise primarily from the optic nerve papilla and from large vessels of the retina. These vessels have only a weak wall, so that bleeding can occur, especially if the blood pressure rises suddenly. If it bleeds into the vitreous humor, this leads to a sudden and drastic deterioration in visual acuity . At a later stage, the resulting vascular trees on the retina can shrink scarred and thus lift the retina off the ground (tractive retinal detachment ), which can lead to blindness or even loss of the eye. The effects of the vascular-active messenger substances are also visible in other places in the eye. In severe cases, new vessels can also form on the iris , the so-called rubeosis iridis . This in turn can lead to an (sometimes even painful) increase in intraocular pressure ( rubeotic secondary glaucoma ) by obstructing the drainage pathways for the aqueous humor .

Proliferative retinopathy is more common in type 1 diabetics than in type 2 diabetics. After 15-20 years of the disease, 50% of type 1 diabetics and 15-30% of type 2 diabetics suffer from this stage of the disease. It develops particularly quickly in phases of hormonal changes, such as puberty or pregnancy.

Diabetic maculopathy

Diabetic fundus with macular edema

In maculopathy, the point of sharpest vision in the center of the retina ( macula ) is damaged, which leads to a progressive loss of central visual acuity and thus often e.g. B. also leads to loss of reading ability and loss of driving ability. The reasons for this are fat deposits (lipid exudates) and edematous swelling of the retina in the area of ​​the macula ( macular edema ) due to damage to the small vessels. A lack of blood supply can also damage the macula early in the course. Maculopathy is the most common cause of severe visual impairment in patients. It can occur at any stage of the disease.

examination

In addition to mirroring the fundus of the eye ( ophthalmoscopy ), depending on the stage of the disease, methods such as fluorescence angiography , which can depict the blood vessels of the retina, are part of the diagnosis. This is particularly mandatory before laser treatment. For some years now, optical coherence tomography (OCT) has also been used, with which cross-sectional imaging of the macula is possible. This method is particularly suitable for the detection and assessment of the course of diabetic macular edema. The retinal vascular analysis can detect disorders of the autoregulation of the small blood vessels in the retina, often before retinopathy occurs. Such disorders of the vascular behavior can indicate an increased risk of stroke. All forms of retinopathy usually remain symptom-free for the patient for a very long time. Only in the late stage with involvement of the macula or vitreous hemorrhage does the patient notice deterioration in vision. This can progress slowly, but it can also become symptomatic with sudden blindness due to a vitreous hemorrhage in the eye.

treatment

There are different approaches to treating diabetic retinal disease, depending on the stage. What they all have in common, however, is that adequate treatment success can only be achieved if diabetes as an underlying disease is treated correctly and consistently.

A real "cure" of the diabetic retinal disease, like a cure for diabetes itself, is not possible. Nevertheless, through various treatment measures and a good control of the diabetes, an improvement in the vascular damage or at least a halt in the disease can often be achieved. In general, the earlier the diabetic retinal disease is detected and the sooner the treatment starts, the better the chances of success. The later treatment for a derailed metabolism begins, the higher the risk of diabetic retinopathy.

The patient plays the most important role in the therapy: through consistent implementation of diabetes therapy with adequate nutrition, renouncing nicotine and excessive alcohol consumption . The permanent good setting of the blood sugar values is a basic requirement for protection against diabetic retinopathy (and all other complications of diabetes). As a patient, you should be well informed about the quality of your blood sugar control. To serve u. a. the diabetic pass and the knowledge of the so-called long-term sugar value ( HbA1c value), which as a “blood sugar memory ” provides information about the average blood sugar values ​​of the last three months. And knowledge of the blood sugar profile, which can be determined very easily by reading out the blood sugar measuring devices. It provides information as to whether the good HbA1c value may not have been “bought” by just a few hypoglycaemia.

An arterial hypertension must also be treated consistently; There is no evidence of the advantage of certain substance groups of antihypertensive drugs .

Retinal laser therapy (laser coagulation)

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

  • Panretinal laser coagulation: Here the retina is scarred in a grid-like manner in around 1,000 to 2,000 places by laser. The macula as the place of sharpest vision is left out. The scarred areas usually remain able to see because the laser only destroys the outer parts, not the photoreceptors . The laser treatment reduces the oxygen consumption of the scarred parts of the retina, so that the supply situation for the macula is improved. Possible side effects of the therapy are disorders of color vision and adaptation to darkness. With extensive scarring, the field of vision can also be restricted. As a long-term consequence, especially in large-scale operations, the retina can become overgrown with membranes ( epiretinal gliosis ), which damages the ability to see.
  • Focal laser coagulation: This method is the method of choice when macular edema occurs. The leaky new blood vessels responsible for the edema are scarred. As a result, both the edema and the lipid exudates are reversible. The treatment usually only leads to a stabilization of the visual acuity, only rarely to an improvement. Panretinal laser treatment is not indicated for macular edema as it can worsen it.

Injection therapies

In the treatment of diabetic macular edema, new treatment options have recently emerged with the introduction of new forms of treatment and drugs. Injections of active substances directly into the vitreous humor of the eye ( intravitreal injections) have become established as a therapeutic method in recent years, even if they are not yet an absolute standard method in the field of diabetic maculo / retinopathy. Two groups of active ingredients are available:

  • The corticosteroid preparation dexamethasone can have a positive effect on diabetic macular edema, but it must be injected repeatedly into the vitreous humor. However, this is an off-label use , about which the patient must be informed. The previously used triamcinolone caused an increase in intraocular pressure and cataracts more frequently than dexamethasone .
  • Anti- angiogenesis drugs. These substances block the substances in the eye that promote vascular growth directly and can lead to a swelling of the center of the retina. They are often injected into the eye several times at intervals of a few weeks. The drugs used are bevacizumab , which was borrowed from cancer therapy, ranibizumab and pegaptanib . Ruboxistaurin is a PKC-beta inhibitor that is taken as a tablet.

surgery

If there is persistent bleeding into the vitreous or a detachment of the retina with membrane formation, removal of the vitreous ( vitrectomy ) and exfoliation of the blood is indicated. The vitreous humor is replaced by gas or silicone oil to reattach the retina as it is only held in place by the pressure of the vitreous humor. Laser therapy is usually also performed during the operation.

prevention

Successful treatment of diabetic retinopathy depends on early diagnosis of diabetes mellitus, early diagnosis of retinopathy, and consistent therapy. With timely therapy, progression and thus loss of vision can be prevented. Since diabetic retinopathy can progress for a long time without causing any major discomfort, the diabetic should generally see an ophthalmologist once a year. If there are signs of diabetic eye disease, the examinations should be repeated at shorter intervals (usually every 3–6 months).

In the event of acute deterioration in vision, new problems with reading, color perception or phenomena such as soot rain , an immediate ophthalmological examination should be carried out.

In the case of diabetics who are planning a pregnancy , the blood sugar should be optimized before pregnancy and intensively monitored during pregnancy (see also gestational diabetes ). Before the beginning of the pregnancy, otherwise as soon as possible after admission, an ophthalmological examination should be carried out, as the hormonal changes can lead to a worsening of the eye findings. In 10–26% of patients who had little or no retinopathy prior to pregnancy, the findings worsen.

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

literature

Web links

Individual evidence

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  2. ↑ a b c d Jack Kanski: Clinical Ophtalmology. 6th edition. Munich 2008, pp. 581-599.
  3. ↑ Aris N. Kollias, Michael W. Ulbig: Diabetic Retinopathy . In: Deutsches Ärzteblatt . tape 107 , no. 5 , 2010, p. 75–84 , doi : 10.3238 / arztebl.2010.0075 ( aerzteblatt.de ).
  4. ↑ a b c d J. Nasemann: Retina (Retina) in Matthias Sachsenweger (Ed.): Dual series - ophthalmology. Stuttgart, 2003, pp. 259-262.
  5. ↑ MM Nentwich, MW Ulbig: Diabetic Retinopathy. In: The Diabetologist. Edition 6, 2010, p. 491 ff.
  6. ↑ Richard Daikeler, idols Use, Sylke Waibel: diabetes. Evidence-based diagnosis and therapy. 10th edition. Kitteltaschenbuch, Sinsheim 2015, ISBN 978-3-00-050903-2 , p. 170 f.
  7. ↑ Mandecka A et al .: Abnormal retinal autoregulation is detected by provoked stimulation with flicker light in well-controlled patients with type 1 diabetes without retinopathy. Diabetes Res Clin Pract. 2009 Oct; 86 (1): 51-5.
  8. ↑ Bettermann K, Slocomb J, Quillen D et al .: Impaired Retinal Vasoreactivity: An Early Marker of Stroke Risk in Diabetes. J Neuroimaging 2017; 27: 78-84.
  9. ↑ Gerhard Lang u. a .: Ophthalmology. 4th edition. Stuttgart, 2008, pp. 311-317.
  10. ↑ MM Nentwich, MW Ulbig: Diabetic Retinopathy. In: The Diabetologist. Edition 6, 2010, p. 491 ff., Springer
  11. ↑ D. Kook, A. Wolf, T. Kreutzer et al. a .: Long-term effect of intravitreal bevacizumab (avastin) in patients with chronic diffuse diabetic macular edema . In: Retina. 2008 Oct; 28 (8), pp. 1053-1060. PMID 18779710
  12. ↑ JF Arevalo, RA Garcia-Amaris: Intravitreal bevacizumab for diabetic retinopathy. In: Curr Diabetes Rev. 2009 Feb; 5 (1), pp. 39-46. PMID 19199897
  13. ↑ GP Giuliari, DA Guel, VH Gonzalez: pegaptanib sodium for the treatment of proliferative diabetic retinopathy and diabetic macular edema. In: Curr Diabetes Rev. 2009 Feb; 5 (1), pp. 33-38. PMID 19199896
  14. ↑ Effect of fenofibrate on the need for laser treatment for diabetic retinopathy (FIELD study): a randomized controlled trial. In: The Lancet. 2007; 370, no. 9600, pp. 1687-1697. accessed March 2, 2014.
  15. ↑ Nentwich et al. a .: Diabetes and the eye. In: The Diabetologist. Springer 2014, accessed March 2, 2014.