One of the main complications of diabetes mellitus which is well-known by the patients and affects their daily life is ocular involvement. Diabetic retinopathy implies changes related to diabetes in the retina layer, which is responsible of vision. The changes are secondary to diabetes-emergent impairment of vessels at this layer. Diabetic Retinopathy is one major cause of poor vision; while it is the most common third cause of blindness in middle- and advanced-age people in developed countries.

Frequency is positively correlating with time elapsed since diagnosis of diabetes mellitus. Retinopathy is rare before fifth year of the diagnosis, but metabolic control is also utmost important, in addition to duration. Diabetic retinopathy may not be observed in a patient whose HbA1c level has never increased above 7 in 20th year; whereas it may develop in the patient at third year after the diagnosis, if HbA1c level is around 9. One other uncertainity is the time elapsed since diagnosis of diabetes is made. It is hard to determine how long their blood glucose level is above normal limits in a patient who does not attend follow-up visits regularly.

At initial phase of diabetic retinopathy, the permeability of veins is disturbed, and both cellular agents (bleeding) and serous part (edema) begin leaking from the vein. If these leakages occur at your macula, vision may impair; but it may be also silent, if it is far from the macula. At this phase, walls of regional vessels weaken, resulting with microaneurysms. At these segments, ruptures may easily occur and minimal bleedings from microaneurysms to the ocular gelly (vitreus). At early stage retinopathy, two major cause of visual impairment is edema of our vision center (macula) and vitreal bleeding. Visual impairment is not a sign of severeness in diabetic retinopathy and it will easily recover when edema is treated. Anti-edematous agents are injected to eye for treatment. Vitreal bleedings may also spontaneously resolve, without leaving any sequele. All these findings are observed in first phase of background retinopathy (nonproliferative stage). This stage progresses, sometimes, into next stage within a short span of time, i.e., 2-3 years, but it may take 10-15 years if metabolic follow-up is good.

Second phase of background diabetic retinopathy is pre-proliferative phase. In this phase, vessel wall weakening is progressive, and occlusion occur in vessels and vitality of retina is threatened, since blood supply corrupts non-diffusely. At this phase, metabolic alarms start in retina with insufficient blood supply, and a somewhat local hormone is secreted in order to facilitate formation of new vessels, using unhealthy vessels, in order to restore blood supply. Non-viable retinal zones can be identified with angiography and at this phase, the secretion of above mentioned local hormone can be stopped with laser therapy. Since this procedure will completely remove viability of retinal tissue, oxygen demand reduces and hormone secretion ceases. Thus, neovascularization (formation of new vessels) is prevented. Moreover, effects of secreted hormone on eye can be decreased by injecting anti-angiogenic agents. At this phase, treatment is of vital importance. Macular edema and vitreal bleedings may also occur at this phase and they may cause visual impairment.

Formation of new vessels, under effect of hormone, prepares somewhat end of retinal tissue and of eye. Those neovascularizations are characterized with weak, fraying and absence of supportive layer and they are highly tended to bleed. Moreover, there is no healthy vascular lumen, and therefore, they cannot sufficiently supply blood. Occurrence of these vessels is a sign of diabetic retinopathy progressing to second phase (proliferative phase). These vessels spread along retinal vascular structure, and the worst conditions occur when optic nerve is involved. Meanwhile, triggering impaired retinal blood / oxygen supply followed neovascularization, hormone secretion increasingly continues. New vessels can form not only at posterior pole, but also in anterior chamber. At this phase, laser therapy and various intra-ocular injections can cease or reverse the process yet.

The third and the last phase of diabetic retinopathy is the complication phase. Impaired retinal blood supply impairment and neovascularizations on head of optic nerve, retina and iris are all responsible for severe ocular damage. The new vessels bleed into vitreus and cause visual impairments which are not as innocent as they were at the first phase. In addition to bleedings and abnormal vessel structures, membranes grow parallel to retinal surface, resulting with retinal retractions. Those changes result in tractional retinal detachment, in which retina cannot completely line interior surface of globe any more. This type of detachment requires surgical intervention, but this surgery alone is associated with many risks and complications. Other postoperative severe retinal problems may hinder restoration of vision, even if retinal detachment is eliminated. Another important finding of this phase is secondary glaucomas. Vessels forming at anterior side of eye lead to formation of a membrane covering the anterior chamber angle region, which drains intraocular fluid. Intra-ocular pressure increases in an uncontrolled manner, and the clinical picture progressed to painful condition, which is characterized with loss of vision. This condition, known as neovascular glaucoma, does not respond to classic anti-glaucoma medications or surgical methods; primarily, the hormone secretion causing neovascularization should be ceased with injection, and later, intraocular pressure should be decreased with a special series of surgical techniques. Otherwise, this condition will not only result in complete loss of vision; removal of eye may be required secondary to insufferable pain and red eye.

Metabolic control is the best way to prevent development and progression of diabetic retinopathy. One should not delay to switch patient to insulin or new-generation anti-diabetic agents, and blood glucose level should be held within normal ranges. Ophthalmologic follow-up is of vital importance for diabetic patients, since management gets more complex and challenging in every next phase. Following-up the patient, endocrinologist or internist plays a significant role in this manner. As mentioned before, since time elapsed since diagnosis is usually not known, every patient diagnosed with diabetes should be consulted an ophthalmologist immediately. Later on, diabetic patients with no complaint should have routine ophthalmic examination once in a year in 10 years following diagnosis and at semi-annual intervals thereafter. Complaints like visual impairment, dark floaters and ocular pain require immediate consultation with an ophthalmologist. If diabetic retinopathy had already developed, appropriate intervals of follow-up visits shall be determined by your ophthalmologist. Except routine examinations, color fundus photography, optic coherence tomography (OCT) and angiography (FFA) are main diagnostic methods we use in follow-up. Laser photocoagulation, intraocular injections and surgery are principal therapeutic options.

There are other eye problems, excluding diabetic retinopathy. Among them are a special type of cataract, visual fluctuations secondary to abrupt changes in refractive defects and paralysis of extra-ocular muscles. Diabetic cataract develops rapidly; onset time is usually 10 years after diagnosis of Type 2 diabetes mellitus is made. However, it may occur earlier in Type 1 diabetes. It can be found during routine examinations, and the treatment is surgery. Age-related cataract occurs in diabetic patients, and progression is also faster. Fluctuations in refractive defects is manifested by increased myopia, which is almost always secondary to hyperglycemia. Therefore, if a diabetic patient specifies abrupt-onset poor vision despite glasses, one should first consider this possibility. Similarly, if glycemia is not regulated, patient should not have optic examination; otherwise, patient may not have a good sight with correction glasses prescribed. Paralysis of extra-ocular muscles is manifested by abrupt-onset diplopia; however, diplopia is a serious condition in diabetic patient and it should be examined in detail, since many pathologies should be considered, including but not limited to intra-cranial tumors, aneurysms, embolism and severe neurological diseases, in differential diagnosis. One should always remember that diabetic patients are more prone to ocular surface infections and contact lens complications.

Do you know that

  • You should immediately consult your ophthalmologist immediately after you are diagnosed with diabetes,
  • You should have fundus examinations once a year or at semi-annual intervals, if diagnosis of diabetes is made earlier or later than 10 years, respectively.
  • Among all complications of diabetes, diabetic retinopathy is the third most common cause of blindness in developed countries ,
  • The better your metabolic control is, the later ocular complications of diabetes will develop.




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