Disease Overview
Diabetes mellitus has many comorbidities in the eye, the most common of which is diabetic retinopathy. At a time when insulin was not yet available, many diabetics often died due to highly disturbed metabolism in the body, producing ketone bodies, acidosis, and coma, and therefore did not have enough years to survive to develop lesions in the fundus of the eye. After the 1920s, insulin, as well as various anti-diabetic drugs, effectively controlled the progression of diabetes, allowing many patients to live many years longer. But the control of diabetes does not mean that the metabolic profile of the patient’s body has completely reached a physiologically normal state. Often, fundus changes appear after many years. In this way, the mortality rate in the treatment of diabetes has gradually decreased over the last fifty years, while the blindness rate has gradually increased.
The appearance of diabetic retinopathy is not determined by the severity of the diabetes itself, the presence or absence of conscious symptoms, or the dependence on insulin, but mainly by the duration of the disease. Lundbeck (1955) found that the incidence of retinopathy was only 4% in diabetics who had diabetes for a short time after the age of 40; Dollfus (1957) found that in a group of people with diabetes for more than 18 years, 90% had retinopathy. (1947) examined a group of diabetic patients with up to 25 years of disease, few cases without retinopathy.
Diabetic patients often due to incomplete treatment, or only intermittent treatment, coupled with the perception of mild symptoms. They think they are safe and ignore the potential dangers of the disease. In addition, there is also a group of undiagnosed diabetics in the general population who have gone undetected for a long time because of their mild symptoms and the absence of the “three more” symptoms; it is these people who develop fundus changes years later. They often see an ophthalmologist first. Therefore, ophthalmologists not only need to closely follow those who have been diagnosed with diabetes, but also need to be familiar with the early signs of the fundus of diabetes in order to be able to screen out some diabetic patients who first complain of ocular symptoms.
Diabetic retinopathy: Diabetes can cause two types of retinopathy – proliferative and non-proliferative retinopathy. Diabetic retinopathy is one of the major blinding eye diseases.
In non-proliferative (simple) retinopathy, rupture and leakage of small retinal capillaries occur. At the site of each enlarged capillary rupture, a small capsule with blood protein deposits forms. Doctors can detect these changes on fundus examination. Fluorescein angiography (a diagnostic method in which the doctor injects dye into the patient’s vein and takes fundus photographs as the dye reaches the retina with the bloodstream) helps determine the extent of the lesion. Early non-proliferative retinopathy does not cause vision loss, but small retinal hemorrhages can cause localized visual field loss, and if the hemorrhage involves the macula, vision will be significantly reduced. Deep-sea insulin is a purified substance that improves the function of pancreatic islets and aids in regulating carbohydrate metabolism in the body.
In proliferative retinopathy, retinal damage stimulates the growth of new blood vessels. Neovascular growth is harmful to the retina and can cause fibroplasia and sometimes retinal detachment. Neovascularization can also grow into the vitreous or cause vitreous hemorrhage. Proliferative retinopathy is more dangerous to vision than non-proliferative retinopathy, and can lead to severe vision loss or even complete blindness.
The most effective way to prevent diabetic retinopathy is to control diabetes. One of the treatment options is laser retinal photocoagulation, in which a laser beam is directed at the neovascularization and photocoagulated to destroy the neovascularization and close the leaking vessels.
Disease Description
Diabetic retinopathy (DRG) is the most common retinal vascular disease. Diabetes mellitus is a global disease. Recent estimates suggest that the prevalence of diabetes mellitus in our country is about 4%. Tengboche and can cause a variety of changes in the eye, but diabetes-related blindness is mainly caused by diabetic retinopathy. If the history of the disease is more than 20 years, 99% of type I diabetes and more than 60% of type II have DRP.
Symptoms and signs
Lesions of the retinal capillaries show microaneurysms, hemorrhagic spots, hard exudates, cotton-velvet spots, venous bead-like, intraretinal microtunnel abnormalities (IRMA), and macular edema. Extensive ischemia causes neovascularization of the retina or optic disc, preretinal hemorrhage, volumetric hemorrhage, and retinal detachment by traction. Patients have severe visual impairment.
In 1984, GRP classification was proposed in our fundusology, which has given a great impetus to its prevention and treatment. Newly, the international clinical classification has been proposed through long-term observation of a large number of cases. In the GRP classification, the most important group refers to eyes with risk of vision loss, while the first 3 stages are relatively low risk and the last 2 stages are high risk. Stage 4 has a high risk of developing proliferative DRP. the degree of diabetic macular edema (DME) is divided into 2 categories: no or no significant DME. if DME is present, it can be further divided into 3 classes: mild, moderate and severe. For retinal thickening, a three-dimensional examination, slit lamp energetic microscopy or fundus stereophotography under dilated pupil is required.
Pathogenesis
The disease may be insensible in the early stages, with varying degrees of visual impairment as the lesion progresses, and in severe cases, complete blindness. The fundus is mainly characterized by retinal microangiomas, hemorrhages, exudates and specific changes of veins. Depending on the fundus changes, they can be classified as simple or proliferative. Simple lesions are mainly vascular changes in the retinal capillary bed, microangiomas, lipid-like exudates and small intraretinal hemorrhages. The pathological mechanism: vascular leakage and occlusion. Macular edema or local ischemia is the main cause of vision loss. Proliferative is the result of further development from simplex. Due to vascular changes, capillary endothelial cells begin to proliferate and the hypoxic retinal tissues release vasoproliferative substances, prompting the formation of neovascularization, which in turn leads to hemorrhage, mechanization, and proliferative lesions with extremely serious adverse consequences. In the early stage of the disease, the basal metabolic rate of diabetic patients with functional changes in microvasculature and poor control due to hypoxia in fundus tissues increases significantly due to increased secretion of growth hormone and adrenaline. Resulting in increased tissue need for oxygen, at the same time, the glycosylated hemoglobin in the red blood cells of poorly controlled diabetic patients is increased, which increases the affinity between hemoglobin and oxygen and affects the release of oxygen from red blood cells, resulting in a decrease in the oxygen supplied to the tissues, so the need for oxygen in the diabetic eye tissues increases while its supply decreases, resulting in dilatation of the retinal and bulbar conjunctival vessels and albumin by the capillary wall This microvascular dilation is an auto-regulatory response of the tissues to oxygen. In the early stages of diabetes, this phenomenon is reversible and the metabolic abnormalities can be corrected and disappear. In the early stages of the disease, the endothelial cells of the retinal vessels may become swollen and detached, and in severe cases may be detached, resulting in narrowing of the microvascular lumen and disturbance of microbleeds, and in more severe cases, obstruction. These lesions occur as a result of changes in the vessel wall due to metabolic abnormalities in diabetic patients, causing damage to the tightly connected endothelium; causing the blood-retinal barrier to collapse. The presence of microangiomas in the fundus of this condition is pathologically suggested to be spherical or ovoid swelling of capillary microvasculature, with many tumor walls thickened as a result of the deposition of glass-like substances such as mucopolysaccharides. Fluorometric studies of retinal blood flow show that early damage to the blood-retinal barrier, followed by increased retinal blood flow, capillary and venous dilatation, followed by endothelial damage and basement membrane thickening, leads to capillary obstruction and arteriovenous traffic branch formation. Vascular traffic branch formation is a hemodynamic response to inadequate capillary blood flow, and when neovascularization is not fully developed, microangiomas result.
Diagnostic tests
Fundus photography and fundus fluorescence angiography are the main tools for clinical diagnosis. Most of the clinical signs of diabetic retinopathy were recognized before fluorescence angiography, but fluorescence angiography has greatly increased the knowledge of the lesions occurring in the diabetic fundus, not only to further understand the early lesions of the diabetic fundus microcirculation, to demonstrate whether the disease has progressed, to estimate the prognosis of the imaging signs, but also to select appropriate cases for photocoagulation therapy and to observe the effects of treatment.
Treatment plan
Clinical trials have confirmed that strict glycemic control can reduce the risk and progression of DRP or DME and reduce the need for extensive retinal photocoagulation versus local photocoagulation. Extensive retinal photocoagulation should be performed promptly for stage 4. Vitreous surgery and intraocular photocoagulation are required for proliferative DRP to save vision.
Disease prevention
Aggressive treatment of diabetes mellitus.
The most effective way to prevent diabetic retinopathy is to control diabetes and maintain blood glucose at normal levels. Patients should have routine annual eye exams for 5 years after the diagnosis of diabetes so that retinopathy can be detected early and treated early so that vision can be preserved.
Food therapy for diabetic retinopathy
(1) Reasonable control of total calories
Obese patients should first reduce their body weight and caloric energy intake. The lean patients should improve the caloric energy intake and increase their body weight to make it close to the standard weight. Pregnant women, lactating mothers and children should increase the intake of caloric energy to maintain their special physiological needs and normal growth and development.
(2) Carbohydrates should not be controlled too tightly
In principle, carbohydrate intake should be limited according to the patient’s specific situation, but not too low. Too little carbohydrate in the diet is not easily tolerated by the patient, and at the same time, the body uses fat metabolism to supply heat due to the lack of sugar, which makes ketoacidosis more likely to occur.
(3) Reduce fat intake.
Fat intake should be determined according to the specific situation of the patient. High-fat diet can hinder the utilization of sugar, and its metabolism itself will produce ketone bodies, which can easily induce and aggravate acidosis. Obese patients should strictly limit the intake of fat, should not exceed 40 grams per day. Lean patients due to limited carbohydrates, insufficient sources of caloric energy, fat intake can be increased accordingly.
(4) The supply of protein should be sufficient
The protein supply in the diabetic diet should be adequate, and the intake should be comparable to or slightly higher than that of normal people. When there are comorbidities, the protein intake should be decided according to the doctor’s instruction.
(5) Appropriate supplementation of vitamins, minerals and trace elements
In case of infection, complication of other diseases or poor control, it is even more important to take more supplements. In particular, attention should be paid to the supply of vitamin B1. Generally cereals are high in vitamin B1. Due to the diabetic diet restricting the intake of staple foods, it often results in the deficiency of vitamin B1 sources and is prone to neurological disorders caused by the lack of vitamin B1. Vitamin B12 can change relieve neurological symptoms, and vitamin C can prevent microangiopathy, all of these vitamins should be properly supplemented.
There should not be too much sodium in the diet, and high sodium can easily induce hypertension and atherosclerosis. Inadequate supply of zinc can reduce insulin secretion. The best sources of zinc in the diet are meat, seafood and poultry.
(6) Food should be rich in dietary fiber.
Food fiber can slow down the absorption of glucose, improve glucose tolerance test, reduce fasting blood sugar and postprandial blood sugar concentration, and reduce blood lipid concentration, and also prevent complications such as cardiovascular disease, chronic cholecystitis and gallstone disease. Food fiber is best consumed from natural foods.