Older Man With Visual Symptoms of Acute Onset

For more than a week, a 74-year-old man has had diminished vision in his left eye. He reports that the problem started acutely with a sensation of flashing lights in the affected eye, followed by the presence of dark floaters for several days. He initially had minimal vision loss in the lateral (temporal) field, but with each day the loss has become more profound and central; it now significantly impedes his ability to read and perform activities of daily living. He denies headaches or other neurological symptoms either before or during this episode.

HISTORY

The patient is relatively healthy for his age. He has had mild hypertension for about 10 years, which is well controlled with lisinopril, 10 mg/d; he has no history of coronary disease or diabetes mellitus. He sees an optometrist regularly and had a complete examination 4 months earlier, with no change in his eyeglass prescription.

PHYSICAL EXAMINATION

Heart rate is 76 beats per minute; respiration rate, 14 breaths per minute; and blood pressure, 110/68 mm Hg. Eyes appear normal, without inflammation, and cranial nerves are intact. Funduscopy is deferred until consultation with an ophthalmologist. The remainder of the physical findings are normal.

LABORATORY RESULTS

A complete blood cell count and chemistry panel are normal. Total cholesterol level is 175 mg/dL, with a high-density lipoprotein cholesterol level of 62 mg/dL. Triglyceride level is 98 mg/dL.

CORRECT ANSWER: C

This patient experienced an acute unilateral ocular syndrome followed by subacute deterioration in vision. On the basis of the clinical findings, primary retinal detachment (choice C) is the most likely diagnosis.

Epidemiology and symptoms of primary retinal detachment. Primary retinal detachment is an extremely common and age-dependent event. Roughly 10% of cases are in persons younger than 60 years; 27% are in persons between the ages of 60 and 70 years; and 63% are in persons older than 70 years.¹ This patient's symptoms are classic: flashing lights and floaters followed by a progressive loss of visual field.

Pathophysiology of primary retinal detachment. Lifelong liquefaction of the vitreous is responsible for floaters, which result from debris being able to move in the more liquid vitreous. This more liquid vitreous may also dissect into atrophic holes or tears in the retina; the herniated fluid can then force the retina into the subretinal space, thereby detaching the neural retina from the posterior structures of the eye (the pigmented epithelium and the choroid). This separation distorts the visual anatomy and can cause further retinal tears in areas of strong vitreoretinal adhesion. If detachment progresses to include the macula, profound loss in visual acuity occurs. (Nonmacular detachments produce lesser degrees of vision loss.)

Treatment of primary retinal detachment. Retinal detachment is an ocular emergency. Most studies have shown that posttreatment visual acuity is inversely proportional to the time between onset of symptoms and repair. The most cited studies indicate that 1 week is the critical time window for repair; results are inferior when surgical repair is not performed within 7 days.^1,2

A variety of surgical techniques are available, including pneumatic retinopexy, scleral buckling, and vitrectomy.¹ Repair can usually be performed in the ophthalmologist's office. Determining the most appropriate technique depends on the particular findings in a given case and is beyond the scope of this discussion.

Age-related macular degeneration. This potentially blinding disease affects, at least to some degree, as many as one-third of persons older than 75 years. Unlike the syndrome in this patient, age-related macular degeneration (choice D) has an insidious rather than an abrupt onset; it develops gradually and painlessly.³

Amaurosis fugax. This condition is characterized by an acute partial loss of vision often described as "a shade covering one eye." However, the vision loss is transient, usually lasting only seconds to minutes before reversing. Amaurosis fugax (choice B) is caused by ischemia in the ophthalmic artery, typically resulting from carotid atherosclerosis. Episodes are often premonitions of more serious cerebrovascular events.⁴ This patient's history of progressive loss of vision over a period of days does not fit this diagnosis.

Scintillating scotoma. This is another acute-onset ocular syndrome. Scintillating scotoma (choice A) is characterized by the presence of a flickering spot, followed by a spreading arc of flashing lights that prevents vision within the scotoma. Its pathophysiology puts it within the spectrum of migraine syndromes (it is a type of acephalgic migraine). As with amaurosis fugax—but again, unlike the syndrome in this man—the symptoms of scintillating scotoma are transient; they almost always pass within 60 minutes, and usually within 5 to 20 minutes.

Outcome of this case. An ophthalmologist was consulted, and funduscopy with pupil dilation confirmed a retinal detachment involving the macula, with tears at superior fundus positions. Pneumatic retinopexy was performed in the office, with good results. The patient was advised that subsequent procedures may be required and that careful monitoring is mandatory.