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Patient History

HPI:
A 35 year-old convenient store manager with history of non-insulin dependent DM x 5 years presents to the Eye Clinic for his annual visit. He admits to progressive blurring of vision since his last visit one year ago. Reading street signs while driving seems more difficult. He is unsure of which eye seems worse. He does not wear any glasses or contacts with the exception of over-the counter reading glasses. He denies any flashes or floaters, diplopia, eye discomfort or pain.

The patient reports that he has been going through some tough times recently with a difficult divorce about 6 months ago. As a result of all the stress, his blood sugars have not been under good control and he feels he has been making this worse by eating a lot of junk food and not always taking his diabetic medications. His blood sugar has been as high as 400 and he was admitted to the hospital three months ago for diabetic ketoacidosis.

Past Ocular History:
No prior eye surgeries, no hx of eye trauma, amblyopia or strabismus. No prior diabetes findings in the eye.

Ocular Medications:
None

Past Medical History:
Hypercholesterolemia, Obesity, DM Type 2, Hypertension

Surgical History:
None

Past Family Ocular History:
Negative for macular degeneration, glaucoma, diabetic retinopathy or blindness

Social History:
30 pack year smoking history and drinks alcohol socially.

Medications:
Lisinopril, Hydrochlorothiazide, Metformin, Simvastatin

Allergies:
None

ROS:
Denies any other CNS, heart, lungs, GI, skin or joint symptoms

Visual Acuity (cc):
OD: 20/40
OS: 20/40

IOP (tonoapplantation):
OD: 16 mmHg
OS: 15 mmHg

Pupils:
Equal, round and reactive to light. No APD

Extraocular Movements:
Full OU. No nystagmus

Confrontational Visual Fields:
Full to finger counting OU

External:
Normal, both sides

Slit Lamp

Lids and Lashes	Normal OU
Conjunctiva/Sclera	Normal OU
Cornea	Clear OU
Anterior Chamber	Deep and quiet OU
Iris	Normal OU; no neovascularization of the iris OU
Lens	Clear OU
Anterior Vitreous	Clear OU

Dilated Fundus Examination:

OD	Clear view, CDR 0.35; neovascularization of the disc involving ~ 50% of disc; flat macula with multiple microaneurysms and hard exudates > 500 microns away from the fovea, no clinically significant macular edema; multiple dot-blot hemorrhages in the retina periphery in all 4 quadrants without retinal detachment
OS	Clear view, CDR 0.40 with sharp optic disc margins; flat macula with multiple microaneurysms and hard exudates > 500 microns away from the fovea, no clinically significant macular edema; peripheral retina with multiple dot-blot hemorrhages in the periphery in all 4 quadrants

Other:
Fluorescein angiography with evidence of abnormal vasculature (microaneurysm with leakage in later frames) and areas of capillary dropout. In the R eye there is hyperfluorescence in the area of the neovascularization of the disc.

Diagnosis
Proliferative diabetic retinopathy in both eyes

Discussion

Differential Diagnosis:
This case describes a patient with proliferative diabetic retinopathy (PDR) in both eyes. Other conditions that could present with retinal hemorrhages include retinal vein occlusions, retinal ischemia from artery occlusions, radiation retinopathy, anemias or other blood disorders, retinal vasculitis (either due to infection, neoplasms or systemic vasculitides), severe hypertensive disease, carotid related ocular ischemia, Purtscher retinopathy (a hemorrhagic and vaso-occlusive retinopathy due to systemic disease) and Terson's syndrome (associated with acute intracranial hemorrhage).

Definition:
Retinopathy due to diabetes can be classified as non-proliferative diabetic retinopathy (absence of new vessels) or proliferative diabetic retinopathy (presence of new vessels). In non-proliferative diabetic retinopathy (NPDR) the high blood sugars disturb the normal retinal vascular, especially the capillaries, causing the formation of microaneurysms and ghost capillaries. Weaken capillaries have the tendency to bleed. This is seen clinically as microaneurysms, dot-blot hemorrhages and hard exudates. NPDR can range from mild to severe, and roughly 40% of patients with the severe form will develop proliferative diabetic retinopathy within one year. Proliferative diabetic retinopathy (PDR) is defined by the development of small abnormal blood vessel (neovascularization) on the surface of the retina or on/near the optic disc (NVD). These are the results of high levels of vascular endothelial growth factor (VEGF) released by ischemic retina. These new vessels are also fragile and can cause significant intraocular (vitreous) bleeding. PDR is responsible for the majority of vision loss from diabetes. The vision loss is due to recurrent vitreous hemorrhages and tractional retinal detachment. This type of retinal detachment is a result of the contraction of fibrous tissue which accompanies the new vessel formation and is difficult to surgically repair.

Examination:
Since diabetic retinopathy is the leading cause of blindness in working age individuals in the United States, it is very important that individuals with diabetes have a dilated fundus exam at least yearly to monitor for diabetic retinopathy. Key exam elements include visual acuity, IOP, iris examination for neovasculature, vitreous exam for evidence of bleeding and examination of the retina for abnormal vessels, bleeding and ischemia. Fluorescein Angiogram (FA) can also aid in diagnosis because abnormal neovascularization is hyperfluorescent.

Treatment:
According to The Diabetic Retinopathy Study, panretinal laser treatment (the burning of the peripheral ischemic retina with laser) decreases vision loss in patients who have PDR with “high risk characteristics.” These high risk characteristics include neovascularization of more than one third of the optic disc surface, neovascularization of the disc with preretinal or vitreous hemorrhage, and any neovascularization away from the disk with preretinal or vitreous hemorrhage. Performing laser photocoagulation reduces the metabolic oxygen demand of the retina, helping the neovascularization to regress. Once complications such as a non-clearing vitreous hemorrhage or traction retinal detachment have occurred, laser treatment may no longer be effective and an intraocular surgery called a pars plana vitrectomy could be necessary.

The most important factor in the development and progression of diabetic retinopathy is blood sugar control. Tight control is associated with reduced likelihood of vision loss from diabetic retinopathy. Diabetic patients are recommended to keep their HgA1c under 7 to decrease the likelihood of retinopathy. Good communication between the primary care provider and the ophthalmologist is imperative to maintain good eye health and prevent retinopathy and its consequences.

1. How often should a person with diabetes have a dilated eye exam?
   • When they notice any vision changes, even if it is mild
   • If Type 2 DM, at the time of diagnosis and then at least annual exams
   • Every 6 months
   • Every 2 years
   • Every 4 months
2. True or False : Complications due to diabetic retinopathy is the number one cause of blindness in the USA in working-age people.
3. What is not a sign of retinopathy due to diabetes?
   • Abnormal blood vessel growth (neovascularization) on the optic nerve
   • Retinal dot-blot hemorrhages
   • Macular edema
   • Retinal exudates
   • Optic nerve atrophy

1. How often should a person with diabetes have a dilated eye exam?
b. If Type 2 DM, at the time of diagnosis and then at least annual exams
Since some patients with a diagnosis of Type 2 DM might have had significant and chronic hyperglycemia prior to the diagnosis, an exam at time of diagnosis and yearly after is recommended.

2. True or False : Complications due to diabetic retinopathy is the number one cause of blindness in the USA in working-age people.
TRUE

3. What is not a sign of retinopathy due to diabetes?
e. Optic nerve atrophy
Retinal disease can cause optic nerve dysfunction but optic nerve atrophy, as a single entity, would signal a direct injury to the nerve itself and not necessary diabetic retinopathy.