Flashes and floaters are the most common emergency complaints the patient presenting to an ophthalmologist. Symptoms occur in approximately 50% of patients over fifty years of age and increase in frequency with age. These symptoms are worrisome since they may be a manifestation of a retinal tear or detachment which visual threatening events. As such, all patients complaining of flashes and floaters should be evaluated by an ophthalmologist.


Historically, floaters have been described since the Roman Empire and were called “musce volatante” (a floating fly). This is a descriptive term for the condensations of the vitreous cavity casting a shadow on the retina producing the floaters. The vitreous gel maintains the volume of the spherical shape of the eye and is located between the posterior aspect of the lens-iris diaphragm and the retina. The vitreous is a gel-like substance derived from collagen and hyaluronidase. The vitreous collagen forms fibers which consolidate to attach to the peripheral and posterior retina (actually the outer most layer of the retina, the internal limiting membrane). Hyaluronic acid is the resin filling the vitreous cavity. With age hyaluronic acid liquefies enhancing the mobility of the vitreous precipitating detachment of the vitreous from its anterior or posterior base. In addition, the vitreous collagen fibers thicken and become tortuous creating pockets of liquid vitreous. When the vitreous is detached posteriorly the entire vitreous body can shake with ocular movement. This shimmering is similar to shaking a bowl full of Jell-O. Motion of the collagen fibers within the eye will be perceived as floaters. Floaters can appear as different shapes such as dots, circles, lines, clouds or cobwebs. If vitreous traction is significant, pulling the peripheral retina will create flashing lights or lightening strikes. Flashes of lights can appear intermittently for months after a posterior vitreous detachment. However with time this will gradually subside. When the vitreous detaches it may result in a hemorrhage increasing floaters and severity can reduce visual acuity. If adhesions with the macula are broken this can result in the formation of a macular hole with a dramatic reduction of visual acuity.

Posterior vitreous detachments are more common in people who are:
*following cataract surgery
*inflammations or trauma


Flashes of light may appear as jagged lines or heat waves in both eyes lasting 15-30 minutes. These symptoms are caused by a spasm of blood vessels within the brain and are called an ophthalmic migraine. Only approximately 30% of ophthalmic migraines progress to a classic migraine with a severe headache. The key to ophthalmic migraines is transient in nature and these may occur individually or in clusters.


Retinal holes or tears occur when the retina is pulled away from its normal position. If the detached retina no longer functions is perceived as a shadow. Usually the peripheral vitreous separates from the retina without problems. However stronger adhesions occur at the peripheral base and a hole or tear develops with vitreous separation. Fluid can pass through the tear lifting the retina and creating a retinal detachment. Symptoms of retinal detachments are:
*flashing lights
*new floaters
*gray shadows or curtain across visual field
*loss of visual acuity
As you can see, retinal tears and posterior vitreous detachments share symptoms. As such, it is imperative to have patient’s evaluated to insure there are no visual threatening sequela.


There is no medical or surgical treatment for posterior vitreous detachment. Most floaters gradually resolve with time and are well tolerated. Very rarely one would remove the vitreous if symptoms were extremely debilitating.

However, if symptoms persist or worsen a retinal hole may develop. This occurs in approximately 1-2% of patients with a posterior vitreous detachment. Surgical treatment is performed by a specialist in retinal disease. This may consist of focal laser treatment to reduce choroidal-retinal adhesions or more formal surgical intervention. A scleral buckle with an associated vitrectomy to reduce traction may be required to compress the globe to reattach the retina.

The important concept is flashes and floaters are significant ocular sequela and should be properly addressed to rule out significant retinal pathology.

When the vitreous separates from the peripheral retina it may tear a retinal vessel creating a vitreous hemorrhage. Depending on the severity of the bleeding will produce fine floaters or a generalized clouding of the visual acuity. If vitreous adhesions with the macula are violated a macular hole may develop with a sudden and dramatic reduction of visual acuity.


Fluctuations of visual acuity would not be complete without addressing amaurosis fugax. Transient ischemic attacks of the retinal arterial auscultation are known as amarousis fugax (fleeting blindness). This is a transient visual lens usually progressing from the periphery toward the central vision. Vision loss may vary but can progress to complete blindness. Generally visual acuity returns in 1 to 20 minutes. Etiology of these attacks is micro embolic material in the form of fibrin platelet aggregates that momentarily occlude retinal vessels. These aggregates then disintegrate with reconstitution of blood flow. If the fibrin platelet aggregate does not dissolve then permanent ischemic damage results to the inner retinal layers. (Figure ). The major source of retinal micro emboli is the extra cranial internal carotid artery especially at the level of the bifurcation. This may occur in 50-65% of patients and is evident by the presence of a carotid bruit. Evaluation of the carotids is imperative if symptoms are suggestive.