9
Vitreous
Steve Charles, MD
INTRODUCTION
During the past four decades, there has been an explosion of interest in the vitreous due to the development of vitreoretinal surgery. Previously large numbers of patients were blinded by vitreoretinal diseases. One goal of this chapter is to help the medical student, intern, resident, general ophthalmologist, and optometrist become aware of the indications for vitreoretinal surgery, many of which are time sensitive. Many vitreoretinal conditions have implications for the family medical practitioner, internist, and emergency physician.
VITREOUS ANATOMY AND ITS RELEVANCE TO PATHOLOGY
The vitreous fills the space between the lens and the retina and consists of a three-dimensional collagen fiber matrix and a hyaluronan gel (Figure 9–1). The outer surface of the vitreous, known as the cortex, is in contact with the lens (anterior vitreous cortex) and adherent in varying degrees to the surface of the retina (posterior vitreous cortex) (Figure 9–2).
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Figure 9–1. The vitreous consists of a three-dimensional matrix of collagen fibers and a hyaluronan gel.
Figure 9–2. The vitreous cortex is adherent to the lens and especially to the retinal surface to varying degrees.
Aging, hemorrhage, inflammation, trauma, myopia, and other processes often cause hypocellular contraction of the vitreous collagen matrix. The posterior vitreous cortex then separates from areas of low adherence to the retina and may produce traction on areas of greater adherence. The vitreous base extends from the equator anteriorly and is a zone of permanent and strong adherence. The vitreous never detaches from the vitreous base. The vitreous is also more adherent to the optic nerve and, to a lesser extent, the macula and retinal vessels. Adherence to the macular region is a significant factor in the pathogenesis of epimacular membrane, macular hole, vitreomacular schisis, and vitreomacular traction syndrome.
Previously it was taught that the vitreous developed cavities from a process known as syneresis, ultimately resulting in “collapse” of the vitreous. It is now believed that collagen cross-linking and selective loss of retinal adherence rather
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than cavity formation are the primary events. Even though the vitreous may migrate inferiorly when separated from the retina, this process causes less force at the zones of vitreoretinal adherence than the traction caused by saccadic eye motion. Saccadically induced, dynamic forces play a significant role in the development of retinal breaks (tears), damage to the retinal surface, and bleeding from torn vessels (Figure 9–3). Further contraction of the vitreous caused by invasion of retinal pigment epithelial, glial, or inflammatory cells may result in sufficient static traction to detach the retina without retinal tears.
Figure 9–3. Motion of partially detached vitreous (white arrow), induced by saccades (black arrow) and resulting in a retinal break (arrowhead).
Prior to vitreoretinal surgery, vitreous “bands” were thought to cause traction on the retina, and largely unsuccessful attempts were made to cut them with scissors. The visualization provided by vitreoretinal endoillumination systems has contributed to our knowledge of anatomy and demonstrated that these bands are contiguous with the transparent posterior vitreous cortex, which is also responsible for substantial traction. Traction bands virtually only exist when penetrating trauma creates a path through the vitreous or from severe necrosis, usually from Toxocara canis infection. Even these bands are usually contiguous with the posterior vitreous cortex.
EXAMINATION OF THE VITREOUS AND VITREORETINAL INTERFACE
Normal vitreous is essentially transparent but is capable of exerting substantial force on the retina. Vitreoretinal traction can often be inferred by the
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configuration of the retinal surface (Figure 9–4). Transparent vitreous is best seen with a narrow, off-axis slitbeam using a three-mirror contact lens and stereo biomicroscopy (Figure 9–5). Visualization is significantly enhanced by dark adaptation of the observer. A biomicroscope with a broad, on-axis slitbeam or a direct ophthalmoscope is not suitable for observing the vitreous.
Figure 9–4. Abnormal retinal configuration (white arrows) indicating vitreoretinal traction (black arrows).
Figure 9–5. Narrow, off-axis slitbeam, contact lens, and biomicroscope offer the best view of transparent vitreous.
Indirect ophthalmoscopes provide a large field of view, are capable of looking “around” some lenticular and vitreous opacities, and provide a stereoscopic view. Many observers only attempt to look “through” the vitreous, ignoring the opportunity to look “at” the vitreous, especially if it is abnormal. Visualization of vitreoretinal traction is enhanced rather than adversely affected by eye motion. In addition, mobility of the vitreous is an excellent gauge of the extent of vitreoretinal traction. It is often possible to see some portion of the retina in eyes with substantial vitreous hemorrhages by looking at the periphery first to establish a plane of focus, known as the visual horopter. The viewing path length through semi-opaque vitreous is much less in the periphery than when
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attempting to visualize the optic nerve. The vitreous is often clearer superiorly. Sitting the patient up for a period of time may cause blood to migrate inferiorly, enabling a better view of the retina.
If the vitreous is too opaque to visualize the retina, B-scan ultrasonography should be used to determine if the retina is attached or a tumor, foreign body, dislocated lens, dislocated intraocular lens, or choroidal detachment is present (Figure 9–6).
Figure 9–6. B-scan ultrasonogram.
Optical coherence tomography (OCT) uses light to construct a threedimensional (3D) model of the macula and posterior retina. The 3D model is constructed from a series of optical B-scan images (see Chapter 2). Spectral domain OCT with tracking produces much better resolution and has much shorter acquisition times than the initial time domain OCT (Figure 9–7). The resolution is approximately 5 μm. OCT is ideal for visualization of vitreomacular traction, epimacular membranes, macular holes, macular cysts, macular edema, vitreomacular schisis, subretinal fluid, pigment epithelial detachments, and choroidal neovascular membranes.
Figure 9–7. Spectral domain optical coherence tomography.
SYMPTOMS OF VITREORETINAL DISEASE
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FLOATERS
Most people experience “floaters” at some point during their life. These may be described as strings, spider webs, small saucer-like objects, or a transparent ring. Posterior vitreous detachment occurs in at least 70% of the population and causes the majority of floater complaints. Most floaters prove to be clinically insignificant after examination of the retina fails to reveal any retinal breaks or other pathology. Careful, timely, peripheral retina examination using an indirect ophthalmoscope through a widely dilated pupil is essential any time a patient complains of the onset of floaters. Any change in the nature of floaters is also an indication for peripheral retinal examination within a few days. Floaters secondary to posterior vitreous separation are better termed vitreous “condensations” to emphasize their origin from preexisting vitreous collagen fibers and surfaces. Erythrocytes and, on occasion, inflammatory cells can result in the patient seeing floaters, often described as saucer-like. A ring-like floater is usually a result of visualizing the zone of posterior vitreous cortex previously adherent to the optic nerve. Vitreous hemorrhage (Figure 9–8) requires careful examination to determine if an avulsed vessel or vascular disease such as diabetic retinopathy, venous occlusive disease, hemoglobinopathy, or leukemia is present. The presence of inflammatory cells demands a workup for lymphoma, sarcoidosis, candidal infection, and other systemic disorders. Although floaters are common, it is crucial that careful retinal examination be done before a patient is reassured that only posterior vitreous separation has occurred.
Figure 9–8. Vitreous hemorrhage.
Small, uniform, spherical, golden objects known as asteroid hyalosis
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frequently occur in the vitreous (Figure 9–9). Although they have an impressive appearance, they almost never interfere with vision and need no treatment. It was once taught that asteroid hyalosis is associated with diabetes, but this was subsequently disproved.
Figure 9–9. Asteroid hyalosis.
Vitrectomy is very rarely indicated for floaters. Many patients overreact to floaters and need counseling rather than surgery with its risk of retinal detachment and cataract. Although some ophthalmologists perform YAG laser vitreolysis for floaters, this is rarely effective and also has risk of retinal detachment and cataract.
LIGHT FLASHES (PHOTOPSIA)
Light flashes, better termed “photopsia,” are caused by mechanical stimulation of the retina, usually secondary to the vitreous separating from the retina. Jagged, lightning-like, bilateral scintillating scotomas secondary to migraine (50% are not accompanied by a headache) are often mistakenly confused with photopsia. The majority of patients experiencing posterior vitreous separation will experience light flashes, especially during saccades, until separation has stabilized. Posterior vitreous separation is never “complete” as the vitreous always remains attached to the peripheral vitreous base. Any patient with the recent onset of photopsia must have a timely, careful examination of the retinal periphery with a dilated pupil and indirect ophthalmoscope.
VITREORETINAL DISEASES
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VITREOMACULAR DISEASE
In many vitreomacular diseases, OCT is superior to clinical examination and essential to diagnosis and treatment decisions.
Epimacular membranes (EMM) are usually caused by posterior vitreous separation. It is thought that excessive adherence of the posterior vitreous cortex to the retinal surface results in a partial-thickness retinal defect during the process of separation. Glial cells migrate through the defect onto the retinal surface and cause hypocellular contraction. EMM is treated by vitrectomy and membrane peeling, best performed with end-opening forceps, although pics and other tools are used as well. Peeling the internal limiting membrane (ILM) after peeling the EMM hastens visual recovery and eliminates striae. Patients with EMM complain of metamorphopsia and reduced vision. Usually they experience dramatic improvement after the EMM and ILM are removed.
Vitreomacular traction syndrome (VMT) was thought to be rare until the availability of OCT. It is thought that excessive adherence of the posterior vitreous cortex to the retinal surface, coupled with hypocellular vitreous contraction, results in VMT. In some cases, a layer of posterior vitreous cortex separates from the vitreous body, remaining attached to the retina and then contracting. More typically, the taut posterior vitreous cortex adherent to the macula creates macular elevation, distortion, and reduced vision. Vitrectomy usually with ILM peeling is extremely effective in managing these cases.
Macular hole development is related to posterior vitreous separation, but the exact mechanism is unknown. The Gass classification adds nothing to management decisions. The core issue is to determine by OCT if the hole is partial or full thickness. Partial-thickness holes require vitrectomy, ILM peeling, and SF6 gas if they are symptomatic or if macular cysts or schisis is present, but otherwise, they can be observed. Full-thickness holes require vitrectomy, ILM peeling, and SF6 gas, which results in at least 90% chance of significant visual improvement.
RETINAL BREAKS & RHEGMATOGENOUS RETINAL
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DETACHMENT
As described earlier, posterior vitreous separation in eyes with abnormal vitreoretinal adherence can result in retinal tears (breaks). Retinal breaks occur more commonly in patients with myopia as they may have lattice degeneration, which is genetically linked to myopia. Symptomatic retinal breaks are said to be more significant than asymptomatic, although patients vary widely in their reporting of symptoms. Large tears are more significant than small tears, although very small flap tears often cause retinal detachment. Small round holes, especially those inside lattice degeneration, seldom cause retinal detachment. Operculated holes or round atrophic holes are less likely to cause retinal detachment than flap (horseshoe) tears (Figure 9–10).
Figure 9–10. Passage of liquid vitreous through horseshoe retinal tear leading to retinal detachment.
DIABETIC RETINOPATHY
Patients with proliferative diabetic retinopathy may bleed into the vitreous from retinal neovascularization. These patients must be managed aggressively with eye-saving panretinal photocoagulation, often combined with anti-VEGF (vascular endothelial growth factor) therapy with intravitreal injections of ranibizumab (Lucentis), aflibercept (Eylea), or bevacizumab (Avastin), although such anti-VEGF therapy is not approved by the US Food and Drug Administration. If the blood prevents visualization of the retina, ultrasound examination must be performed to rule out traction retinal detachment.
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Vitrectomy can be done to improve vision and apply endopanretinal photocoagulation (Figure 9–11).
Figure 9–11. Endolaser retinal photocoagulation.
Diabetic traction retinal detachments are managed using vitreoretinal surgery, incorporating techniques such as scissors segmentation (Figure 9–12) and delamination (Figure 9–13) of epiretinal membranes. Coagulation of transected neovascularization preferably is accomplished using endolaser or optionally bipolar diathermy probes (Figure 9–14).
Figure 9–12. Scissors segmentation of epiretinal membrane to release tangential traction.
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Figure 9–13. Scissors delamination to remove adherent epiretinal membrane.
Figure 9–14. Coagulation of transected vessels with bipolar endoilluminator during segmentation or delamination.
COMPLICATIONS OF CATARACT SURGERY
Approximately 0.5–1% of cataract surgery patients ultimately develop rhegmatogenous retinal detachment, presumably related to alterations in the vitreous during or after surgery. These patients present with light flashes, photopsia, loss of peripheral vision, and loss of central vision if the macula is detached. Posterior capsule rupture and vitreous loss are often said to occur after 1% of cataract surgeries, but some evidence suggests that the incidence probably is closer to 5%. Retinal detachment is more common after capsule rupture, vitreous loss, and anterior vitrectomy, especially if cellulose sponge vitrectomy is used (Figure 9–15).
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Figure 9–15. Vitreous traction during and after cataract surgery can lead to retinal breaks and detachment.
Capsule rupture during cataract surgery may result in displacement of lens material or occasionally the entire lens into the vitreous. Inflammation and phacolytic glaucoma usually develop unless only a small amount of cortex is dislocated. Vitrectomy plus lens fragmentation is very effective in removing posterior dislocated lens material (Figure 9–16).
Figure 9–16. Vitrectomy with contact lens and endoillumination to allow fragmentation and removal of posterior dislocated lens material.
Endophthalmitis may occur within a few days after cataract surgery and can rapidly result in loss of the eye unless recognized and treated rapidly. Most cases can be treated by performing a vitreous tap for culture and sensitivity and injecting intravitreal antibiotics. Severe cases with retained view of the retina are treated with vitrectomy as well. Even with prompt diagnosis and appropriate treatment, eyes with certain aggressive organisms often are still lost. Any patient with pain, decreased vision, or increasing inflammation soon after cataract surgery should be seen immediately to determine if endophthalmitis is present. Endophthalmitis can also result from a leaking filtering bleb, trauma, or
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endogenous sources such as an intravenous line or indwelling catheter, especially in immune-incompetent patients.
TRAUMA
Penetrating ocular trauma often results in a vitreous hemorrhage, which may be accompanied by significant retinal damage. Vitreous mobility as judged by indirect ophthalmoscopy and ultrasonography helps determine the timing of vitrectomy after penetrating trauma without a foreign body. Mobile vitreous, even if completely opaque from hemorrhage, can be observed if ultrasound demonstrates the retina to be attached and no foreign body is present. Vitrectomy is typically performed 7–10 days after initial wound repair after posterior vitreous separation occurs, active bleeding subsides, and the cornea is clearer. If early vitreous contraction is indicated by decreased mobility, vitrectomy should be performed before fibrosis and secondary traction retinal detachment occur.
If a metallic (ferrous or copper), toxic, or potentially infectious (biologic material) intraocular foreign body is present, prompt vitrectomy and forceps removal of the foreign body are indicated (Figure 9–17) (see Chapter 19). Occasionally, a plastic or glass foreign body or a shotgun pellet can be observed without surgery or until vitreoretinal traction occurs.
Figure 9–17. Removal of intraocular foreign body with diamond-coated forceps.
SUMMARY
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Study of vitreoretinal diseases is fascinating and can have a major impact on visual outcomes. New technologies and techniques are being developed at an explosive pace, producing great improvement in outcomes after vitreoretinal surgery. Many eyes formerly untreatable have had vision restored. Advances in biotechnology and OCT imaging are likely to produce phenomenal advances in the upcoming years.
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