VMT & PVD - RethinkVMT.com

Vitreomacular Traction (VMT) — Often Responsible for Progressive Sight-Threatening Symptoms and Irreversible Vision Loss 1-4

An increasingly recognized clinical entity, vitreomacular traction (VMT) is a condition of the vitreoretinal interface resulting from incomplete posterior vitreous detachment (PVD). 1-4 Tractional forces caused by partial adhesion of the vitreous to the retina can compromise the structural and functional integrity of the macula, and are implicated in macular hole formation1,5-7 Patients with vitreomacular traction (VMT) — in the past, referred to as vitreomacular traction syndrome, commonly present with symptoms such as metamorphopsia, decreased visual acuity, and central vision defect. preconcertedly

Because of advances in imaging (ultrasound and optical coherence tomography [OCT]), clinical diagnosis of vitreomacular traction (VMT) can be made earlier and more reliably. 3,5,10 Treatment advances, too, are changing the landscape of vitreomacular traction (VMT) and macular hole management. 1,9,11,12

The Evolution and Management of Vitreomacular Traction
(VMT)


Dr. Arnd Gandorfer discusses aspects of vitreomacular traction
(VMT), from natural history to treatment considerations.


Dr. Arnd Gandorfer discusses aspects of vitreomacular traction
(VMT), from natural history to treatment considerations.

Welcome to
The Evolution and Management of Vitreomacular Traction (VMT)
An educational presentation for healthcare professionals

The Evolution of VMT
In the human eye, posterior vitreous detachment, or PVD, marks the culmination of age-related changes in the vitreous.

Defined as a separation between the posterior vitreous cortex and the internal limiting membrane of the retina, posterior vitreous detachment, or PVD, generally occurs uneventfully.

However, in some individuals, the detaching vitreous remains firmly tethered to focal areas of the retina, including the macula. When the adhesion exerts tractional forces that are sufficient to compromise the structural and functional integrity of the retina, the patient has vitreomacular traction and is at risk for macular hole and a variety of other retinal pathologies.

I’m Dr. Arnd Gandorfer, I’m a vitreoretinal surgeon with a particular interest in the pathology of the vitreoretinal interface. I'll be discussing aspects of vitreomacular traction, its natural history, complications, and management considerations.

To begin with, the symptoms of vitreomacular traction, as you can see in your patients, can disrupt activities of daily living and quality of life.

Symptoms of vitreomacular traction include diminished visual acuity, metamorphopsia, and central visual field defect.

VMT and Patient Well-being
In addition to a clinical assessment, it’s important to consider how patients perceive their vision-related functioning and well-being. Subjective perceptions are crucial to characterizing the magnitude of disability that results from visual impairment.

Data from the 2004 Survey of Health, Ageing and Retirement in Europe—which involved over 22,000 individuals with a median age of 64 in 10 European countries—showed that lower vision was associated with a highly significant negative impact on all measured aspects of well-being. Persons with low vision had a higher probability of concentration problems during reading and entertainment, of losing interest and enjoyment in their activities, or of feeling fatigued, irritable, or sad.

The authors concluded that effective measures of early detection, prevention, and rehabilitation might help counter these problems and thereby improve mental and physical health, as well as reduce the economic impact of low vision.

Patients who can no longer drive or read well, if at all, may no longer be able to work. In one fairly large study, the age at onset of symptoms of VMT ranges from 36 to 83 years, with a median age of 67.5 years. In other words, many patients are still in their economically productive years.

Clearly, in addition to clinical assessments, it’s important to factor in quality of life and well-being when considering how—and how quickly—to make a therapeutic intervention in patients with VMT.

VMT and Other Retinal Pathologies
The relationship between VMT and other retinal pathologies has become increasingly clear. Clinical studies have pointed out the increased prevalence of incomplete posterior vitreous detachment in association with exudative age-related macular degeneration, diabetic macular edema, and retinal vein occlusion. It has been suggested that vitreomacular traction plays a role in the progression of diabetic retinopathy and may play a role in the progression of AMD.

The Management of VMT
Until recently, the only available intervention for vitreoretinal traction and macular hole has been vitrectomy, generally after a period of watchful waiting. While vitrectomy often has good outcomes, there are associated risks and recovery after the procedure can be challenging. For this reason, vitrectomy is normally reserved for patients who suffer from more severe symptoms and who show morphologic findings of disease progression with worsening visual function.

Enzymatic Vitreolysis
However, with the availability of enzymatic vitreolysis in some countries, VMT may now be managed pharmacologically, while it is still in its early stages, including when associated with macular hole of diameter less than or equal to 400 microns. This makes it increasingly relevant to understand the evolution and complications of early-stage PVD.

Two critical processes underlie posterior vitreous detachment. The first is a gradual liquefaction of the vitreous gel and the development of fluid pockets, typically beginning in front of the macula and in the central vitreous cavity. Liquefaction of at least 50% of the gel is observed in most individuals older than 70 years. A second factor is progressive age-related weakening of the adhesion between the posterior vitreous cortex and the internal limiting membrane. Collapse of the vitreous gel and weakening of the adhesion normally lead to an innocuous complete PVD.

During enzymatic vitreolysis, intravitreal injection of a proteolytic agent lyses the protein components of both the vitreous body and the vitreoretinal interface. These components include laminin, fibronectin, and collagen. This promotes further liquefaction of the vitreous body, plus dissolution of the protein matrix that is responsible for abnormal vitreomacular adhesion—in effect, working both within the vitreous and at the point of adhesion to help complete the natural process of posterior vitreous detachment.

Rate of PVD
In the past, complete PVD was thought to be a sudden event because it was accompanied by acute symptoms, namely floaters, photopsia, or both. However, the introduction of optical coherence tomography — or OCT — which provides high-resolution cross-sectional images of retinal structures—has clarified that the pattern and rate of PVD evolution are actually gradual. This spectral domain OCT image demonstrates an insidious early shallow perifoveal vitreous detachment, which tends to extend slowly, and usually asymptomatically over time, until vitreous separation from the optic disc margin results in complete PVD. OCT can precisely characterize the intimate relationship of the posterior vitreal face and the retina, supporting early diagnosis of retinal pathologies and differentiation of anomalous posterior vitreous detachment—which we see here—from other clinical entities, such as vitreoschisis.

Several longitudinal studies conclusively demonstrate that early PVD stages persist chronically and progress slowly and usually asymptomatically to complete PVD, over months to years. Certain populations are at greater risk for incomplete posterior vitreous detachment, and, therefore, VMT. For example, patients with diabetes who also have clinically significant diabetic macular edema.

In general, the vitreous is attached to the retina most firmly in areas where the internal limiting membrane is thinnest, including the vitreous base, along the large retinal vessels, the optic nerve disc margin, and the foveola. It is hypothesized that especially strong vitreofoveal adhesion delays or prevents a smooth and complete separation. This results in tractional forces that can act on the macula. The specific macular disorder that may develop depends in part on the size of the persistent vitreomacular adhesion.

It is predicted that tractional stress acting on the fovea increases as the area of vitreous attachment decreases. Thus, small vitreous adhesions of 500 microns or less impart greater tractional stress and are more likely to result in macular hole or in localized cystoid foveal thickening.

In contrast, the lower tractional stress caused by larger adhesions—typically 1500 microns or more—will more likely result in diffuse macular thickening, traction macular detachment, or possibly exacerbation of conditions such as age-related macular degeneration. Now, with the availability of enzymatic vitreolysis, the opportunity exists to help patients by inducing vitreal separation at an earlier stage in patients with vitreomacular traction, and possibly avoid late-stage complications or surgery.

Thank you



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