DISEASE
Diabetic retinopathy represents microvascular end-organ damage as a result of diabetes. It ranges from non-proliferative diabetic retinopathy (NPDR) and its stages to proliferative diabetic retinopathy (PDR).
As the disease progresses, associated diabetic macular edema (DME) may also become apparent. Among patients aged 25-74, diabetic retinopathy is a leading cause of vision loss worldwide.
By 2030 an estimated 191.0 million people globally will have diabetic retinopathy, and approximately 56.3 million will have vision-threatening diabetic retinopathy.
The Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) Cohort showed that after 20 years of diabetes mellitus, 99% of patients with type 1 and 60% of patients with type 2 show some degree of retinopathy.
There are several other key risk factors for the development of diabetic retinopathy beyond years since diagnosis and type of diabetes.
Additionally, elevated hemoglobin A1c (HbA1c) levels and blood pressure are associated with increased risk of diabetic retinopathy.
Type 1 diabetes mellitus (T1DM) is characterized by the destruction of beta cells in the pancreas by an autoimmune mechanism, whereas type 2 diabetes mellitus (T2DM) is a relationship between lifestyle and genetics.
The etiology of these two subtypes describes the etiology of diabetic retinopathy, as the retinal disease is an end-organ manifestation of the principal disease.
There is a stronger genetic association between T2DM compared to T1DM. Multiple genetic factors have been named in the development of T2DM including TCF7L2, NOTCH2, KCNQ1, JAZF1, and MODY (a heterogeneous disorder with autosomal dominant transmission). Poor lifestyle, in conjunction with genetic influences, increases the risk of developing T2DM.
Over 90% of people with a new diagnosis of T1DM have measurable antibodies against specific pancreatic β-cell proteins (insulin, islet antigen 2, zinc transporter 8, etc.).
These antibodies lead to a chain of progressive loss of β-cells, decreased insulin release, and recognizable diabetes.
The main types of diabetic retinopathy are non-proliferative diabetic retinopathy (NPDR) and proliferative diabetic retinopathy (PDR).
The distinguishing feature between these two categories is the presence (proliferative) or absence (non-proliferative) of abnormal new blood vessels (retinal, optic disc, or iris/angle neovascularization).
Of primary concern are the factors that lead to visual impairment in this patient population. The three items listed below are the foundation of this disease process, and their presence can be correlated with disease severity.
- Capillary leakage (DME)
- Capillary occlusion
- Sequelae of retinal ischemia (retinal neovascularization, vitreous hemorrhage, tractional retinal detachment, neovascular glaucoma)
Diagnosis
History:
Symptoms of decreased vision or fluctuating vision (lens or macular edema), presence of floaters (vitreous hemorrhage), or visual field defects (tractional detachment). It is important to know the hemoglobin A1c and whether or not the patient’s blood pressure is under control.
Physical Examination and Signs:
A slit lamp examination and dilated fundus examination should be performed. One should look carefully for the presence of abnormal blood vessels on the iris [neovascularization of the iris (NVI) or rubeosis], cataracts (associated with diabetes), and vitreous cells (blood in the vitreous or pigmented cells if there is a retinal detachment with hole formation).
Intraocular pressure (IOP) should be checked especially when NVI is seen. Dilated fundus examination should include a macular examination (contact lens or non-contact lens) to look for microaneurysms, hemorrhage, hard exudates, cotton wool spots, and retinal swelling (DME).
The optic disc and area surrounding it (for one disc diameter) should be examined for the presence of abnormal new blood vessels (neovascularization of the disc, NVD), optic nerve head pallor, or glaucomatous changes.
The remainder of the retina should also be examined for the presence of abnormal new blood vessels (neovascularization elsewhere, NVE).
Symptoms
Clinical Diagnosis:
The central retinal area that is located between the main branches (superior and inferior arcades) of the central retinal vessels (central retinal artery and central retinal vein) in the eye is known as the “macular area.”
The retina beyond this is considered the “peripheral retina.” The central retinal area can develop abnormal findings in diabetic retinopathy.
These findings can be present in the non-proliferative or the proliferative forms of the disease. These changes in the macula include the presence of abnormally dilated small vessel outpouchings (called microaneurysms), retinal bleeding (retinal hemorrhages), and yellow lipid and protein deposits (hard exudates).
The macula can get thicker than normal, which is referred to as macular edema.
MANAGEMENT
General Treatment:
The systemic status should be optimized by
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Strict metabolic control of diabetes,
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Maintaining HbA1C levels under 7%,
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Lifestyle modifications like routine exercises and a proper diabetic food diet,
Patients should visit diabetologists for proper follow-up visits and take timely antidiabetic medications.
Read more about management strategies
Other systemic ailments like hypertension, dyslipidemia, hypoproteinemia, anemia, nephropathy, neuropathy, cardiac ailments, and others should also be taken care of by respective medications and excellent interprofessional collaboration.
Would you have interest in taking retinal images with your smartphone?
Fundus photography is superior to fundus analysis as it enables intraocular pathologies to be photo-captured and encrypted information to be shared with colleagues and patients.
Recent technologies allow smartphone-based attachments and integrated lens adaptors to transform the smartphone into a portable fundus camera and Retinal imaging by smartphone.
RETINAL IMAGING BY YOUR SMARTPHONE
REFERENCES
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- Davis MD, Fisher MR, Gangnon RE, Barton F, Aiello LM, Chew EY, Ferris FL 3rd, Knatterud GL. Risk factors for high-risk proliferative diabetic retinopathy and severe visual loss: Early Treatment Diabetic Retinopathy Study Report #18. Invest Ophthalmol Vis Sci. 1998 Feb; 39:233-52
- Diabetes Control and Complications Trial Research Group. Clustering of long-term complications in families with diabetes in the diabetes control and complications trial. Diabetes. 1997 Nov; 46:1829-39.
- Diabetic Retinopathy Clinical Research Network. A randomized trial comparing intravitreal triamcinolone acetonide and focal/grid photocoagulation for diabetic macular edema. Ophthalmology. 2008 Sep;115(9):1447-9, 1449.e1-10. Epub 2008 Jul 26.
- Diabetic Retinopathy Clinical Research Network (DRCR.net), Beck RW, Edwards AR, Aiello LP, Bressler NM, Ferris F, Glassman AR, Hartnett E, Ip MS, Kim JE, Kollman C. Three-year follow-up of a randomized trial comparing focal/grid photocoagulation and intravitreal triamcinolone for diabetic macular edema. Arch Ophthalmol. 2009 Mar;127(3):245-51.
- Diabetic Retinopathy Clinical Research Network, Elman MJ, Aiello LP, Beck RW, Bressler NM, Bressler SB, Edwards AR, Ferris FL 3rd, Friedman SM, Glassman AR, Miller KM, Scott IU, Stockdale CR, Sun JK. Randomized trial evaluating ranibizumab plus prompt or deferred laser or triamcinolone plus prompt laser for diabetic macular edema. Ophthalmology. 2010 Jun;117(6):1064-1077.e35. Epub 2010 Apr 28.
