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Diabetic retinopathy (DR) is one of the leading causes of morbidity and vision loss worldwide, and its diagnosis is based on retinal vascular stasis found during clinical examination. This disease is divided into nonproliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR).1

PDR occurs in less than 2% of patients with type 2 diabetes within 5 years of diagnosis.

NPDR is also divided into 4 categories: mild, moderate, severe, and severe. Diabetic macular edema (DME), a complication characterized by abnormal leakage and accumulation of fluid affecting central vision, can occur at any stage.

There is a strong relationship between chronic hyperglycemia and the development of DR. The pathophysiology of microvascular damage is unclear, with a number of chemical mechanisms implicated as the cause.3

Minorities have higher rates of microvascular complications compared to Caucasian adults. The estimated prevalence of DR is 38.8% in African Americans, 31% in Hispanics, and 26.4% in non-Hispanic Whites.

DR is managed with anti-vascular endothelial growth factor (anti-VEGF), panretinal photocoagulation (PRP), and vitrectomy. These drugs aim to reduce new vessel growth (neovascularization), reduce inflammation (ie, macular edema), and eliminate vitreous hemorrhages, respectively.

The global prevalence of DR is 22.27%: 6.17% of these cases are sight-threatening and 4.07% include clinically significant macular edema (CSME).6 In South Asia, Africa, Latin America, and people of Indian descent they have a high incidence of DR, vision. -threaten DR, and CSME more than Caucasian people.7

In mild cases of DR, patients may be asymptomatic, and symptoms are only seen on fundus examination. In more severe cases, symptoms include blurred vision, central metamorphopsia, floaters, and severe vision loss.

DR is a microvascular disease caused mainly by the metabolic effect of chronic hyperglycemia, and theories abound regarding its pathophysiology. Pain depends on the type of diabetes, the time since the beginning, the level of glycemic control, and the presence of smoking and having problems such as blood pressure, chronic kidney disease and hyperlipidemia.

Type I DM is a genetic disease in which insulin is not produced. In type II DM, the pancreas cannot produce enough insulin, or the insulin does not work properly.8 The blood-retinal barrier is damaged in DR, which leads to leakage and damage to the blood vessels. nerves in the retina.

Vascular endothelial growth factor (VEGF) also plays a role in vascular permeability. The molecular mechanisms involved include the polyol pathway, advanced glycation endocytosis, protein kinase C activation, renin-angiotensin aldosterone system activation, oxidative stress, and loss of pericyte function.2,9 ,10.

Pericytes are specialized mesenchymal cells in capillaries that regulate arterial tone and blood pressure. The relationship between pericyte and endothelial cells may be disrupted by thickening of the basement membrane, hyperglycemia, advanced production of glycation products, and hypoxia leading to pericyte apoptosis and neovascularization.10

DR can occur unilaterally or bilaterally and produce any HbA1c level. Clinical findings in NPDR include microaneurysms, retinal hemorrhages, changes in venous caliber, cotton wool spots, and microvascular abnormalities. According to the Modified Airlie House Classification, DR can be proliferative and nonproliferative (Table).

Categorization

In nonproliferative retinopathy, there are mild, moderate, severe and severe stages. Mild NPDR consists only of microaneurysms. To see also : It said RBC would explore opportunities for a European custody business. Moderate includes more microaneurysms but less severe NPDR; eyes will show increased IRH, microaneurysms, hard exudates, and cotton wool spots (CWS).

Severe NPDR follows the 4-2-1 rule: IRH and microaneurysms in all 4 retinal quadrants, venous beading in 2 or more quadrants, and intraretinal microvascular abnormalities (IRMA) in 1 or more pass the quadrants. Severe NPDR is greater than or equal to 2 values ​​from severe NPDR without signs of neovascularization.

PDR is characterized by neovascularization of the iris angle (rubeosis iridis), optic disc, or in other areas and preretinal and vitreous hemorrhages.11 PDR can also include vitreous or preretinal hemorrhage. High risk factors are the presence of neovascularization in other areas (NVE), neovascularization of disc (NVD), and vitreous or preretinal hemorrhage.12

CSME occurs as a result of a breakdown of the blood-retinal barrier and can produce any of the DR conditions.13

The Early Treatment Diabetic Retinopathy Study (ETDRS) defined CSME as retinal thickening within 500 μm of the foveal center, retinal detachment within 500 μm of the foveal center with a thickness of close, and retinal thickness greater than 1 disc diameter in size within a single disc. foveal center.14

Due to the widespread use of OCT to investigate macular edema, many doctors no longer follow the strict ETDRS criteria for CSME but prefer to define DME as central and non-central.

Depending on the location of the edema and its effect on the vision, the doctor decides whether it is better to treat immediately or to watch closely.

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Differential diagnosis

Variations in PDR include high blood pressure, retinopathy, sickle cell retinopathy, central retinal vein occlusion or retinal vein occlusion, and retinal vein occlusion. This may interest you : Type-2 diabetes in children: 5 symptoms of lifestyle disorders in children.

Hypertension retinopathy is associated with high blood pressure and ocular symptoms such as retinal hemorrhages, inflammation of the blood vessels, arteriovenous nicking, and papilledema.

Sickle cell retinopathy can occur in patients affected by sickle cell disease and involves “beaches” of neovascularization. If left untreated, sea fans can lead to retinal detachment.

Retinal and retinal vein occlusions are caused by blockages similar to thrombus and emboli and may be associated with diabetes and high blood pressure.15

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Treatment and management

Diabetic macular edema

Treatment for vision-threatening DME includes anti-VEGF agents, the FDA-approved ranibizumab (Lucentis, Roche), and aflibercept (Eylea, Regeneron). Bevacizumab (Avastin, Roche) is used off-label as an alternative treatment option. Anti-VEGF is the first-line treatment for DME involving the fovea. On the same subject : Lifestyle Interventions Help Aging with Diabetes.16 Other treatment options are focal/grid laser photocoagulation and intraocular steroids.

Dexamethasone (Ozurdex, Allergan) is a vitreous compound that releases steroids slowly to reduce inflammation associated with macular edema. Its side effects include cataract development and IOP elevation.17 Depending on the visual acuity, observation is the appropriate management for non-central DME.15,16

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Proliferative diabetic retinopathy

PRP has proven to be an effective treatment for PDR that reduces the risk of severe vision loss. PRP is intended to improve retinal oxygenation by eliminating hypoxic areas of the retina. Anti-VEGF can be used in combination with PRP, or without pars plana vitrectomy (PPV). PPV is indicated in cases of dense vitreous hemorrhage, traction, and severe retinal neovascularization.18

Systemic blood sugar control

Blood sugar control is very important to reduce the risk of diabetes complications and complications such as kidney disease, retinopathy, stroke, and heart failure. It is important to discuss these risks with patients and coordinate care with their primary care providers and endocrinologists.

Recent research shows that a rapid decrease in blood sugar can lead to worsening of DR. A rapid decrease in blood glucose can be caused by blood pressure control, changes in osmotic pressure, and diabetes treatment such as insulin therapy.

The theory of osmotic pressure states that water moves from high to low pressure levels, such as small vessels in the eye, with rapid drops of HbA1c, thus worsening retinopathy.

Another recent study of retinal imaging in patients with type 2 diabetes who participated in the Diabetes Program at Harbor-UCLA Medical Center in West Carson, California, showed that a 4% reduction in HbA1c over a 13-month period resulted in worsening retinopathy. by 23% compared to the control group.

The patient discussed in the case report experienced a 3.8% reduction in HbA1c levels over a 5-month period, from July 2021 to November 2021 (Table 1). It is hypothesized that tight control of HbA1c in the short term may worsen DR. Worsening, in these cases, is defined as the appearance of cotton wool spots, soft exudates, hemes, and intraretinal microvascular abnormalities. The underlying mechanism of exacerbation includes abnormal microvascular perfusion, inadequate blood supply to arteriosclerotic vessels, and impaired autoregulation.19

The Diabetes Control and Complications Trial (DCCT) states that tight glycemic control reduces the incidence and progression of diabetes complications in type 1 diabetes. It is not certain whether this is true for type 2 diabetes, as research has shown that tight control can lead to hyperinsulinemia, increased hypoglycemia, and weight gain.20

Research conducted by the United Kingdom Prospective Diabetes Study (UKDPS) has provided guidelines for the management of type 2 diabetes. It found that lowering blood sugar reduces the risk of microvascular complications in type 2 diabetes. sugar and that controlling blood pressure helps to reduce the rates of heart problems. 21

The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial showed that intensive treatment to lower HbA1c levels for 3.5 years increased mortality and did not reduce cardiovascular events in patients those with type 2 diabetes. However, it delayed the onset of albuminuria and other eye problems. ACCORD also showed that targeted control of blood pressure below 120 mm Hg versus below 140 mm Hg did not reduce the rate of fatal and non-fatal cardiovascular events.22

Systemic comorbidities impacting DR progression

There are different types of diabetes, including retinopathy, obesity, heart disease, kidney disease, neuropathy, nephropathy, metabolic syndrome, neovascular glaucoma and cataracts.

In this case, the patient had retinopathy, macular degeneration, chronic kidney disease, hypertension and hyperlipidemia. Glucose intolerance appears to be associated with an increased risk of heart problems. Treatment of high blood sugar and blood pressure in patients with glomerular hyperfiltration can reduce the risk of kidney damage.23

Public health outreach and education

In the United States, DR disproportionately affects racial and ethnic groups and people of lower socioeconomic status. About 13% of the US population has diabetes; of that group, 14.7% are Indian/Alaska Native, 12.5% ​​are Hispanic, 11.7% are African American, 9.2% are non-Hispanic Asian, and 7.5% are non-Hispanic White. 14

African Americans and Hispanic adults also have higher rates of retinopathy and poorer glycemic control than non-Hispanic whites. Microvascular complications such as retinopathy, nephropathy, and lower limb amputations also occur more frequently in the minority population.

Studies show that poor patients are less likely to receive preventive care for diabetes such as annual examinations and examinations. 15 Recent research aims to better understand the difference in the incidence rate between different races.

Socio-economic issues, transportation problems, and lack of health literacy can be barriers to health care for minorities. And patients of low socio-economic status are less likely to receive preventive services due to language barriers, refusal of care and lack of trust in the medical system.

In another study by Walter et al, only 36% of African American patients had heard of retinopathy, and only 8% defined it correctly. Patient education is very important in reducing the incidence of diabetes and complications of diabetes. 24

Conclusion

The prevalence of diabetes continues to increase at an alarming rate worldwide. To prevent vision loss, eye care providers must recommend annual examinations to monitor changes in diabetes and initiate appropriate treatment and management.

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