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Diabetic retinopathy

  1. Gastroepato
  2. Diabetology
  3. Diabetic retinopathy
  4. Diabetic nephropathy
  5. Diabetic neuropathy
  6. Type 1 or type 2 diabetes
  7. Diabetes. What are we talking about?
  8. The cardiometabolic risk in type 1 diabetes mellitus
  9. The checks to be performed
  10. Pregnancy and risk of diabetes during pregnancy

notes by dr Claudio Italiano

Why implement a good glyco-metabolic control

The prospective controlled studies have shown with certainty that chronic hyperglycemia is the necessary condition for the development of diabetic microangiopathy, even if in determining it, genetic factors contribute. The hyperglycemia toxicity is mainly due to the glycation processes and subsequent oxidation of various protein molecules (basal membranes, circulating proteins, etc.) which undergo irreversible denaturation processes.
The glucose itself gives rise to oxidative phenomena with the formation of free radicals. Activation of the polyol pathway is also oxidative stress. An important mechanism of glucotoxicity has been recognized in the activation of protein-kinase C.
So what if I'm diabetic?
Certainly I must implement a good metabolic control, which is the basis for the prevention of microangiopathy.
 The most important clinical forms of diabetic microangiopathy are:
Retinopathy
Nephropathy
Neuropathy
Tissue damage, however, affects all tissues (skin and myocardium in particular)

Diabetic retinopathy

Diabetic retinopathy is the most prevalent and potentially serious complication of the diabetic patient, especially if suffering from type 1 diabetes mellitus, as according to studies by Wisconsin, in 71% of cases it is present in such patients; vice versa in the subject with diabetes mellitus type 2 is present in 39% of cases, in Italy, fortunately, unlike the US, the percentage is between 46 and 58% for type 1 diabetes and for 14-35 % in type 2 diabetes.

Retinopathy, especially in adults, can lead to maculopathy with blindness, while the most frequent form in the young is proliferative retinopathy.

Classification of retinopathy

Retinopathy is the consequence of three fundamental alterations of the retinal capillaries:
- Capillary exclusions
- Wall waterproofing
-Proliferation of newly formed vessels

We distinguish different degrees of retinal damage that are at the base of the classification:
- basic retinopathy or background
- preproliferant
- proliferative
The background form is characterized by microaneurysms, haemorrhages and hard exudates and cottony; hard exudates are due to extravasation of plasma proteins and especially lipoproteins.
Fortunately, they are not stable lesions, in the sense that microaneurysms can regress. Hemorrhages have a point-like or flame-like appearance. The cottony exudates are an expression of the accumulation of an axoplasmic material at the border of a microvascular infarct.
When the lesions compromise the retina, then we talk about the maculopathy that underlies the serious reductions in the visus. Preproliferative retinopathy is characterized by ischemic areas caused by multiple capillary occlusions.
Retinal hypoxia underlies local release of endothelial growth factors. The result is a revascularization process called "proliferating retinopathy". The haemorrhages are followed by the development of fibrous branches that can also cause detachment of the retina with permanent loss of the visus.
Still other complications are the rubeosis of the iris when the proliferation of the vessels reaches the anterior segment of the eye.

Treatment of retinopathy

Makes use of :
- good diabetes therapy with particular attention to the control of glycated or HBA1C values ​​which must tend, according to the modern guidelines to be <6.5%;
- control of arterial hypertension
- laser photoglulation that reduces the incidence of blindness from proliferating retinopathy by 50%
- in cases of repeated vitreous hemorrhage there is cloudiness of the vitreous and retinal detachment and it is necessary to resort to vitrectomy.
 

Hence the need for a screening program on the entire population of diabetics; patients, that is, must be controlled starting from the diagnosis of diabetes with a direct ophthalmoscopic examination and, if there are evolutionary lesions, they must undergo retinal fluorangiography, an examination obtained by coloring the retinal vessels with an injected intravenous dye and studying the end retinal circulation under the microscope. Controls are scheduled at 6 months in case of serious complications and at 12 months if there are none, as routine screening.
Finally we remember that diabetes is responsible for cataracts, glaucoma and ophthalmoplegia, ie the paralysis of the eyeball due to neuropathic suffering.

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