HOW TO DIAGNOSE AND MANAGE DISORDERS OF THE VITREOUS

A FEW MONTHS ago, I noticed an annoying “floater” that failed to go away in my right eye, though I didn’t experience flashes of light or changes in my vision. It was large and stringy and persisted for two days. Like any self-respecting optometrist, I didn’t panic. Instead, I asked a colleague to perform a dilated fundus exam on me.

The good news: I didn’t have a retinal tear, macular hole (MH) or detachment. The bad news: A partial posterior vitreous detachment (PVD) causing a vitreomacular adhesion (VMA) was discovered, indicating the aging process was catching up to me.

Here, I discuss the vitreous and its associated complications, viewing the vitreous to arrive at a definitive diagnosis and the management of vitreous disorders.

THE VITREOUS/COMPLICATIONS

The vitreous is the largest structure within the eye and functions as the pathway for oxygen and nutrients to the lens, ciliary body and retina.

It is a transparent hydrophilic gel that is 99% water and 1% solid. The solid portion contains collagen, hyaluronan and proteoglycans, which form the supportive network of the gel, allowing for its strong adherence to the underlying retina.

At birth, the vitreous gel is firm. As it ages, the gel gradually liquefies (synchysis), leading to the development of fluid-filled pockets within it that coalesce and enlarge. This process results in a breakdown of collagen fibers (syneresis) within the vitreous, causing weakened vitreous adhesion, which allows liquefied vitreous to enter the posterior hyaloid space and causes PVD.

PVD is defined as a separation of the posterior cortex of the vitreous, or the posterior hyaloid membrane, from the internal limiting membrane (ILM) of the retina. The PVD process occurs in stages: Stage 1 is perifoveal PVD with vitreofoveal attachment; stage 2 is macular PVD; stage 3 is near-complete PVD with a vitreopapillary adhesion; and stage 4 is the presence of a visible Weiss ring, which may or may not indicate total separation and may require additional testing.

In most patients, the process may take months to years and is typically benign.

However, incomplete or partial PVD, with persistent traction (stages 1 to 3) can contribute to these significant sight-threatening retinal complications: vitreomacular traction (VMT) syndrome, MH, epiretinal membrane (ERM), vitreous hemorrhage (VH), retinal breaks, tears or holes and retinal detachment.

The risk factors for PVD are age — specifically age 45 to 65, family history of retinal tears or detachments, ocular trauma, previous eye surgery, prior intravitreal injections and high myopia (≥-6.00). Other factors that accelerate the PVD process are local conditions (uveitis) and systemic conditions (diabetes or inflammatory disease). Although PVD occurs in both genders, there is a higher incidence in post-menopausal women, a finding that may be due to the effects of decreased estrogen on collagen tissues within the vitreous gel.

Typically, patients who have acute PVD complain of new onset floaters or flashes of light (photopsias) or both. Photopsias are seen peripherally, are more noticeable in dim lighting and are often described as arc-shaped. Meanwhile, patients who have a VH, retinal tears or retinal detachment, among other vitreous-associated complications, complain of worsening floaters, or those described as “pepper,” and a shade or a curtain of vision.

VH can occur from diabetes, retinal vein occlusions, oral anticoagulant or aspirin use, ocular trauma, sickle cell disease and acute PVD. The literature shows it can happen in about 7.5% of PVDs, with the risk of having an underlying retinal tear increasing to nearly 70% in the case of a hemorrhagic PVD, according to Ophthalmology. A prominent symptom: significant decreased vision secondary to dispersed blood in the vitreous cavity.

As in my case, a partial PVD may be complicated by persistent VMA, which may progress and cause morphological alterations to the underlying retina, known as VMT. VMT can result in symptoms of photopsia, metamorphopsia, blurred vision and complications, such as cystoid macular edema (CME), ERM or a full-thickness MH. The risk of developing a MH in the fellow eye without a PVD is about 15%, whereas patients with a PVD are at low risk for MH development, reports the American Journal of Ophthalmology.

Retinal breaks, especially horseshoe or flap tears, occur in up to 26% of patients who have acute, symptomatic PVD, reports the latest American Academy of Ophthalmology guidelines. Also, those who previously had an acute PVD and no retinal breaks/tears on initial presentation have a 5% chance of developing a retinal break/tear (missed or new) in the weeks that follow, reports the American Journal of Ophthalmology. A retinal tear, in and of itself, does not have a poor prognosis, but left untreated, it may progress to a retinal detachment.

VIEWING THE VITREOUS

The following tools can aid you in the definitive diagnosis of PVD or a vitreous-associated complication:

• Biomicroscopy. Use this to scrutinize the vitreous for pigment cells (“tobacco dust” or Shafer’s sign), white blood cells indicating inflammation or red blood cells in the anterior vitreous — signs of retinal break/tears, a retinal detachment or VH. In cases of VH, gonioscopy should be performed to check for neovascularization of the angle. Also, the slit beam (Watzke-Allen) is useful for diagnosing a full-thickness MH. Perform a peripheral assessment with your condensing lens or three-mirror lens if a retinal break/tear is suspected with a PVD.
• Indirect ophthalmoscope combined with scleral depression. This should be performed on any patient experiencing new floaters and/or flashes of lights. A compete 360° enables the view of the peripheral vitreoretinal interface, especially when looking for small retinal breaks, tears or traction with acute PVD. Both eyes should be examined thoroughly, even the asymptomatic eye, to ensure no pathology exists.
• Retinal photography. This is excellent for documenting structural changes, monitoring disease progression through time and patient education. Widefield retinal imaging offers a panoramic view of the peripheral retina, allowing for the detection of retinal breaks/tears or detachments associated with PVD.
• SD-OCT. This allows for the visualization of details of the vitreous cavity, including vitreous opacities, such as degenerative asteroid hyalosis, and vitreous cells (indicating inflammation or a retinal break/tears) and VH. Imaging of the vitreoretinal interface can aid in the accurate staging of PVD and detection of adhesion or traction of the hyaloid membrane traction, which causes a focal or broad VMA and VMT, CME, ERM, MH or complete PVD.
• B-scan ultrasonography. This is an important tool when media opacities (mature cataracts) obscure the view of the retina. It aids you in detecting pathologic conditions, such VH, retinal tears and detachments associated with PVDs.

MANAGING VITREOUS DISORDERS

While “floaters” can be bothersome, identifying the underlying cause is imperative to determining the best course of action management-wise. For example, for those who have VHs or vitritis (vitreous cavity inflammation), a systemic work-up may be necessary, as diabetes, sickle cell disease or inflammatory disease, such as sarcoidosis, or infectious disease, such as ocular toxoplasmosis retinitis, may be an underlying cause.

If the PVD is hemorrhagic or other more concerning signs, such as red blood cells, are present, follow closely within one week initially, followed by three to six weeks. Also, advise these patients to avoid heavy exertion, lifting or bending. In patients taking blood-thinning drugs, there is no evidence that the discontinuation of antiplatelet or anticoagulant agents speeds the recovery of vitreous hemorrhage.

For patients who have acute PVD with no complications, such as retinal breaks/tears, follow-up with them in one to two weeks initially, depending on other risk factors, associated signs or symptoms, or both, until the condition becomes asymptomatic and no retinal breaks/tears are found. Advise these patients to return immediately if they experience an increase in signs or symptoms, such as flashes, floaters or a curtain, in their vision.

A retinal consult is necessary for acute symptomatic PVD with retinal breaks/tears because of the risk of a retinal detachment. Laser treatment is performed to prevent progression to a retinal detachment. Even when a patient has undergone adequate treatment, long-term follow-up is important because between 5% and 14% of patients who have an initial retinal break/tear will develop additional breaks/tears during long-term follow-up, reports the American Journal of Ophthalmology. A retinal detachment warrants immediate referral, especially if the macula is attached, to a retinal specialist for surgery.

Regarding symptomatic VMT or an impending MH, the clinical course is unpredictable, as some cases remain stable for years or resolve with spontaneous PVD. For patients who have persistent or worsening symptoms, possible treatment with ocriplasmin (Jetrea, ThromboGenics) intravitreal injection may be an option. However, complications, such as retinal tears, floaters, blue-yellow vision, dyschromatopsia, vision loss and VF abnormalities can occur from this treatment.

Surgical intervention for vitreous disorders include vitrectomy for VH, ILM peeling for ERM, laser treatment for retinal tears (described above) or surgery for retinal detachment.

In many cases, acute PVD symptoms (flashes of light) diminish over time, and most patients adapt to their floaters. For those who don’t, vitreolysis or vitrectomy, may be an option. However, both are controversial options because of the risk of complications, such as retinal breaks/tears and detachment, as well as CME.

STAYING A STEP AHEAD

Although vitreous complications remain a challenge, our understanding of the vitreous and related diseases has vastly improved in recent years. Advanced imaging techniques have enhanced analysis of the vitreous and are invaluable in the early diagnosis and management of related retinal diseases. OM

DR. REYNOLDS is an associate professor at the Nova Southeastern University College of Optometry and clinical preceptor/attending in the college’s diabetes and macular clinic. She is a fellow of the Optometric Retina Society and chairperson for the Florida Optometric Association Healthy Eyes Healthy People Committee.