Diabetic retinopathy
By diabetic retinopathy (lat. Retinopathia diabetica) we mean a set of changes in the blood vessels and adjacent structures of the eye background, primarily the retina, which are caused by a long duration of diabetes mellitus (lat. diabetes mellitus).
Origin and division of the disease:
It is not possible to say with precision when changes in the blood vessels will occur. Research shows that this is very rare in the first five years of diabetes, and after 10 years about 20-30% of people suffer from diabetic retinopathy. This percentage increases with the duration of diabetes. Factors that influence its occurrence are the duration of diabetes, the type of diabetes (we distinguish between insulin-dependent type of diabetes or type 1 and insulin-independent type of diabetes or type 2, and changes occur earlier in insulin-dependent type), successful treatment, i.e. maintenance of blood sugar in within the limits of normal and some other factors such as pregnancy.
The initial changes of diabetic retinopathy occur in the capillaries (tiny blood vessels). Namely, some types of cells thicken the walls of capillaries and thus slow down the flow of blood through the vessel and weaken the supply of oxygen to the retina. Then, in that area of the retina, substances that stimulate the formation of new blood vessels (neovascularization) begin to be released with the intention of enabling its oxygen supply again. But even those newly created blood vessels are of poorer quality, so their blockages occur again and thus they do not deliver a sufficient amount of oxygen to the tissue. Thus, the vicious circle continues on a larger and larger scale. On the other hand, the capillary wall is also damaged and more permeable. It is no longer able to retain blood and its components inside it, so exudates (appearance of blood plasma outside the blood vessel), edema (swelling) and bleeding occur. This further slows the blood flow and worsens the disease.
Retinopathy can be divided into three stages.
Nonproliferative diabetic retinopathy (lat. Retinopathia diabetica nonproliferative)
This is the initial stage of retinopathy characterized by initial changes in blood vessels and small hemorrhages and exudates, while the formation of new blood vessels is absent to a greater extent.
Preproliferative diabetic retinopathy (lat. Retinopathia diabetica preproliferativa)
It is characterized by somewhat more extensive bleeding and exudates throughout the fundus, but there are still no major neovascularizations (newly formed blood vessels).
Proliferative diabetic retinopathy (lat. Retinopathia diabetica proliferative)
This is the most severe stage of the disease in which we find extensive bleeding and edema that often affect the macula itself and the formation of many new blood vessels and membranes that cover large areas of the retina and sometimes enter the vitreous body.
Symptoms:
The patient himself is not able to determine when the retinopathy occurred. Namely, peripheral areas that are not crucial for vision are often affected in the beginning. Only when the disease progresses and affects the area of the macula does vision weaken, which is a bad sign. In patients with diabetes who are treated normally and regularly carry out controls, it is customary to regularly perform eye background examinations in order to establish the occurrence of retinopathy at the earliest stage. Although retinopathy itself cannot be directly treated at that stage, its presence or absence is an indirect sign of the success of diabetes treatment.
Establishing a diagnosis:
It is essential to have a detailed eye examination by a specialist. Such examination includes determination of visual acuity, examination of all parts of the eye and measurement of eye pressure. Advanced changes in diabetic retinopathy are also visible on the blood vessels of the conjunctiva and iris, and in particularly severe cases, cataracts and changes in the vitreous body sometimes occur. An examination of the fundus of the eye with a device called an ophthalmoscope and various types of prisms are decisive for establishing a diagnosis, because with them it is possible to see the blood vessels directly.
As an auxiliary search, it is good to do an examination of the visual field, which can show the extent and degree of retinal damage.
Fluorescein angiography is a test in which a contrast medium is injected into a blood vessel on the arm, which further reaches the blood vessels of the retina and retina via the bloodstream. The arrival and passage of contrast through these blood vessels is monitored and photographed with a special camera. On the basis of the images obtained, it can be assessed whether they are sufficiently permeable to blood flow and whether fluid is leaking out through their walls. These data are particularly important for laser treatment.
Treatment:
Diabetic retinopathy should be prevented so that it does not occur at all. This is achieved by treating diabetes, i.e. by maintaining the blood sugar concentration within normal limits without large daily oscillations, by means of medicines and physical exercises that must not be forgotten. When retinopathy occurs, it is a good idea to have eye fundus examinations at least once a year, which depends on the success of regulating diabetes and previous findings of the fundus fundus.
In the case of initial retinopathy when the macula area is not affected, no special therapy is applied that would refer exclusively to the eyes. With the appearance of swelling and bleeding in the macular area and beyond, laser treatment with argon laser, so-called argon laser photocoagulation, is used. In this method of treatment, a laser beam is directed at the affected areas to reduce swelling (edema) and bleeding and prevent the formation of new blood vessels. Laser treatments are carried out on several occasions, and they are supplemented as the disease develops. Although the laser beam actually leaves a mark or destroys the retina where it hits, this method is very good and useful in treatment because without it the development of diabetic retinopathy would be much faster and the consequences more severe.
When, due to retinopathy, membranes begin to form that threaten complete vision loss, newly formed blood vessels, large hemorrhages in the vitreous, and sometimes glaucoma, the only possible treatment becomes vitrectomy. With this operation, the entire vitreous and, if there is blood, is removed, and the membranes are removed. During it, it is also possible to perform laser treatment. The operation is extremely complex and demanding, and although it is performed in patients with the most endangered and damaged eyes, it gives relatively good results. Sight recovers to a degree determined by the severity of the retinal disease and the overall condition of the eye.
Hypertensive retinopathy
Origin and division of the disease:
Arterial hypertension (lat. Hypertensio arterialis) or high blood pressure is a systemic disease that affects all the blood vessels of the body. Since only the blood vessels of the retina are directly visible in our body, it is common for the disease to be controlled and assessed precisely on the basis of the findings of these vessels.
There are three basic indicators that show the condition of a blood vessel: vasoconstriction, arteriosclerosis and leakage of fluid from the vessel to the outside.
Vasoconstriction is the name for squeezing and narrowing of a blood vessel. It represents the normal reaction of healthy blood vessels to elevated pressure. However, in the elderly population, this phenomenon is not particularly pronounced due to arteriosclerosis.
Arteriosclerosis is a complex of biochemical and structural applications of the blood vessel. They occur as a result of age, smoking, increased fat in the blood and many other factors. The result is a thickening of the wall of the blood vessel, which becomes rigid, and its lumen narrows until a possible complete blockage and cessation of blood flow.
Leakage of fluid from the vessel to the outside is a consequence of disturbances in the structure and function of its wall due to the previously mentioned factors. Blood plasma (the liquid part of blood without blood cells) or whole blood comes out of it and forms edemas and bleedings of various intensities.
Based on this, hypertensive retinopathy is divided into four stages:
Hypertensive changes of the first degree (lat. Fundus hypertonicus gradus I) include a slight narrowing of smaller arteries and dilation of veins.
Hypertensive changes of the second degree (lat. Fundus hypertonicus gradus II) are characterized by stronger narrowing of all arteries and dilation of veins and changes in the places where they cross (Gunn-Salus phenomenon).
Hypertensive changes of the third degree (lat. Fundus hypertonicus gradus III) include the appearance of bleeding and edema on the back of the eye.
Hypertensive changes of the fourth degree (lat. Fundus hypertonicus gradus IV) in addition to all the earlier signs, which are now strong, also include swelling of the optic nerve.
Symptoms:
Most of the symptoms actually originate from the blood pressure itself. The main symptom on the part of the eyes is a decrease in visual acuity that occurs when the area of the macula is affected. Another symptom is the loss of vision, i.e. the appearance of certain areas in the field of vision where vision is partially impaired, but this change is difficult to notice, especially if it is not very pronounced and large.
Establishing a diagnosis:
The level of blood pressure is determined by standard measurements, so the condition of the blood vessels can be roughly evaluated based on this indicator. We make a definitive assessment after examining the fundus of the eye with an ophthalmoscope. Retinal function and possible outages are evaluated using the visual field.
Treatment:
Systemic treatment is carried out, i.e. regulation of blood pressure with antihypertensive drugs, thus improving the condition of retinal blood vessels. Edemas and bleeding that may occur will mostly resolve on their own, but the changes in the vessel wall for the better are very discreet.
Retinal ablation
Retinal ablation (lat. Ablatio retinae) is the name for detaching a certain layer of the retina from its substrate.
Origin and division of the disease:
Ablation occurs only in those eyes where there are factors that promote its formation. These factors are very numerous and diverse. Here we primarily include various degenerative changes in the retina that weaken it and cause it to tear, among which are changes due to high myopia (above -6 diopters). Diabetic retinopathy in its proliferative form creates pathological connections between the retina and other tissues that stretch the retina and can even tear it. An eye injury or impact mechanically changes the relationships within the eye and thus causes ablation. In all these cases, fluid accumulates under the raised retina, which does not allow it to return to its place and swells it even more.
An important fact in determining the type of ablation, as well as for its further development, is the presence of a retinal tear. Namely, if we understand ablation as a raised balloon, then we can imagine that it is tense and whole or it can have a crack of various shapes. Precisely according to the presence of this crack, ablation is divided into so-called rhegmatogenous (with a crack) and non-rhegmatogenous (without a crack).
Symptoms:
It is not possible to predict the occurrence of ablation, but there are signs that speak in favor of its occurrence, as well as those that occur after it has developed.
Flashes in front of the eyes occur most often in the dark, or rather they are more noticeable in the dark, but they can also occur in the light. The result is stimulation or stretching of the retina. Flashes are a rather non-specific sign because they occur both before and after ablation, and are common in some other diseases, for example circulatory disorders. If you have such disturbances, contact your doctor and he will assess their importance.
Flying clouds (opacity) in front of the eyes can be small or large, and appear quite suddenly. They are the result of a change in the density of the vitreous, i.e. its threads (fibrils) after retinal ablation. Very small and dense opacities are most often the result of bleeding into the vitreous, caused by the rupture of a blood vessel in the retina. As these changes occur in a large number of diseases that affect the vitreous body, a complete examination must be performed in order to discover their cause.
The basic sign of ablation is the outages in the field of vision, which can be of various sizes depending on the size of the ablation. In cases of larger ablations, there are dramatic symptoms of vision loss in certain parts of the visual field, which patients describe as the appearance of a veil before their eyes. In general, the detached retina loses its normal nutrition and dies. As the retina is the “photographic film” of the eye, its death also results in the loss of vision in that area.
Establishing a diagnosis:
First of all, it is necessary to do a general ophthalmological examination, which includes an examination of visual acuity, the front and back segment of the eye and eye pressure. Central visual acuity does not have to be weakened if the ablation does not affect the central part of the retina and there are no major vitreous opacities. Examination of the fundus using a method called direct and indirect ophthalmoscopy and special prisms proves the diagnosis in the vast majority of cases. When there is clouding of the lens due to cataract or the bleeding in the vitreous is so dense that the fundus cannot be seen with these methods, an ultrasound examination of the eye is performed, which can assess the position, size and type of ablation.
Treatment:
When the existence of ablation is determined, it is necessary to proceed with the operative procedure as soon as possible. It aims to bring the retina back to its place before it dies. There are two basic methods for ablation surgery that have many sub-variants. With the classic method, the fluid that has accumulated under the retina is emptied, and a seal or cerclage is attached to the sclera from the outside, which ensures permanent contact between all layers of the retina and the retina, thus reducing the possibility of reoccurrence of ablation. The second method is more complex, and is used in strictly defined cases. With it, the vitreous is removed with an instrument, the threads that pull the retina and which caused the ablation are cut, and the retina is returned to its place. During the surgery itself, it is possible to perform a laser treatment to fix the retina. Instead of vitreous, silicone oil or special gases are inserted, which additionally cling to the retina. After a certain time, the oil is removed.
Such interventions are absolutely necessary in the treatment of ablation, but they are not omnipotent. After large and long-term ablations, the visual acuity is somewhat weaker than before its appearance, which depends on the localization of the ablation and the vitality of the detached retina. After such operations, cataracts and increased eye pressure sometimes occur as a complication. Despite the quality of the treatment, ablation reoccurs in some cases.
Retinal artery occlusion
Origin of the disease:
The retina is supplied with blood by a blood vessel called the central retinal artery (lat. Arteria centralis retinae), which branches into several branches that go to all parts of the retina, distributing blood.
Clogging of blood vessels, occlusion or embolism, can be caused by cholesterol particles, calcium compounds that are on the walls of sclerotic blood vessels, blood clots, air bubbles that can enter the vessel after injury, and many other substances, all of which are collectively called emboli. They travel through the body through larger vessels, so when they reach a smaller vessel through which they cannot pass, a blockage occurs. So, blockage of a blood vessel in the retina mostly occurs by accident, because the embolus that blocked it could have strayed into any other small vessel in another organ.
Depending on the location of the blockage, we distinguish the blockage of the central retinal artery (lat. Oclusio arteriae centralis retinae) and its branches (lat. Oclusio rami arteriae centralis retinae). The location of the blockage significantly affects its symptoms and consequences.
Symptoms:
The severity of the symptoms directly depends on the size of the affected blood vessel and the place where the blockage occurred. Due to reduced or completely absent blood flow through a certain area of the retina (ischemia), its function is lost. Vision in that area is significantly weakened or disappeared. Patients notice outbursts in the field of vision in the area corresponding to the area of the retina affected by ischemia. Of course, therefore, central outbursts are immediately noticeable, while peripheral ones, especially if they are smaller, are less noticeable and thus relatively less important. When the central retinal artery is blocked, temporary blindness occurs in that eye.
Establishing a diagnosis:
The diagnosis is made on the basis of a clinical examination. Changes on the background of the eye are clearly visible, and depending on their localization, vision is also weakened. An examination of the visual field objectively determines the size of the defect as well as the degree to which the retina has been damaged.
Treatment:
As the retina is very sensitive to changes in the concentration of oxygen in the blood and dies easily, it is necessary within a very short time from the occurrence of the occlusion, approximately 6 to a maximum of 48 hours, to apply methods that try to re-establish blood flow to the retina, such as lowering the eye pressure, massage eyeballs, placing the patient in the supine position and some others. Unfortunately, all of them are unknown and inaccessible to laymen, especially because it is difficult to assert with certainty that an artery blockage has occurred before a real specialist examination. Therefore, when the above symptoms appear, the only real solution is to immediately seek the help of an ophthalmologist. If this help is provided too late, there is a high probability that permanent damage to the retina will occur. However, it should be said that this condition is extremely serious and that even the most urgent and professional help cannot guarantee success.
Retinal vein occlusion
Origin and division of the disease:
Along with diabetic retinopathy, vein occlusion is the most common retinal blood vessel disease. Factors that influence its occurrence are old age, high blood pressure, diseases of the blood and blood vessel walls, and various others.
Similar to the case of blocked arteries, here the severity of the disease and its symptoms depend on the size of the affected blood vessel. In the case of occlusion of a peripheral, smaller vein (lat. Oclusio rami venae centralis retinae) in the area from which it collects blood, swelling (edema) and major or minor bleeding occurs, and vision will be impaired in that segment. If the function of the surrounding veins is preserved and orderly, the symptoms will be less pronounced and will disappear more quickly. In the case of occlusion of the central retinal vein (lat. Oclusio venae centralis retinae), i.e. the vein in which the blood coming from all its branches, i.e. all retinal veins, is united, the consequences will be reflected on the entire retina. In doing so, we distinguish between partial occlusion of the central retinal vein in which circulation is partially preserved (non-ischemic type of occlusion) and complete occlusion in which circulation has completely stopped (ischemic type). In this disease, hemorrhages and edema occur all over the retina, so the area of damage in the field of vision is larger and the visual acuity is weaker.
If the disease is not recognized and treated in time, new blood vessels will begin to form, the role of which is to feed the damaged area of the retina. Such blood vessels swell uncontrollably and are not fully functional, causing many complications such as bleeding and increased eye pressure (so-called neovascular glaucoma). The process of forming new blood vessels is called neovascularization.
Symptoms:
The only symptoms that the patient notices are the loss of the field of vision corresponding to the area of the retina where the affected vein is located and the weakening of visual acuity. The loss of the visual field can be complete, so that the patient cannot see in that part at all, or, which is more often partial, that is, the vision is preserved but weakened. If the area of the macula is not affected, the central visual acuity is the same as before the onset of the disease.
Establishing a diagnosis:
Based on an examination in a specialist outpatient clinic, it is possible to confirm or rule out the existence of vein occlusion with certainty. In order to accurately determine the state of the blood vessels, it is sometimes necessary to perform a test called fluorescein angiography, which has already been described earlier.
Treatment:
The basis of the treatment is the treatment of the affected, ischemic areas with laser beams with the aim of preventing the formation of new blood vessels. This simultaneously prevents all complications caused by neovascularization, which, once they occur, are almost impossible to successfully treat.
At the very beginning of the disease, treatment with retrobulbar corticosteroid injections is applied, which accelerates the withdrawal of the resulting edema.
Senile macular degeneration
Origin and division of the disease:
Senile degeneration of the macula (lat. Degeneratio maculae senilis) is a disease that is primarily caused by weakened circulation, resulting in changes in the structure and function of the macula
(the macula is a part of the retina also known as the yellow spot and represents the place of the clearest vision). As its name suggests, it affects the elderly population. We know two basic forms of this disease:
Dry senile macular degeneration (lat. Degeneratio maculae senilis forma sicca) is the most common form and represents 90% of all senile macular degenerations. The first visible change in the macula is the formation of drusen, small yellowish formations that are predominantly lipid content. The disease develops slowly, develops over months and years, and only moderately affects the weakening of vision.
The wet form of senile degeneration of the macula (lat. Degeneratio maculae senilis forma exudativa) is a much rarer but also more dangerous form. A significant loss of vision occurs within a few days or weeks. In the course of the disease, the ablation of some layers of the retina in the area of the macula and the formation of new blood vessels may occur. The latter leads to bleeding in the retina or in the vitreous body and can result in the formation of a scar.
Symptoms:
In both types of the disease, there is a noticeable drop in visual acuity in the central part of the visual field. Patients describe it as not seeing what they are directly looking at, but seeing the surroundings of that object. This is logical because macular degeneration does not affect the remaining parts of the retina in any way, so vision is preserved in them. Sight is lost gradually, with the dry form slowly, and with the wet form suddenly.
Establishing a diagnosis:
In most cases, the disease is recognized at the first examination by an ophthalmologist without special tests. However, in order to get a better insight into the severity and course of the disease, it is necessary to perform a visual field examination and fluorescein angiography. The latter will give us more information about the state of blood vessels and thus be a decisive test for determining therapy.
Treatment:
A successful treatment for the dry form of macular degeneration has not yet been discovered. Combinations of vitamins and minerals are used as a therapy that contributes to a more positive development of the disease, which participate in the nutrition of the macular area and thus help preserve its function.
In the treatment of wet form, laser treatment is indispensable. Today, there are several types of lasers that are used for this purpose, and more and more sophisticated methods are being discovered that aim to destroy the newly formed blood vessels while preserving other structures of the macula. However, it must be clear to every patient who accesses this treatment that it is not possible to significantly improve visual acuity with it, but that the great success lies in stopping the progression of the disease.
Literature:
M.Sc. sc. Pavan Dr. Joško, “Eye Diseases”, Zagreb 2003.
