Patient with diabetes reports blurred vision in one eye

Leo P. Semes

A 63-year-old man with a 15-year history of type 2 diabetes came in for new glasses stating his right eye had not seen well for several months. There was no history of pain or flashes or floaters.

His medical history included diabetes, chest pain, mitral valve disorder, cerebrovascular disease, prior myocardial infarction, hyperlipidemia, hypertension and general osteoarthrosis.

The patient’s current medications were: amlodipine 10 mg daily, hydrochlorothiazide 12 mg daily, metoprolol tartrate 50 mg twice daily for high blood pressure, nitroglycerin 0.4 mg as needed and nitroglycerin patch 10 mg/24 h for heart disease, warfarin 2 mg at bedtime for blood clots, metformin 500 mg once daily for diabetes, simvastatin 40 mg tablet once daily for cholesterol, multivitamin/mineral supplement daily and acetaminophen 325 mg as needed for pain.

Visual field results. Images: Bockin DG

His visual acuity was 20/200 OD and could not be improved with pinhole or refraction. With –3.50 D sphere before the left eye, visual acuity was 20/20. Versions were smooth and full, and confrontation visual fields were full in the left eye with overall constriction in the right. Pupils were unequal (5 mm OD and 3 mm OS), round and reactive to light with a moderate relative afferent pupillary defect in the right eye.

No hemorrhages or exudates were seen in either eye.

The patient’s IOP was 12 mm Hg OD and 13 mm Hg OS. Examination of the anterior segment was unremarkable except for mild nuclear sclerosis in both eyes.

A visual field was ordered.

Fundus examination revealed a pale optic disc and attenuated blood vessels in the right eye. The left eye was unremarkable. There were no hemorrhages or exudates in either eye.

What is your diagnosis?

Blurred vision

Possible diagnoses include diabetic retinopathy, arteritic ischemic optic neuropathy, central retinal vein occlusion and central retinal artery occlusion.

Arteritic ischemic optic neuropathy (AION) occurs in patients older than 50 with acute severe vision loss. There usually is a history of temporal headache with scalp tenderness, jaw claudication, muscle pains, weakness, weight loss, a significant afferent pupillary defect, pale optic disc swelling and markedly increased erythrocyte sedimentation rate (ESR).

AION is attributed to ischemia at the optic nerve head due to structural crowding that may impair perfusion to the nerve and thereby cause edema. The condition is divided into two subcategories: nonarteritic (NAION) and arteritic (AAION). The latter is most commonly associated with temporal arteritis.

The patient demographic for AION is typically older than age 50; the median age group for NAION is older than 60, and with AAION the median age is 70 years. There is a gender predilection for females, but only in cases of AAION. Incidence of AAION is 5% to 10% of cases, while NAION accounts for 90% to 95% of AION cases.

A tiny amount of hard plaque was seen in the posterior wall of the carotid bulb and perhaps also at the origin of the right internal carotid artery. However, normal Doppler tracings were obtained in the right common carotid artery, carotid bulb and its internal and external branches. A small amount of hard plaque was also seen in the left carotid bulb and the origins of the left internal and external carotid arteries. Normal Doppler tracings were obtained in the left common carotid artery and carotid bulb. Mild turbulence was seen in the left internal and external carotid arteries, but no velocity shift was measured. Normal antegrade flow was seen in both vertebral arteries. A small amount of hard plaque was seen in the left carotid bulb and its internal and external branches. Only a minimal amount of hard plaque was seen in the right carotid bulb. No significant stenosis was seen by Doppler measurement.

Patients with either form of AION typically report a rapid onset of painless, unilateral visual loss manifested by decreased visual acuity, visual field or both. Vision loss is more severe in AAION, typically less than 20/200.

The most common visual field defect with either form of AION is altitudinal, but it may also present as a general depression, an arcuate scotoma or a cecocentral defect. A retrospective study using Goldmann perimetry suggested that the most common field loss was actually inferior nasal and, when combined with overall inferior field loss, it is highly indicative of NAION. The inferior nasal defect is explained by the location of the watershed zone of the posterior ciliary arteries, which is often temporal to the optic nerve head and the most susceptible to ischemia.

Signs of an AION are a pale and hyperemic optic nerve head with edema (diffuse or segmental) in the acute phase and optic atrophy in later stages. The edema may be present several weeks to months before vision loss is reported. One source suggests that in AAION the disc is more pallid than hyperemic, which is more common with NAION. Flame hemorrhages and narrowed peripapillary arterioles are other signs associated with AION. Also, because the presentation is typically unilateral, a relative afferent pupillary defect is often expected. Systemic associations with the arteritic form are symptoms common with temporal arteritis (i.e., headache, jaw claudication and scalp tenderness). Vision loss in the arteritic form may be preceded by episodes of transient vision loss, which is also highly indicative of arteritis.

Central retinal artery occlusion (CRAO) is a unilateral, painless, acute vision loss that occurs over several seconds. There may be a history of amaurosis fugax, which did not present in this case. There is a marked afferent pupillary defect, narrowing retinal arterioles, box-carring or segmentation of the blood column in the arterioles. Occasionally, retinal emboli or cilioretinal artery sparing of the foveola is evident.

The etiology is an embolus more often from the carotid arties, but possibly cardiac in origin.

Sudden onset of CRAO may be treated using heroic measures with immediate ocular digital massage, anterior chamber paracentesis, acetazolamide 500 mg IV or two 250-mg tablets or a topical beta blocker. All treatment is aimed at reducing intraocular pressure to help restore blood flow.

The diagnosis of CRAO was based on the carotid studies, in that the patient had an abnormal result. In addition, no retinal hemorrhages were present, which, in CRVO, may be present for several months after the occlusion.

The patient was referred to his primary care physician for re-evaluation of bloodwork and a carotid Doppler ultrasound.

On follow-up examination the patient’s vision was stable. His primary care doctor changed no medications but will administer more frequent physical evaluations. Discussion with the patient’s primary care physician for a referral for a carotid endarterectomy was considered, but the patient was in poor health and may not survive the surgery.

References:

• Arnold AC. Ischemic optic neuropathies. Yanoff & Duker Ophthalmology. Elsevier.
• Ehlers JP, Chirag PS. The Wills Eye Manual, 5th ed. 2008. Baltimore, MD: Lippincott Williams & Wilkins.
• Hayreh SS, Zimmerman B. Visual field abnormalities in nonarteritic anterior ischemic optic neuropathy: Their pattern and prevalence at initial examination. Arch Ophthalmol. 2005;123:1554-1562.

• Donald G. Bockin, OD, can be reached at 1174 Windy Hill, Salado, TX 76571; donbockin@gmail.com.
• Edited by Leo P. Semes, OD, a professor of optometry, University of Alabama at Birmingham and a member of the Primary Care Optometry News Editorial Board. He may be contacted at 1716 University Blvd., Birmingham, AL 35294-0010; (205) 934-6773; fax: (205) 934-6758; lsemes@uab.edu.