Complete Nurse's Guide to Diabetes Care, 3rd Edition

Chapter 12:

Ocular Changes with Diabetes

Roger H. Phelps, OD, FAAO, CDE1

1Phelps has type 1 diabetes and for many years has taught and lectured locally and internationally on diabetes and the eyes. He practices at OjaiEyes Optometry, Ojai, CA.

Diabetic retinopathy is the leading cause of new blindness in Americans ages 20–74 years, and most diabetes-related blindness is preventable.1–3 Nurses can participate in this prevention by

• knowing the range of effects that diabetes has on the eyes;

• assessing the patient’s glycated hemoglobin A1c (A1C) history, level of retinopathy (if any), and date of last dilated eye examination; and

• encouraging diabetes self-management knowledge and skills to promote glycemic and blood pressure control.

For every 1% lowering of A1C, there is an ~35% risk reduction for the development or progression of retinopathy. Timely detection and treatment of proliferative diabetic retinopathy (PDR) can reduce the risk of severe visual loss by 50%.4,For patients with diabetes, regular follow-up with early detection and treatment of vision-threatening retinopathy is recommended.

The American Diabetes Association (the Association) recommends the following:

• Dilated eye examinations should be performed by an ophthalmologist or optometrist who is knowledgeable and experienced in diagnosing diabetic retinopathy (see the Dilated, Comprehensive Eye Exam Schedule for Diabetic Retinopathy).

• Although high-quality fundus photographs can detect most clinically significant diabetic retinopathy when interpreted by a trained eye care provider, they are not a substitute for a comprehensive eye exam.

• Result of the eye examination should be documented and transmitted to the referring health-care professional.

• An eye doctor who finds any level of diabetic macular edema (DME), severe nonproliferative diabetic retinopathy (NPDR), or any PDR should promptly refer that patient to an ophthalmologist who is knowledgeable and experienced in the management and treatment of diabetic retinopathy.1

The term retinal specialists will refer to ophthalmologists who have had specific retinal fellowship training beyond their general ophthalmological training. All eye doctors are licensed to do comprehensive dilated eye examinations and are responsible for detecting diabetic retinopathy.4,6 Nurses working with patients who have diabetes should get to know which eye doctors are in their area or on their referral lists to establish a two-way communication link to benefit their mutual patients. It is helpful for the nurse to be aware of the patient’s eye exams and the reported results.

If a patient has been referred or is having treatment done for advanced diabetic retinopathy, the nurse should know whether the treating ophthalmologist wants to limit exercise for a period of time.7

Dilated, Comprehensive Eye Exam Schedule for Diabetic Retinopathy

Patient group

Recommendation for exam

Minimum routine follow-up

Type 1 diabetes

An initial dilated and comprehensive exam is recommended > or = age 10 or after puberty has started, whichever is earlier, once the youth has had diabetes for 3–5 years

Annual exams generally recommended. Less frequent, every 2 years on the advice of an eye care professional

Type 2 diabetes

At time of diagnosis of diabetes

Yearly, more or less frequently depending on prior exams

Pregnancy with preexisting diabetes

Before conception or during first trimester

Every trimester and for 1 year postpartum, at the physician’s discretion, pending results of first trimester exam

TEMPORARY REFRACTIVE CHANGES

Temporary blurry vision can occur any time individuals with diabetes have a major change in their average glycemic control. Either a major increase or a major decrease in A1C can change the osmotic balance between the aqueous and the crystalline lens in the eye. This change usually is temporary and is reversible with glycemic stabilization. It remains important, however, that patients have a dilated eye examination any time they complain of blurry vision to rule out any serious cause. Most eye doctors will discuss the costs versus benefits of purchasing a pair of glasses for temporary use while driving or reading until the refractive error stabilizes.

Practical Point

The nurse should encourage all patients with diabetes to learn how to establish and maintain glycemic control. When working with individuals who are experiencing significant changes in glycemic control, inform the eye doctor of these changes and send a copy of the most recent A1C value. If no active retinopathy is found, the eye doctor may recommend a temporary change in their prescription for work or driving purposes.

Figure 12.1—Illustration of a normal eye

Figure 12.1—Illustration of a normal eye.

Source: From Funnell et al. Life with Diabetes: A Series of Teaching Outlines. 5th ed. Alexandria, VA, American Diabetes Association, 2014, p. 298.

Eye Anatomical Terms

• Aqueous: The clear fluid constantly produced by the eye. It drains out of the eye in a circular canal near the iris root.

• Iris: The diaphragm that forms the pupil, located in the front portion of the eye. The color of the iris is considered the “eye color.”

• Lens: The crystalline lens is just behind the iris and is responsible for about one-third of the optical power of the eye. It can change focus until about the age of 40 years.

• Vitreous: The vitreous body is the clear gel-like body that fills the large posterior portion of the eye. It is bathed in aqueous fluid, as is the entire inside of the eye, and tends to liquefy with increasing age.

• Retina: The photosensitive membrane that lines the inside back of the eye and acts like the film in a camera. It is connected to the brain’s seeing mechanism through the optic nerve. It is nourished by its own capillary bed as well as by vessels that underlie it.

• Optic disk: The opening in the retina where the optic nerves and major retinal vessels enter and exit the back of the eye (see Figure 12.2).

• Macula: This small area of the retina is the most sensitive and central part of our vision. This is a specific area of concern in diabetes (see Figure 12.2, and cross-section of the macular area by optical coherence tomography in Figure 12.3).

Figure 12.2—Retinal photograph of healthy retina

Figure 12.2—Retinal photograph of healthy retina. The macular area is the critical central part of your vision. The circular area is the optic nerve (disk) that transmits information from the retina to the brain.

Figure 12.3—Spectral domain optical coherence tomography with the lower scan showing a healthy macular area in the center

Figure 12.3—Spectral domain optical coherence tomography with the lower scan showing a healthy macular area in the center. The three top scans show increasing levels of clinically significant DME.

Levels of Diabetic Retinopathy

Microvascular disease of the retina is best predicted by the A1C history and duration of diabetes in a patient.5 The continued hyperglycemia of inadequately controlled diabetes can lead to blindness by the following process. First, high glucose levels damage the capillary walls of the retina, leading to leakage and small blot hemorrhages and microaneurysms. Continued glycemic insult leads to more capillary nonperfusion and the development of intraretinal microvascular abnormalities, venous beading, and the stimulation of chemical factors, such as vascular endothelial growth factor (VEGF). New fragile vessels then grow out from the retina into the vitreous. These leak and bleed easily, forming adhesions between the retina and vitreous, which then lead to traction retinal detachment, vitreous bleeding, and blindness.9

Surgical and pharmacological interventions are available to stop or slow this process,4,10 but the best intervention is to optimize glycemic control to keep the retinal capillaries healthy. Often, if the retinopathy is severe, improving glycemic control too quickly first can lead to increased retinopathy; however, after 2–3 years, the benefit of maintained glycemic control will be realized.

No Diabetic Retinopathy

This level of no diabetic retinopathy indicates that no disease is visible on the retina. Although this has been historically uncommon after a long duration of diabetes, it is now becoming more probable with ongoing, consistent glycemic control combined with a timely diagnosis of diabetes.

Nonproliferative Diabetic Retinopathy

NPDR, also called background retinopathy, indicates that some damage has occurred to the retinal capillary bed but not to the point that new vessel growth has been stimulated into the vitreous body, which would signify PDR. These background changes are usually put into three categories: mild, moderate, and severe (or preproliferative).11

Practical Point

The health of the retinal capillary bed can be diagnosed best by clinical exam along with fluorescein angiography and optical coherence tomography. In angiography, a dye is given through an intravenous line. Carefully timed photographs then are taken of the retina to show areas of capillary nonperfusion and leakage. Optical coherence tomography is a newer, noninvasive test that is sensitive to macular edema resulting from both diabetes and macular degeneration (see Figure 12.3).

Mild NPDR

In mild NPDR, some scattered small blot hemorrhages and microaneurysms begin to appear on the retina. These can be difficult to see and are easily missed during a nondilated eye examination (see Figure 12.4). There have been documented incidences of patients at this mild stage improving their glycemic control and reversing these changes.

Figure 12.4—There are fine red dots and blotches in the upper left part of this retinal photo

Figure 12.4—There are fine red dots and blotches in the upper left part of this retinal photo, indicating mild NPDR. These can be best detected with a careful dilated retina exam.

Moderate NPDR

In moderate NPDR, the number of small blot hemorrhages and microaneurysms increases significantly, with the additional findings of intraretinal microvascular abnormalities or venous beading. This is the point at which the experienced eye doctor will consider a consultation with a retinal specialist.

Severe NPDR (Preproliferative)

In severe NPDR (preproliferative), retinal changes become a real threat to vision. The retina capillary bed is severely compromised, and more of the retinal findings of the previous moderate stage are present. Chemical mediators, such as VEGF, are now strongly calling out for new vessel growth. The patient should immediately see a retinal specialist or other experienced treating ophthalmologist for special testing, such as fluorescein angiography and optical coherence tomography, with probable retinal treatment.

Proliferative Diabetic Retinopathy

PDR indicates that the insult to the vessels has been sufficient enough that the body has started to try to fix the problem by growing new vessels (see Figure 12.5). This “fix,” however, results in more problems for the eye, such as rubeosis iridis, retinal detachment, and vitreous hemorrhage (see Figure 12.6).

Figure 12.5—A patch of new vessels is growing up out of hte optic disk in PDR

Figure 12.5—A patch of new vessels is growing up out of the optic (nerve) disk in PDR. The vision is still 20/20 in this eye.

Figure 12.6—Advanced PDR

Figure 12.6—Advanced PDR. New vessels have grown, hemorrhaged, and are causing traction on the retina.

Rubeosis Iridis

The new vessels most commonly grow from the optic nerve head, but they also can grow elsewhere in the retina and on the iris (called rubeosis iridis). Rubeosis iridis can lead to neovascular glaucoma. A retinal specialist needs to be involved immediately at this stage to minimize the high probability of blindness.

Retinal Detachment

In retinal detachment the proliferative new vessels are leaky and cause adhesions and tractions that can then pull apart the two layers of the retina, in turn detaching them from the eye wall. If the retina is not surgically reattached, it will deteriorate quickly. Many times, this finding is the first indication of an eye problem in a patient with suboptimally controlled diabetes who has not had an eye examination or routine annual screening. It is not always possible to reattach the retina, and the result is permanent blindness.

Vitreous Hemorrhage

A vitreous hemorrhage occurs when the fragile new vessels growing in PDR break and bleed into the vitreous body. This can be seen as an oily, pink haze or sometimes as a total blockage of vision. Again, this may be the first indication of a diabetes-related eye problem. A retinal specialist usually does a vitrectomy at this point. This surgical procedure removes the jelly-like vitreous material, allowing clear aqueous fluid to fill the eye.

Clinically Significant Macular Edema

Retinal edema can appear at almost any level of retinopathy and usually is accompanied by some hard exudates (see Figure 12.3). Sometimes these changes can be subtle and missed by an inexperienced examiner who fails to dilate the pupil. Anti-VEGF intravitreal injections and sometimes laser treatment, guided by fluorescein angiography and tomography needs to be done as soon as possible to minimize the damage caused by the edema to the sensitive macular area.10–13

Other Retinal Changes Associated with Diabetes

Hypertensive Retinopathy

High blood pressure combined with weakened retinal capillary beds in suboptimally controlled diabetes can cause a rapid progression in diabetic retinopathy. Hypertensive effects include infarcts in the retinal nerve fiber layer evidenced by cotton wool spots and flame-shaped retinal hemorrhages. These can resolve with better control of blood pressure; however, continued hypertension, even without diabetes, can lead to sight-threatening retinal changes.

Interventions for Diabetic Ocular Complications

• Glycemic control

• Blood pressure control

• Panretinal photocoagulation: A retinal specialist will use a laser to carefully place hundreds of microburns to the peripheral retina. This will decrease the peripheral vision somewhat but will reduce the demand for new blood vessel growth. This usually dries up the neovascular growth in PDR, thus preserving the central vision.

• Intravitreal injections: If clinical exam, optical coherence tomography, or fluorescein angiography determines areas of leakages around the macula, intravitreal injections of anti-VEGF are now the primary intervention for clinically significant macular edema, but laser treatments still may be indicated.

• Grid laser treatment: A small-grid pattern of microburns will be placed, usually drying up the clinically significant macular edema to prevent further permanent loss to the macular function.

• Subthreshold diode laser micropulse photocoagulation: This technique is being developed as a less destructive alternative to grid laser treatment of the retina for DME.

• Vitrectomy: A retinal specialist, in microsurgery, will remove some of the vitreous bodies while carefully protecting the retina from detachment, removing traction membranes.

• Follow-up: Most retinal specialists do not do routine eye care or prescribe low-vision aids, so the optometrist or general ophthalmologist will continue to monitor the patient’s visual needs and, if necessary, refer the patient to a low-vision specialist for visual rehabilitation.

• Visual rehabilitation: Similar to physical therapy after a stroke, many patients can learn to adapt to their reduced vision with various new low-vision aids and techniques.

• Pharmacological interventions: Many new pharmacological interventions, including implantable intraocular devices, eye drops, and oral and injectable medications, are being studied and show some promise in turning off the chemical mediators in the eye that call out for new blood vessel growth.

Central Retinal Vein Occlusion

Central retinal vein occlusion (CRVO) appears as a hemorrhagic stroke resulting from an occlusion in the central vein of the eye or a branch of it (BRVO). This problem threatens sight and is more related to the macrovascular changes in diabetes. Cholesterol management together with blood pressure control best prevents CRVO (see Chapter 2, Diagnosis and Classification). Some of these branch occlusions can resolve, but others need laser treatment similar to that used to treat PDR. Intravitreal anti-VEGF also is used to control damaging retinal edema. Central retinal artery occlusions can result as well, severely limiting the blood supply to the retina.

Age-Related Macular Degeneration

Although not specifically associated with diabetes, age-related macular degeneration is the leading cause of legal blindness in senior adults. Injections of pharmaceutical agents that block VEGF have shown remarkable success in maintaining and even restoring vision when given at the beginning signs of macular edema.

If a patient with diabetes already has lost vision from retinopathy or macular degeneration, special devices, low-vision aids, and proper training can greatly assist patients in their self-management needs, such as in reading blood glucose meters and drawing insulin. There are a number of catalogs and websites that offer aids and adaptive devices for those with low vision.14 The National Eye Institute has a large-print booklet and a series of videos that is a resource for low-vision adaptive devices. Since the type and degree of vision loss may vary from person to person, it may be a matter of trial and error to find the low-vision device that is most helpful.

Vision rehabilitation services include:

• training to use a magnifier and other adaptive devices

• learning new daily living skills to remain safe and live independently

• develop strategies to navigate inside and outside the home

• provide resources and support to help patients with vision loss (from www.nei.nih.gov/lowvision)

NONRETINAL CHANGES ASSOCIATED WITH DIABETES

Diplopia

A sudden onset of double vision in a patient with diabetes commonly is associated with a complete or partial paresis of cranial nerves III, IV, and VI, which affect the extraocular muscles that control eye position and movement. Most of these patients can be followed conservatively for 2–3 months, and many times, they experience a dramatic recovery. The important exception is when either a third nerve palsy affects the pupil or any palsy lasts >3 months. This situation requires an extensive neuroradiological workup to rule out the possibility of a brain aneurysm or other serious cranial problems.

Cataracts

Because the lens of the eye becomes less clear throughout the natural aging process, most people who live long enough will benefit from cataract extraction. When the crystalline lens is removed, an artificial lens (intraocular lens) usually is put behind the iris to keep it in proper focus. Although cataracts are more common in individuals with suboptimally controlled diabetes, they are detected easily in routine eye examinations and can be treated easily when they sufficiently interfere with vision. No surgery is without risk, however, and individuals with diabetes who have a significant amount of retinopathy are at a higher risk of complications during and after the surgery. In these cases, many cataract surgeons will request a consultation from a retinal specialist to determine the best time for surgery.

Glaucoma

The three basic types of glaucoma are primary open-angle glaucoma, primary angle-closure glaucoma, and neovascular glaucoma. All three types are associated with an intraocular pressure that is too high for the health of the optic nerve fibers.

Primary Open-Angle Glaucoma

The population with diabetes is at higher risk of developing primary open-angle glaucoma (also known as chronic open-angle glaucoma), which is the most common type of glaucoma. The potential for loss of vision can be higher in individuals with suboptimally controlled diabetes because of compromised microvascular circulation. Detection and continuous treatment of this condition are important to minimize or prevent vision loss. Almost all routine eye examinations check for glaucoma. Because it is usually asymptomatic, patients are unaware of its presence until much of their peripheral vision is lost. Most patients can be controlled successfully with daily eye drops that lower their eye pressure.

Primary Angle-Closure Glaucoma

Primary angle-closure glaucoma (also called narrow-angle glaucoma) is an ocular emergency and usually is painful. The cause is an anatomical closure of the drainage canal by the iris. Quick treatment usually prevents any visual loss. Prevention of this condition begins when a narrow drainage angle is discovered during a routine eye examination. The patient should be referred to an ophthalmologist who has a special laser to open a drainage hole in the iris. This procedure (called YAG iridotomy [neodymium:yttrium aluminum-garnet-pulsed laser]) can be performed during an office visit, usually permanently prevents closure, and requires no ongoing medication.

Neovascular Glaucoma

Neovascular glaucoma is a serious condition and is associated with suboptimally controlled diabetes. In this form of PDR, new blood vessels form and proliferate along the iris (rubeosis iridis) and into the normal drainage canal of the eye, blocking the normal outflow of the aqueous, causing a painful increase in eye pressure. It is treated in the same way as other PDR, with panretinal laser photocoagulation and other medical and surgical interventions. Treatment, however, is not always successful in saving vision.

Abbreviations Commonly Used in Ocular Charts and Reports

A1C: Glycated hemoglobin A1c

AMD: Age-related macular degeneration (sometimes ARMD)

BDR: Background diabetic retinopathy (same as NPDR)

CIDME: Central involved diabetic macular edema

CRVO: Central retinal vein occlusion

CSME: Clinically significant (diabetic) macular edema

CW: Cotton wool spots (on retina)

DME: Diabetic macular edema

DR: Diabetic retinopathy

FA: Fluorescein angiography

H/ma: Small-blot hemorrhages and/or microaneurysms

IRMA: Intraretinal microvascular abnormalities

NPDR: Nonproliferative diabetic retinopathy (same as BDR)

NVD: New vessels on the optic disk (this is PDR)

NVE: New vessels elsewhere in the retina (this is PDR)

NVG: Neovascular glaucoma

OCT: Optical coherence tomography

OD: Oculus dexter (right eye)

OS: Oculus sinister (left eye)

OU: Oculus uterque (both eyes)

PACG: Primary angle closure glaucoma

PDR: Proliferative diabetic retinopathy

POAG: Primary (or chronic) open-angle glaucoma

PRP: Panretinal laser photocoagulation

RD: Retinal detachment

RI: Rubeosis iridis (this is PDR)

VEGF: Vascular endothelial growth factor

VB: Venous beading (with retinal veins)

VH: Vitreous hemorrhage

SUMMARY

The nurse plays an important role in reducing the incidence of diabetic retinopathy by providing education in maintaining blood glucose control, helping ensure timely eye examinations, and assisting individuals to achieve better control of blood pressure and lipids. Optimal diabetes control has been shown to prevent or reduce the severity of diabetic retinopathy. Early detection and treatment also decreases the incidence of blindness. Encouragement by the nurse to achieve optimal control and to have annual dilated eye exams is important. The nurse educator may be the health-care professional in any practice group most knowledgeable about low-vision devices and aids for self-monitoring of blood glucose and injections.

REFERENCES

1. Diabetic retinopathy: a Position Statement by the American Diabetes Association. Diabetes Care 2017;40:412–418

2. Chous AP. Diabetic Eye Disease: Lessons from a Diabetic Eye Doctor: How to Avoid Blindness and Get Great Eye Care. Auburn, WA, Fairwood Press, 2003

3. Centers for Disease Control and Prevention. National diabetes education program. Available from www.cdc.gov/diabetes/ndep/index.htm. Accessed 28 July 2014

4. American Academy of Ophthalmology (AAO) website. Available from www.aao.org. Accessed 28 July 2014

5. Diabetes Control and Complications Trial Research Group. The relationship of glycemic exposure (HbA1c) to the risk of development and progression of retinopathy in the Diabetes Control and Complications Trial. Diabetes 1995;44:968–983

6. American Optometric Association (AOA) website. Available from www.aoa.org. Accessed 28 July 2014

7. U.S. National Library of Medicine. Diabetes and exercise. Available from https://medlineplus.gov/ency/patientinstructions/000083.htm. Accessed 2 March 2017

8. Centers for Disease Control and Prevention. Keep an eye on your vision health. Available from www.cdc.gov/features/healthyvision. Accessed 30 July 2014

9. Aiello LP, Aiello LM, Cavallerano JD. Visual loss. In Therapy for Diabetes Mellitus and Related Disorders. 4th ed. Lebovitz HE, Ed. Alexandria, VA, American Diabetes Association, 2004, p. 340–343

10. Nguyen QD, Brown DM, Marcus DM, et al.; RISE and RIDE Research Group. Ranibizumab for diabetic macular edema; results from 2 phase III randomized trials: RISE and RIDE. Ophthalmology 2012;119:789–801

11. Aiello LP, Aiello LM, Cavallerano JD. Ocular complications. In Therapy for Diabetes Mellitus and Related Disorders. 4th ed. Lebovitz HE, Ed. Alexandria, VA, American Diabetes Association, 2004, p. 344–357

12. Luttrull JK, Dorin G. Subthreshold diode micropulse laser photocoagulation (SDM) as invisible retinal phototherapy for diabetic macular edema: a review. Curr Diabetes Rev 2012;8:274–284

13. National Eye Institute. Facts about diabetic eye disease Available at https://nei.nih.gov/health/diabetic/Accessed 2 March 2017

14. National Eye Institute Low Vision. Available at http://www.nei.nih.gov/low vision. Accessed 17 Feb 2017