Posterior vitreous detachment

How to approach sudden-onset floaters and flashing lights

Curtis E. Margo, MD, MPH; Lynn E. Harman, MD

VOL 117 / NO 3 / MARCH 2005 / POSTGRADUATE MEDICINE

CME learning objectives

• To review the composition of the vitreous and how aging causes its separation from the retina and the optic nerve
• To become familiar with the symptoms of acute posterior vitreous detachment and the optical basis for floaters
• To be able to identify a management strategy for symptomatic posterior vitreous detachment on the basis of results of an eye examination

The authors disclose no financial interests in this article and no unlabeled uses of any product mentioned.

Preview: Acute posterior vitreous detachment (PVD) is the most common cause of unilateral floaters and flashing lights. These visual experiences are frightening to the patient, and they are usually accompanied by few, and often subtle, physical findings on eye examination. Patients with symptomatic PVD are at risk for retinal detachment and vision loss. In this article, the authors discuss the evaluation and management of unilateral floaters and flashing lights.
Margo CE, Harman LE. Posterior vitreous detachment: how to approach sudden-onset floaters and flashing lights. Postgrad Med 2005;117(3):37-42

The sudden perception of flashing lights or of objects that do not correspond to those in the environment is an alarming experience that often causes persons to seek urgent medical attention from their primary care physician or local emergency department. When these startling visual images are due to PVD, usually few or subtle objective findings are evident on ocular examination. The disparity between a patient's complaint and the paucity of physical findings in this setting can lead to unnecessary neuroradiologic studies.

Although a wide variety of diseases cause entoptic images and visual hallucinations, the differential diagnostic considerations are substantially reduced to disorders of the anterior visual pathway when the symptoms are reliably localized to one eye (table 1). Acute PVD is the most common cause of sudden-onset entoptic imagery and photopsias.

Table 1. Causes of visual hallucinations and entoptic images
Monocular	Comments
Posterior vitreous detachment, spontaneous	Age-related; occurs at younger age in high myopia; 15%-30% of cases associated with related retinal disease
Posterior vitreous detachment, traumatic	Risk of retinal tear; needs thorough fundus examination
Anterior visual pathway migraine	One third of cases occur in persons with history of common or classic migraines; diagnosis of exclusion
Retinal ischemia	Positive visual phenomenon has been reported with arterial and venous circulatory impairment
Multiple evanescent white-dot syndrome	Occurs in young to middle-aged women; subtle retinal findings
Acute idiopathic big blind spot syndrome	Occurs in young to middle-aged women; subtle peripapillary and retinal changes; overlaps with multiple evanescent white-dot syndrome
Optic neuropathy	Sound-induced phosphenes associated with demyelinating disease
Mass lesion of choroid or retina	Retinal phosphenes as a manifestation of choroidal melanoma or other mass lesions
False localization to one eye	Often found in hemianopia visual phenomenon
Binocular	Comments
Migraine	Ranges from classic fortification scintillation scotoma to photopsias; acephalgic migraine
Epilepsy	Pattern and type of hallucination depend on anatomic site of neural discharge
Vertebrobasilar insufficiency	Lacks stereotypical pattern of migraine; does not enlarge or "march" across visual field
Midbrain infarct	Varies from colored lights to complex visual forms
Acute confusional state	Secondary to metabolic, nutritional, infectious, or organ system failure diseases
Drug-related hallucination and imagery	Sedative-hypnotics, opioids, anticholinergics, and recreational drugs are most often implicated
Severe blindness	Charles Bonnet syndrome; occasionally affects one eye
Narcolepsy	Lasts minutes; occurs on entering sleep or awakening

Entoptic imagery and hallucinations

Visual experiences that do not correspond to any external environmental object can be placed into two broad categories: (1) entoptic imagery (visual perceptions produced by intrinsic structures of the eye) or (2) hallucinations (1). See glossary at end of article for definitions of visual terms used in this article.

When entoptic images are caused by an ocular media opacity, the opacity can usually be identified on eye examination. Visual hallucinations, on the other hand, are attributed to abnormal stimuli or the release of inhibitory control at susceptible points in the visual pathway, visual association areas or, rarely, the brainstem. Vitreous traction on the retina is a common stimulus for flashing lights (eg, retinal phosphenes, photopsias), which, depending on definition, can be considered either an entoptic image or a visual hallucination.

Pathophysiologic factors

The vitreous, which makes up 80% of the volume of the ocular globe, occupies the space bound by the lens and retina and has the physical and chemical properties of a dilute gel. It is composed mostly of water and contains various amounts of salts, soluble proteins, glycoproteins, and glycosaminoglycans (mostly hyaluronic acid). It is interwoven by a network of collagen fibrils (2).

The vitreous minimally scatters light and is acellular except for a small number of modified macrophages called hyalocytes. Small amounts of acellular debris from the embryonic hyaloid vascular system are found in the normal vitreous and are responsible for most physiologic floaters. The vitreous is adherent to the ora serrata anteriorly and to the optic nerve head and macula posteriorly. Adhesions to some superficial retinal vessels also occur.

The most common abnormality of the vitreous is liquefaction, or syneresis. A number of conditions (eg, high myopia, inflammation) are associated with or cause abnormal vitreous liquefaction, which is also a consequence of aging. Once liquefied, the vitreous cannot be reconstituted. Although the mechanism of age-related syneresis is not fully understood, the process is linked to cortical vitreous separation from the sites of attachment to the retina and optic disc. Early signs of posterior vitreous collapse and separation from the macula begin in middle age (3). Nearly two thirds of persons aged 65 years and older have identifiable PVD (2).

Optical basis for floaters
Floaters are perceived as shadows cast on the retina by vitreous opacities. Patient awareness of floaters depends on the opacities' size, optical density, and distance from the retina and, to a lesser extent, on pupil size and type of background illumination (4). The closer a small vitreous opacity is to the retina, the larger its central, dark shadow becomes. Movement of the eye stirs the vitreous so that any suspended debris causes the shadows to move correspondingly.

Attempts to look directly at off-center floaters are frustrated by the seemingly elusive movements of these particles away from fixation. When a vitreous opacity is anterior to the axis of ocular rotation, movement of the entoptic image is in the opposite direction of gaze; when the opacity is behind the axis, movement of the entoptic image is in the same direction of gaze. As the diameter of the pupil increases, entoptic shadows become smaller. Thus, vitreous floaters are less noticeable after pharmacologic mydriasis.

Vitreous floaters are most apparent when there is uniform background illumination, such as a pale blue sky or a white wall. The patterns of visual sensation caused by vitreous opacities are highly specific and are not easily mistaken for other types of entoptic imagery or hallucination.

Clinical history

The abrupt separation of vitreous from its attachments on the retina and optic disc is usually heralded by the onset of flashing lights in the temporal field of vision and one or more new floaters. The luminous flashes usually have a vertical orientation, are exacerbated by rapid eye movement, and exhibit physiologic fatigue. The process is painless. The description of floaters as "numerous" or "too many to count" suggests that red blood cells, pigment cells, or pigment granules (from the retinal pigment epithelium) are present in the vitreous.

Ocular examination

Patients with unilateral flashes and floaters require a complete eye examination that includes measurement of visual acuity, tests of pupillary light reaction and confrontation fields, slit lamp biomicroscopy of the anterior and posterior segments, thorough inspection of the vitreous, and dilated fundus examination with indirect ophthalmoscopy and scleral depression.

On examination, the detached posterior hyaloid can be visualized with careful ophthalmoscopy. This diaphanous tissue has a variety of configurations. The posterior hyaloid attachment to the optic disc, for instance, typically appears donut-shaped. Signs of inflammation are usually absent with an uncomplicated PVD. Red blood cells in the vitreous indicate that a retinal vessel has been severed. Cellular, or free, melanin, which is described as "tobacco dust," is presumptive evidence of a full-thickness retinal tear.

Prognosis

Between 15% and 30% of patients with symptoms of acute PVD have a retinal hole when first examined (5,6). Prophylactic treatment is often recommended for symptomatic retinal holes because of the risk of retinal detachment and vision loss (5). The risk of a retinal tear is substantially increased when symptomatic PVD is associated with "clouds" of small floaters (ie, vitreous red blood cells or pigment cells) (6,7). Patients with symptomatic PVD without a retinal hole need to be told what symptoms to expect should a retinal tear or retinal detachment occur. Instructions on how to obtain prompt follow-up evaluation are critical (table 2).

Table 2. Management of symptomatic posterior vitreous detachment

If retinal detachment is detected, refer patient immediately for treatment. If retinal tear, signs of vitreous hemorrhage, or presence of vitreous pigment cells is identified, refer patient immediately to rule out retinal detachment or to obtain prophylactic treatment for retinal tear as needed. If examination rules out retinal lesions and presence of vitreous cells, educate patient about symptoms of retinal tears and detachment (ie, increase in flashing lights or floaters or decrease in central or peripheral vision) and why any of these symptoms requires prompt follow-up with an ophthalmologist. Fundus examination in 5 to 6 wk will increase detection of retinal tears. If patient has symptoms of posterior vitreous detachment but dilated fundus examination is inadequate or incomplete, promptly refer patient to an ophthalmologist for dilated fundus examination with scleral depression. The optimal and acceptable time frame for referral in this setting is subject to debate. We recommend consulting an ophthalmologist and allowing him or her to decide on a case-by-case basis the appropriate time frame for referral.

Occasionally, patients who have symptomatic PVD present with retinal detachment (figure 1). On fundus examination, the elevated neurosensory retina often draws attention away from the more subtle PVD. However, even rhegmatogenous retinal detachments can be difficult to identify when they are peripheral or shallow or when the fundus is obscured by red blood cells. Ocular ultrasonography is useful in identifying a detached neurosensory retina when direct visualization is not possible because of vitreous hemorrhage.

Differential diagnostic considerations

Incomplete PVD, multiple evanescent white-dot syndrome, anterior visual pathway migraine, and a number of other conditions can cause symptoms similar to those of acute PVD.

PVD in evolution
Incomplete PVD, or PVD in evolution, can cause lightninglike flashes but may not have advanced enough for the posterior hyaloid to cast a shadow on the retina. Patients with incomplete PVD need to be informed about the significance of any new visual symptoms and what to do should complete PVD, retinal tear, or retinal detachment occur.

Multiple evanescent white-dot syndrome
This syndrome usually affects young to middle-aged women. Patients present with unilateral, mildly decreased vision and complain of seeing black spots and flashing lights (8). Most are healthy, although some have a recent history of flulike illness. Visual acuity ranges from 20/40 to 20/100. Ocular examination is remarkable for small white dots at the level of the retinal pigment epithelium. The syndrome shares many features of acute idiopathic enlarged blind spot syndrome, which may be part of the same disease spectrum (9).

Anterior visual pathway migraine
The diagnosis of retinal and optic nerve migraine must be made only after other causes of transient, unilateral scintillating scotoma and photopsias have been excluded. Visual episodes of migraine usually last between 15 and 45 minutes, and an ipsilateral headache, eye ache, or feeling of discomfort may develop afterward. Visual aura without headache has similar features to that with headache. As many as one third of patients have a history of common or classic migraine. If the patient is examined during a visual disturbance, transient vasoconstriction of the vessels in the retina or optic disc may be observed.

Miscellaneous conditions
Unilateral photopsias have been reported with ocular ischemic syndrome due to carotid artery disease, retinal vascular disease, tumors and inflammatory conditions of the posterior eye, macular edema, and demyelinating optic neuropathy. Floaters can be caused by any type of vitreous opacity, including red blood cells, inflammatory cells, tumor cells, or amyloid. Objective clinical findings supporting these underlying conditions are usually apparent with complete eye examination (see table 1).

Summary

Symptomatic PVD is a common age-related problem that in some patients is associated with retinal tear and retinal detachment. Thorough ocular examination of patients with unilateral floaters and photopsias is needed to identify those at greatest risk for vision loss. Patients without retinal pathologic findings on initial examination need to be given careful instructions on what to expect and do should symptoms of retinal tear or detachment occur.

Glossary Entoptic imagery: Visual phenomenon that originates inside eye (eg, vitreous cells casting shadows on retina are perceived as floaters). Intraocular structures that produce images may be normal or pathologic. Ocular media: Normally transparent tissues of eye (ie, tear film, cornea, aqueous humor, lens, and vitreous humor). Posterior vitreous detachment: Separation of formed vitreous gel from its attachments to retina and optic nerve head. When associated with sudden onset of visual symptoms, process is usually referred to as acute posterior vitreous detachment. Photopsia: Visual phenomenon consisting of unformed images that do not correspond to environmental objects (usually flashing lights and floaters). Phosphene: Visual sensation of bright or flashing lights from sources other than external light stimulation to retina. Best seen in dark-adapted state. Sources of retinal stimulation include mechanical pressure on globe, vitreous traction on retina, and even gamma radiation when orbiting earth at high altitudes. Rhegmatogenous retinal detachment: Separation of neurosensory retina from its underlying retinal pigment epithelium, caused by retinal tear. Retinal tears are due to tractional forces exerted on neurosensory retina by the vitreous. Scintillating scotoma: Type of visual defect described as bright spot, glowing image, shimmering light, or heat wave. Often, but not exclusively, associated with migrainous episodes. Scleral depression: Examination technique in which sclera is mechanically depressed with blunt instrument while examiner simultaneously inspects peripheral retina with indirect ophthalmoscope. Standard method to identify peripheral retinal disease. Visual hallucination: Visual perception that does not correspond to objects in environment. Vitreous syneresis: Liquefactive degeneration of vitreous gel. Usually an age-related phenomenon, but can be secondary to intraocular inflammation, infection, tumor, or high myopia.

References

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4. Serpetopoulos C. Optical explanation of the gradual disappearance of flying dots in posterior vitreous detachment. Surv Ophthalmol 1997;42(1):92-4
5. Management of posterior vitreous detachment, retinal breaks, and lattice degeneration. San Francisco: American Academy of Ophthalmology, 1998
6. van Overdam KA, Bettink-Remeijer MW, Mulder PG, et al. Symptoms predictive for the later development of retinal breaks. Arch Ophthalmol 2001;119(10):1483-6
7. Brod RD, Lightman DA, Packer AJ, et al. Correlation between vitreous pigment granules and retinal breaks in eyes with acute posterior vitreous detachment. Ophthalmology 1991;98(9):1366-9
8. Friedman SM. White dots in the retina. In: Margo CE, Hamed LM, Mames RN, eds. Diagnostic problems in clinical ophthalmology. Philadelphia: WB Saunders, 1994:542
9. Volpe NJ, Rizzo JF III, Lessell S. Acute idiopathic blind spot enlargement syndrome: a review of 27 new cases. Arch Ophthalmol 2001;119(1):59-63

Dr Margo is an ophthalmologist and pathologist, department of ophthalmology, Watson Clinic, Lakeland, Florida. Dr Harman is a staff physician at the James Haley Veterans Hospital and clinical assistant professor of ophthalmology, University of South Florida College of Medicine, Tampa. Correspondence: Lynn E. Harman, MD, James Haley Veterans Hospital, Bldg 36, 13000 Bruce B. Downs Blvd, Tampa, FL 33612.

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