Funduscopic Examination: Clarifying the Cause of Blurred Vision Proliferative Diabetic Retinopathy Arterial Occlusive Event Ischemic Optic Neuropathy Wet Macular Degeneration Central Retinal Vein Occlusion

October 1, 2006

A 54-year-old woman with a 10-year history of insulin-dependent type 2 diabetes mellitus was referred by her optometrist because of the recent onset of blurrinessin her right eye. Her optometrist told her that new blood vessel growth and leakage had developed.

Case 1:

A 54-year-old woman with a 10-year history of insulin-dependent type 2 diabetes mellitus was referred by her optometrist because of the recent onset of blurrinessin her right eye. Her optometrist told her that new blood vessel growth and leakage had developed.

The patient's best corrected visual acuity was 20/40 in the right eye and 20/25 in the left. Her pupils and intraocular pressures were normal in both eyes. A slit-lamp examination revealed mild nuclear sclerotic changes in the lenses of both eyes. No rubeosis of the iris was found on gonioscopic evaluation.

A funduscopic examination demonstrated neovascularization of the optic disc, with blood in the vitreous directly over the macular area of the right eye. Dot and blot retinal hemorrhages were scattered throughout the posterior pole. A few hard exudates were also seen (A). A large preretinal hemorrhage was detected in the infranasal quadrant of the left eye (B). Because the bleeding was not near the patient's line of sight, she had not experienced visual difficulties in this eye.

Proliferative diabetic retinopathy was diagnosed. The optic disc neovascular vessels had begun to leak, and the blood settling over the macula manifested as a cloud in the patient's vision. The patient's other retinal hemorrhages and hard exudates are common in moderate diabetic retinopathy. The preretinal hemorrhage in the left eye is another sign of proliferative diabetic retinopathy, which is treated with laser panretinal photocoagulation. *

Case 2:

A 73-year-old woman presented for evaluation because of a sudden severe but painless loss of vision in her left eye 2 days earlier. Her medications included ramipril, 2.5 mg/d; aspirin, 81 mg bid; and a multivitamin.

The patient's initial visual acuity was 20/20 in the right eye and light projection in the left eye. She had a left afferent pupillary defect. Results of the funduscopic examination of the right eye were unremarkable. The fundus of the left eye showed a foveal cherry-red spot; retinal whitening and opacification surrounding the fovea; and retinal arterial thinning with segmentation, or "boxcarring." Her seated blood pressure was 200/82 mm Hg in the right arm and 192/80 mm Hg in the left.

This patient had experienced an arterial occlusive event, probably of the central retinal artery in the left eye. This neuroretinal ischemic disorder is often associated with conditions that lead to embolus formation but is also seen in patients with coagulopathies, collagen vascular and inflammatory disorders, and vasculitides and in patients with systemic abnormalities such as untreated or undertreated hypertensionand diabetes.

There is no effective treatment for patients who present several hours or days after onset. In acute presentations, ocular massage, rebreathing in a paper bag, or anterior chamber paracentesis may be tried. Systemic conditions must be identified and treated. This patient was referred to her internist for further evaluation. *

Case 3:

Shortly after awakening, an 82-year-old man with a history of cataracts in both eyes noticed a sudden painless diminution of vision in the left eye. He had no new headaches or jaw claudication. His medications included hydrochlorothiazide and atorvastatin.

The patient's best corrected visual acuity was 20/25 in the right eye and 20/60 in the left. There was no afferent pupillary defect. The slit-lamp evaluation identified mild to moderate nuclear sclerotic cataracts. The fundus of the right eye was unremarkable. The optic disc of the left eye showed edema with blurred disc margins. The rest of the fundus of the left eye was normal.

A diagnosis of ischemic optic neuropathy (ION) was made. It is imperative to differentiate between arteritic ION (temporal arteritis) and nonarteritic ION. Temporal arteritis may lead to bilateral blindness if not treated promptly. Results of immediate evaluations of erythrocyte sedimentation rate and C-reactive protein level were normal. These results, as well as the absence of headaches and jaw claudication, supported the diagnosis of nonarteritic ION.

This condition is seen in elderly patients who have a systemic disorder such as hypertension, diabetes, hyperlipidemia, or generalized arteriosclerosis. A compromised autoregulatory mechanism at the anterior aspect of the optic nerve head results in decreased blood flow and ischemia. Patients experience a sudden, painless monocular loss of vision. Disc edema, often sectoral with a corresponding altitudinal visual field loss, is common during the acute phase. Optic atrophy develops in 4 to 6 weeks.

No treatment is available for nonarteritic ION. Systemic diseases should be identified and treated. *

Case 4:

A 90-year-old woman with a history of dry age-related macular degeneration in both eyes noticed blurred vision in her left eye after she rubbed her right eye. She had undergone cataract surgery in both eyes 10 years earlier and was pseudophakic. She was otherwise in good health and took only aspirin, 81 mg/d, and a multivitamin.

The patient's best corrected visual acuity was 20/25 in the right eye and 20/400 in the left. There was no afferent pupillary defect. The slit-lamp examination showed well-positioned posterior chamber intraocular lens implants in both eyes. The intraocular pressures were normal. The funduscopic examination of the right eye showed a healthy optic nerve and some mild macular mottling. Examination of the left eye showed a healthy optic nerve and revealed evidence of macular edema and hemorrhage.

A fluorescein angiogram identified an occult subretinal neovascular membrane as the cause of this patient's wet macular degeneration.Wet macular degeneration causes more severe vision loss than the dry form does, although the latter is more common. Macular edema and hemorrhaging are classic findings of wet macular degeneration. Special tests--such as fluorescein angiography--are used to differentiate between dry and wet macular degeneration and, in cases of wet macular degeneration, to distinguish between classic and occult subretinal neovascular membranes. Classic membranes may be treated with laser photodynamic therapy; occult membranes (the diagnosis in this patient) are treated with intraocular injections of antivascular endothelial growth factor agents such as pegaptanib sodium. *

Case 5:

An 87-year-old woman complained of a red tinge in the vision of her right eye. She also felt that the vision in the right eye "was just not right." She was pseudophakic in both eyes from previous cataract surgery. She had diet-controlled diabetes and took atenolol for hypertension.

The patient's best corrected visual acuity was 20/40 in the right eye and 20/25 in the left eye. There was no afferent pupillary defect. Her intraocular pressures were mildly elevated at 24 mm Hg in the right eye and 22 mm Hg in the left eye. Funduscopic evaluation of the right eye revealed venous tortuosity and retinal hemorrhages in all 4 quadrants with no significant disc or macular edema (A). A fluorescein angiogram showed no evidence of ischemia. The left fundus was unremarkable. The patient's blood pressure and blood glucose level were normal.

A diagnosis of nonischemic central retinal vein occlusion (CRVO) of the right eye was made. At a follow-up visit 1 month later, the patient reported a deterioration in the vision of this eye. Her visual acuity was now finger-counting at 4 feet. There was still no afferent pupillary defect. Funduscopic examination of the right eye revealed worsening of the venous tortuosity and an increase in the number and density of retinal hemorrhages. There was also a new cotton-wool spot superior to the disc with macular edema and a swollen optic nerve head without neovascularization (B). The worsening visual acuity and the anatomical appearance of the CRVO suggested that it was becoming ischemic.

The patient was referred to a retinal specialist and underwent a pars plana vitrectomy with radial optic neurotomy followed by an intravitreal injection of triamcinolone. The patient's hemorrhages, cotton-wool spots, and disc edema slowly resolved and no neovascularization developed (C). Unfortunately, the patient did not recover vision in this eye.

There are 2 categories of CRVO: nonischemic (perfused) and ischemic (nonperfused). Nonischemic CRVO requires just periodic monitoring; any systemic disorders, such as hypertension or diabetes, must be addressed. The ischemic type is associated with a strong probability of neovascularization of the iris, optic disc, and retina. This often leads to neovascular glaucoma and a blind, painful eye. This condition is usually treated with laser panretinal photocoagulationunless, as in this patient's case, retinal hemorrhaging prevents laser application. Investigational therapies such as radial optic neurotomy are being tested in these severe cases. *