CLINICAL

  POSTERIOR

‘I SEE A DIFFERENT IMAGE SIZE’

WHAT KIND OF VITREOMACULAR INTERFACE DISORDER DID THIS PATIENT HAVE?

SHERROL A. REYNOLDS, O.D., F.A.A.O.

AN 80-YEAR-OLD male presented complaining of gradual onset of aniseikonia, or “different image size,” for one week. He denied symptoms of floaters or flashes of light and any trauma. Ocular history revealed uncomplicated cataract surgery OU. Medical history was significant for hypertension and hypercholesterolemia, for which he was taking amlodipine/benazepril (Lotrel, Novartis) and rosuvastatin calcium (Crestor, AstraZeneca).

The patient’s BCVAs were OD 20/25 and OS 20/25. Pupils, ocular motilities and confrontation visual field testing were unremarkable. IOPs were 11 mm Hg OD and OS. Anterior segment was positive for arcus senilis OU. Dilated exam revealed a well-centered posterior chamber IOL with post YAG capsulotomy in both eyes. Vitreous syneresis and healthy optic nerves were observed in both eyes. The macula in both eyes appeared healthy, however, OCT imaging revealed a persistent adherent vitreous at the vitreomacular interfaces. Scleral depression revealed no evidence of a retinal tear or detachment OU.

Did a vitreomacular traction (VMT), vitreomacular adhesion (VMA), impending macular hole (MH) or an epiretinal membrane (ERM) cause this patient’s aniseikonia and macular change?

Here, I discuss the etiology, symptoms, clinical signs and diagnosis/management of these vitreomacular interface disorders to help you make the correct diagnosis. This is important, as such disorders have the potential to cause sight-threatening complications, such as MH. Therefore, early diagnosis, close monitoring and prompt referrals, when necessary, can improve outcomes.

ETIOLOGY

Vitreomacular interface disorders can occur at any age and in any race, according to Ophthalmology. They can affect either sex, although there is a slightly higher incidence in postmenopausal women, possibly because low estrogen levels cause premature vitreous liquefaction and, therefore, earlier onset of posterior vitreous detachment (PVD), reveals the Eye Journal.

As the vitreous ages, it gradually liquefies, leading to the development of fluid-filled pockets in front of the macula that coalesce and enlarge. This results in weakened vitreous adhesion and the development of a PVD.

PVD, defined as a separation of the posterior cortex of the vitreous or the posterior hyaloid membrane from the internal limiting membrane of the retina, is a common process with aging. It usually occurs between the ages of 45 and 65 or earlier in highly myopic patients, according to Archives of Ophthalmology. In most patients the process, which can occur through months to years, proceeds normally, resulting in the complete separation of the vitreous from the macula and optic nerve, observed as a visible Weiss ring.

Fundus of 80-year-old male patient.

However, if the PVD process is partial or incomplete with persistent traction, sight-threatening complications, including VMA/VMT, ERM or MH, can occur. These adherences may be focal or extensive, affecting the foveola only, or a wide region of the macular area and the optic disc.

SYMPTOMS

Patients who have vitreomacular interface disorders experience the following:

• Blurred central vision

• Central metamorphopsia

• Central scotoma

• Floaters or flashes of light

• Photopsia

• Permanent vision loss when untreated

CLINICAL SIGNS

A group of experts, the International Vitreomacular Traction Study Group (IVTS), published a classification system in Ophthalmology for vitreomacular interface disorders:

• VMA. This is adhesion of the posterior hyaloid membrane without macular abnormalities or morphological changes on OCT. VMA may be sub-classified by the size of the adhesion into focal (≤1500 μm) or broad (>1500 μm). It may resolve spontaneously as part of the normal process of PVD, remain stable or progress due to persistent traction to VMT or an MH. VMA is also associated with concurrent macular disease, such as diabetic maculopathy and AMD.

• VMT. This results from persistent traction due to the progression of PVD. It leads to anatomic changes in the contour of the foveal surface, intraretinal pseudocyst formation and foveal detachment, all of which are observed via OCT. VMT generally results in reduced or distorted vision. Like VMA, it can also be sub-classified as focal or broad (using the same cutoff of 1500 μm), depending on the width of the vitreous attachment. Distortion of the foveal profile, formation of intraretinal cysts, intraretinal cavitation, subretinal fluid and even retinal pigment epithelium detachment can be observed. The IVTS refers to a VMT as an impending MH. (For more on MH, see “Get the Hole Picture” at tinyurl.com/MaculaReynolds.)

• ERM. This commonly occurs in about 40% to 100% of eyes that have VMT, according to the Journal of Ophthalmic and Vision Research. It is residual vitreous tissue left over from perifoveal PVD. Via slit lamp exam, ERM may be visible as a glistening sheet with or without retinal wrinkling. Through OCT, ERM appears as a highly reflective layer on the inner retinal surface.

OCT Evaluation: OD-VMT (left) OD-VMA (right)

DIAGNOSIS/MANAGEMENT

In addition to the slit lamp and OCT, you should also use the following to aid in the diagnosis of vitreomacular interface disorders:

• Amsler grid. Use this to detect any central scotoma or metamorphopsia, which indicate worsening disease.

• Retinal photography. This is necessary for documenting changes through time.

• SD-OCT. This allows for the precise assessment of adhesion of the vitreous to the macula, so you can differentiate VMA, VMT and an impending MH.

• B-scan ultrasonography. This can aid in the diagnosis of VMA/VMT, which is seen as a thin, smooth, continuous membrane with focal attachment anterior to the retinal surface. Specifically, the device can show a partial PVD, which can lead to VMA/VMT complications.

In terms of management, VMA could spontaneously resolve, remain stable or progress to VMT or MH formation. Therefore, close monitoring with OCT every six to 12 weeks is necessary.

However, persistent anterior-posterior (axial) traction could result in VMT or a MH. For patients with symptomatic VMA and VMT or a stage I MH (impending MH), refer to a retinal specialist to determine whether an ocriplasmin (Jetrea, ThromboGenics) intravitreal injection, vitrectomy or ILM peeling surgery is needed.

With regard to ERMs, the majority are observed closely every three to six months and are not treated, as they do not lead to significant symptoms. If vision is compromised, however, surgical removal of the vitreous and ERM with peeling of the ILM becomes necessary.

THE ANSWER

If you diagnosed this patient with VMT OD and VMA OS, you are correct! His aniseikonia was due to VMT OD. Retinal photos and SD-OCT were obtained. He was educated on the finding, given a home Amsler grid and advised to return in six weeks. At this visit, his symptoms improved, vision was unchanged, and OCT imaging showed no change in the macula. He is monitored every three months and remains stable. 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. Comment at tinyurl.com/OMcomment.