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Chapter 9: Vitreous



"Flashing lights" (photopsia) are a common symptom of an abnormal relationship between the retina and the vitreous. The patient is aware of a localized "light," "glow," "streak of light," or "flashing" (as of a neon tube) in the field of vision in the absence of a corresponding light source in the environment. The patient can usually point to the area of the disturbance and often describes an arc-shaped flicker in the periphery of one or two quadrants. The light seldom persists for more than a fraction of a second. It frequently recurs at short intervals for a few minutes and then disappears for hours, days, or even weeks. It is most readily identified on moving the eye and when illumination is dim or absent. Bilateral episodes may occur simultaneously but more commonly are separated by an interval of days to many years.

The light represents a cerebral awareness of the initial physical traction on and excitation of the sensory retina by abnormal vitreous. It is most commonly associated with recent collapse and detachment of the vitreous due to syneresis with focal vitreous traction on vitreoretinal lesions such as lattice degeneration, meridional folds, congenital rosettes, and other vitreoretinal adhesions. A careful history will readily distinguish the light from the scintillating scotoma of migraine, which is characterized by a symmetric quivering scotoma usually in both eyes, of predictable configuration and progression, accompanied by variable nausea or headache.

The vitreoretinal traction may require no treatment. However, as it can induce retinal tears, retinal detachment (Figure 9-6), or vitreous hemorrhage, every new case requires a survey of the vitreoretinal relationship, especially in the periphery.

Figure 9-6

Figure 9-6: Schematic representation of vitreous collapse causing the retina to tear and detach.


Vitreous floaters are by far the most common symptom of abnormal vitreous. A given floater represents the patient's awareness of the shadow of a mobile vitreous opacity cast upon the retina. The mind projects the corresponding dark form onto the appropriate area of the visual field.

The term "vitreous floaters" denotes a common, potentially serious symptom that was formerly called muscae volitantes-Latin for flies that flit, flutter, or fly to and fro.

The onset may be either insidious or acute and unilateral or bilateral. The patient is aware of one or more (or even many) fine, dark forms in the field of vision. Their configuration is usually so pronounced that the patient spontaneously classifies them as "spots," "soot," "particles," "spiders," "cobwebs," "threads," "worms," "dark streaks," "a ring," etc. Combinations are often reported. The objects continue to migrate after the eye comes to rest-hence the name "floaters."

Central, relatively immobile floaters are visually annoying and may even be disabling. Peripheral ones are readily overlooked, as they are intermittent and require large eye motion or special positions merely to be seen. Unlike "flashing lights," they are most readily seen against bright lights or a uniform light background. They are extremely common in myopes and people with syneresis.

Floaters may be caused by small hemorrhages into the vitreous resulting from retinal tears or hemorrhagic diseases such as diabetic retinopathy, hypertension, leukemia, old retinal branch vein occlusions, Eales' disease, Coats' disease, and subacute infective endocarditis. Individual red cells are seen as small round black spots. Recent hemorrhages are often seen as black streaks or cobwebs that later break up into small round spots.

White cell invasion of the vitreous gel associated with pars planitis may also cause "spots before the eyes." Vitreous floaters due to pigment are usually a consequence of long-standing tear-induced detachment of the retina that has not yet reached the macula.

Vitreous floaters should never be dismissed as harmless or imaginary. A careful survey of the vitreous and retina is always indicated in order to identify the nature and origin of floaters and to decide on management. Failure to make such an examination not infrequently leads to missed diagnosis. In the absence of a serious causative pathologic process, the patient may be reassured that the condition is harmless.


Asteroid hyalosis is an uncommon condition that occurs in otherwise healthy eyes in elderly people. Unilateral cases are three times as common as bilateral cases. Hundreds of small yellow spheres consisting of calcium soaps are seen in the vitreous. These move when the eyes move but always return to their original positions because they are attached to interlacing fibers. There are no related ocular or systemic diseases. The opacities have little or no effect upon vision but reflect the examiner's light very strongly. If there are enough asteroid bodies, the fundus is not viewable by ophthalmoscopy.


The vitreous cavity is bounded by the retina, optic disk, pars plana, zonule, and crystalline lens. Normal vitreous fills this cavity and remains firmly attached to the retina and pars plana near the ora serrata.

All types of gels, whether vitreous or gelatin, become increasingly susceptible with the passage of time to a degenerative process known as syneresis, involving the drawing together of particles of the dispersed medium, separation of the medium, and shrinkage of the gel. Syneresis affects at least 65% of persons over 60 years of age. Myopes are especially susceptible, even in childhood.

With age, the center of the vitreous may undergo syneresis and become filled with liquid breakdown products of the degenerated gel (Figure 9-7). The liquid contents of the cavity can migrate into the preretinal space. The more solid, heavier vitreous gel collapses downward and forward to create a posterior vitreous detachment (Figure 9-8). The dynamic forces that accompany this collapse can rupture the last vestiges of the adhesions that once connected the vitreous to the disk, blood vessels, and sensory retina in childhood.

Figure 9-7

Figure 9-7: Large intravitreal cavity filled with liquid breakdown products of syneresis.

Figure 9-8

Figure 9-8: Posterior vitreous detachment.

The patient and examiner can often see portions of the adhesions that remain attached to the collapsed vitreous as opacities. If they arise from the disk margin, the patient and examiner may note a ring-shaped opacity on the back of the vitreous.

Since the front of the vitreous is attached to the globe and the back of the vitreous is collapsed in on itself, abrupt motions of the eye transmit a whip-like force to the back of the vitreous. The vitreous tends to fill out toward its normal configuration; liquid vitreous is drawn into the syneretic cavity, and the posterior separation tends to disappear (Figure 9-9).

Figure 9-9

Figure 9-9: Liquid vitreous tends to be drawn into intravitreal cavity on abrupt eye motion (left) and expelled at rest (right).

The whip-like motions of the vitreous can give rise to photopsia by causing stimulation of the vitreoretinal juncture and may cause a characteristic floating motion of posterior vitreous opacities, or floaters. The floaters move with the eye and float to a resting position after the eye comes to rest.

Since acute vitreous collapse can also cause asymptomatic retinal tears or detachment, it should be assumed that patients with new floaters or photopsia have retinal tears or detachment until proved otherwise by thorough examination of the peripheral retina with an indirect ophthalmoscope.

RETINAL TEARS (See also Chapter 10.)

While retinal tears can be caused by trauma, vitreous shrinkage, or proliferative vitreoretinopathy, most are caused by acute vitreous collapse. Tears following acute vitreous collapse are the result of a dynamic interaction between a focal vitreoretinal adhesion, collapsed mobile vitreous, and normal eye movement (Figure 9-10).

Figure 9-10

Figure 9-10: Local vitreoretinal adhesion.

Since the gel and liquid components of the collapsed vitreous are structurally relatively independent of the retina, they do not move synchronously with the retina. When the eye (and hence the retina) moves, the gel and liquid tend to lag behind the retina, and when the eye stops moving, the gel and liquid tend to continue in motion. The vitreous gel and liquid are said to exhibit inertial lag with respect to the retina. Inertial lag of the gel can cause the vitreous to tear the friable sensory retina at the point where they adhere to each other (Figure 9-11). The torn retina is seen to be pulled inward as a flap or a detached operculum (Figure 9-12). If retinal vessels are broken, they bleed briefly. A variable amount of blood accumulates in the vitreous cavity.

Figure 9-11

Figure 9-11: Left: Retinal tear. Right: Retinal detachment.

Figure 9-12

Figure 9-12: Left: Ophthalmoscopic view of retinal tear. Right: Ophthalmoscopic view of retinal detachment.

Some patients are not aware of the onset of retinal tears but often complain of photopsia and floaters. Some present with gross vitreous hemorrhage. Many retinal tears never lead to retinal detachment, but recent symptomatic tears, especially those with symptomatic vitreous hemorrhage, have a strong tendency to cause retinal detachment. Patients with symptoms of acute vitreous collapse or vitreous hemorrhage should therefore undergo careful examination of the retina from the optic disk to the ora serrata to rule out one or more tears. Management of tears by prophylactic laser therapy or cryopexy is relatively simple and very effective compared to the performance of silicone buckling once retinal detachment has occurred.

Retinal tears are usually located anterior to the equator and are more often in the upper quadrants (Figure 9-12 left). Retinal detachment secondary to retinal tear formation is characterized as rhegmatogenous (see Chapter 10), particularly to differentiate it from serous retinal detachment such as that due to choroidal tumor, choroidal or scleral inflammation, or choroidal neovascularization, and from tractional retinal detachment such as that due to retinal neovascularization.


Vitreous hemorrhage can occur whenever the sensory retina is torn. Retinal neovascularization secondary to diabetic retinopathy, branch or central retinal vein occlusion, and hypertension are also frequent causes of vitreous hemorrhage. Acute collapse of the vitreous with posterior vitreous detachment will sometimes cause bleeding without tear formation. The patient often complains of floaters that suggest red blood cells, a sudden shower of small black dots, or even tiny ring-like forms with clear centers. Visual loss ranges from imperceptible to gross.

The appearance of the retina and its visibility vary with the cause and amount of bleeding in the vitreous cavity (see Chapter 10). Fresh blood is red and tends to be located behind the vitreous gel or within a syneretic cavity (Figure 9-13). Within weeks to months, the blood tends to break down, becomes a pale color, and migrates into the gel (Figure 9-14).

Figure 9-13

Figure 9-13: Acute vitreous hemorrhage. A retinal vessel ruptures due to vitreous traction.

Figure 9-14

Figure 9-14: Chronic vitreous hemorrhage.

Vitreous hemorrhage in association with rhegmatogenous retinal detachment necessitates urgent retinal surgery. This often requires vitrectomy to allow adequate visualization of the retina. Vitreous hemorrhage associated with tractional retinal detachment involving the macula generally requires early vitrectomy. Traditionally, vitreous hemorrhage not associated with retinal detachment is treated conservatively for 3-6 months in the hope of spontaneous resolution. Improvements in the outcome of vitreous surgery have led to earlier surgery, particularly in patients with proliferative diabetic retinopathy.

Vitrectomy is not indicated for 3-6 months if treatment of the underlying cause can wait, as the vitreous may clear adequately without surgery.


In the normal eye, the intact sensory retina is kept opposed to the pigment epithelium by the suction the latter exerts on the watertight space between them. If a retinal tear is present, rapid eye motions and sudden rotation of the globe can readily generate enough inertial force to initiate retinal detachment (Figure 9-15). The space between the two layers of the retina fills with liquid vitreous, and eddy currents develop in this space, further accelerating the detachment process (Figure 9-16). Usually the detachment continues until it is total, particularly if the retinal tear is located superiorly.

Figure 9-15

Figure 9-15: Abrupt rotation of globe generates eddy currents in liquid vitreous, a result of inertial lag (left), that tends to lift the retinal flap and surrounding sensory retina (right).

Figure 9-16

Figure 9-16: Enlargement of retinal detachment due to inertial lag of liquid vitreous within the retina.

Surgery with retinopexy, either by cryotherapy or laser photocoagulation, and usually with silicone buckling, is required (1) to close the hole in the retina, reestablishing a watertight intraretinal space; (2) to restrict the inertial lag of the liquid and gel with respect to the retina; and (3) to approximate and seal together the two layers of the retina around the tear to counter the effects of eddy currents in the vitreous cavity. (See also Chapter 10.)


Traction retinal detachment is detachment of the sensory retina due to vitreoretinal traction, usually secondary to proliferative diabetic retinopathy, proliferative vitreoretinopathy, retinopathy of prematurity, or ocular trauma (Figure 9-17). The detachment typically involves the retina posterior to the equator and has a concave surface. Surgery is indicated if the detachment involves the macula and requires vitrectomy and removal of the tractional elements. Scleral buckling and injection of intraocular gas or silicone oil may also be necessary. In a few cases, tractional retinal detachment is complicated by retinal tear formation, leading to combined rhegmatogenous and tractional detachment. This generally requires early vitreoretinal surgery.

Figure 9-17

Figure 9-17: Traction detachment of retina.


A number of abnormal conditions of the vitreous and retina are characterized by contractile membranes arising metaplastically from abnormally located retinal pigment epithelial cells and retinal glial cells. The membranes can occur on either the inner or outer surface of the sensory retina or on several vitreous surfaces. The membranes may be weak and subtle or strong, easily seen, and capable of causing great distortion of the host tissues.

The causal retinal pigment epithelial cells and retinal glial cells are pluripotential cells, with great metaplastic potential. They may proliferate at remote sites and take on the characteristics of myofibroblasts. These myofibroblast-like cells readily form contractile membranes that may deform the inner and outer surfaces of the retina and the posterior vitreous surfaces (Figure 9-18).

Figure 9-18

Figure 9-18: Proliferative vitreoretinopathy. Left: Contracture of membrane adherent to outer retinal surface. Right: Contracture of inner retinal membrane.

The basic process, or its outcome, is known as massive vitreous retraction, preretinal traction, preretinal vitreous membrane, subretinal fibrosis, macular pucker, or surface wrinkling retinopathy.

Proliferative vitreoretinopathy requires no treatment unless it causes surface wrinkling retinopathy of the macula (also known as macular pucker) or unduly complicates therapy for retinal detachment. While research holds some promise for an antiproliferative pharmaceutical agent, current treatment involves a special surgical procedure that employs dissection, severing, or removal of vitreous tissue (see below).



Because the vitreous is inelastic compared with the adjacent tissues, contusions that abruptly though briefly alter the shape of the eye are apt to cause injuries where the vitreous is adherent.

Disinsertion of the vitreous base is not uncommon. It is frequently associated with tearing of the pars plana or retina, vitreous hemorrhage, or detachment of the retina-as long as 20 years later.

Less commonly, photopsia, vitreous floaters, and even vitreous hemorrhage or detachment of the retina may result from stress behind the vitreous base. The affected sites may be previously subclinical anomalous vitreoretinal adhesions (eg, lattice degeneration) or areas of frank vitreoretinal disease such as diabetic retinopathy.

Rupture of the Globe

Rupture of the globe is always a serious injury that may result in early or late blindness or even loss of the eyeball. Prolapse of the vitreous through the wound is a severe complication often associated with acute secondary tearing or detachment of the retina. A seemingly uncomplicated prolapse may be followed by late retinal detachment with or without tears due to fibrous ingrowth from the orbit and subsequent contraction. The latter may be visible as membranes or bands in the vitreous. Various forms of vitreous surgery are used to prevent or treat such complications.

Penetration of the Globe

An almost endless variety of material may accidentally penetrate the globe. Common examples are needles, airgun pellets, and small particles of metal, stone, or plastic that fly into the eye at high velocity.

Prolapse of the vitreous may occur at the site of entry or exit or both. The part traversed by the foreign body is permanently damaged and is often marked by visible condensation, shrinkage, or fibrous elements. Vitreous surgery is increasingly used to prevent or treat complications such as retinal detachment with or without tears.

Vitreous Loss

Vitreous loss is an iatrogenic complication. The vitreous gel prolapses through a surgical wound, usually at (but not limited to) the corneal limbus during the course of operating on the lens, iris, or cornea.

Fibrous tissue invasion and contraction are frequent sequels that are prone to cause traction complications involving the retina. Corneal edema and iris displacement (eg, "updrawn pupil") may also occur. An acute prolapse can be effectively excised. An old prolapse may require surgery for release of vitreous traction.


Vitreous inflammation includes a wide spectrum of disorders ranging from a few scattered white cells to abscess formation. Most commonly, one or more focal inflammatory lesions in the choroid or retina-as in chorioretinitis or retinitis-are responsible for a secondary cellular invasion of the liquid vitreous or relatively resistant gel. There may be a mild localized blurring of the fundus landmarks and lesions that provoke little or no visual complaint except for a possible vitreous floater effect. With greater infiltration, vision is decreased and the fundus is invisible or almost so. The condition may be so marked that the red reflection is lost and the vitreous appears opaque and white. Since these conditions spare the anterior segment, there is no pain and the external eye appears normal. The prognosis and treatment depend upon the underlying condition. The vitreous usually clears when the primary defect is quiescent. Vitreous surgery is used to remove gross residual opacities that show no sign of clearing spontaneously.

Vitreous Abscess (Endophthalmitis)*

Vitreous abscess may occur following penetrating ocular trauma, including ocular surgery or following bloodstream dissemination from elsewhere in the body, such as colonization by Candida albicans of an indwelling venous catheter. The vitreous is an excellent culture medium; following bacterial or fungal invasion, it undergoes liquefaction and abscess formation.

The diagnosis of vitreous abscess is confirmed by aspirating 0.5-1 mL of vitreous under local anesthesia through a pars plana sclerotomy using a 20- to 23-gauge needle. The aspirate should be examined microscopically.

Once the organism is identified, immediate medical treatment is indicated (see Table 3-1).

In some cases, vitrectomy is indicated to drain the abscess and allow better visualization of the fundus.

Even with optimal treatment, vitreous abscess carries a grave prognosis.

*If all three coats of the eye as well as the vitreous are involved by an inflammatory process, the condition is known as panophthalmitis. The line of demarcation between endophthalmitis and panophthalmitis is usually obscure.

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AccessLange: General Ophthalmology / Printed from AccessLange (
Copyright ©2002-2003 The McGraw-Hill Companies. All rights reserved.