Beware the Floaters

A 59-year-old woman presented with a sudden onset of floaters in her right eye 2 hours earlier. She reported no accompanying flashes of light, curtains, veils, or loss of vision. Her ocular history was remarkable for dry eye disease, an operculated hole in her right eye, cataracts in both eyes, and dermatochalasis in both eyes, for which she had undergone cataract surgery, blepharoplasty, and intense pulsed light therapy. Her medical history was remarkable for hypercholesterolemia, seasonal allergies, and breast cancer, for which she had previously undergone lumpectomy and radiation.

EXAMINATION

On examination, the patient’s UCVA was 20/25-2 OU. Her pupils were equally round and reactive to light. Extraocular movements were full and smooth. Her IOP was 14 mm Hg OU. A slit-lamp examination of the right eye was unremarkable. The pupil in her right eye was dilated with 1% tropicamide and 0.5% proparacaine.

A fundus examination of that eye showed a new Weiss ring and an operculated retinal hole with a cuff of edema in the superotemporal far periphery, which had been noted 2 years prior (Figure 1). A Shafer sign was not observed in the anterior vitreous of the right eye. An examination of the left eye was unremarkable (Figure 2).

DIAGNOSIS, MANAGEMENT, AND FOLLOW-UP

Based on the examination results, the patient was diagnosed with a posterior vitreous detachment (PVD) in her right eye. She was educated on the nature of PVDs and how they occur as a normal consequence of aging due to changes in the vitreous. She was also encouraged to monitor herself for any new symptoms that might develop (eg, flashes of light, curtains, veils) that could be indicative of additional pathology (eg, retinal tears, retinal detachments [RDs]). She was scheduled to return in 1 month for follow-up to reevaluate the PVD and rule out subsequent pathology.

At the 1-month visit, the patient mentioned that, although she still noticed floaters in her right eye, she was getting used to them. She reported no new flashes of light, loss of vision, curtains, or veils.

On examination, her UCVA was 20/20 OD and 20/30 OS. Her pupils were equally round and reactive to light. Her IOPs were 16 mm Hg OD and 15 mm Hg OS. Her right pupil was dilated with 1% tropicamide and 0.5% proparacaine. A fundus examination showed a new horseshoe retinal tear in the superotemporal periphery in the same general location as the previously noted operculated retinal hole (Figure 3). A Shafer sign was not observed in the anterior vitreous of the right eye.

The left eye examination remained unremarkable.

The patient was diagnosed with a horseshoe retinal tear in the right eye. She was educated about the retinal tear and the potential consequences if it were not treated. She was then urgently referred to a retina specialist for laser retinopexy.

DISCUSSION

Posterior Vitreous Detachment

A PVD is a separation of the posterior hyaloid membrane from the internal limiting membrane of the retina. It can be partial or complete and create traction on peripheral vitreoretinal adhesion sites, leading to retinal tears, which can cause a rhegmatogenous RD (RRD).1 PVDs typically occur in patients between 45 and 65 years of age. The vitreous can also detach earlier in patients with a history of trauma, myopia, or diabetes.¹

As a normal result of aging, the vitreous gradually becomes liquefied, a process known as syneresis. As pockets of fluid form within the vitreous gel, the posterior hyaloid membrane pulls away from the neurosensory retina at the macula and optic nerve, leading to a PVD. By 70 years of age, many people will have had a PVD.²

During the acute phase of a PVD, patients may report light flashes that are more noticeable in the dark and an increased number of floaters. The photopsias occur due to vitreous traction on the retina as the posterior hyaloid membrane starts to separate from the posterior retina toward the vitreous base. Floaters can result from condensation of collagen or glial tissue (Weiss ring), which is separated from the optic nerve head.¹

PVDs typically are benign and do not result in a loss of vision. However, if vitreous traction exists on the retina, complications can occur, and vision may be lost over time if not managed appropriately.¹

Operculated Hole

An operculated hole is a full-thickness retinal hole with a free-floating piece of retinal tissue in the vitreous body called an operculum.^3,4 The operculum represents avulsed retinal tissue due to traction from the vitreous body. Operculated holes originate in focal areas of vitreoretinal abnormalities such as vitreoretinal tufts. During the development of an operculated retinal hole, patients can be symptomatic. However, symptoms often resolve once the operculum becomes free-floating and traction is released.4 Due to the lack of significant vitreoretinal traction after the release of the operculum, there is less than a 1% chance of an RRD occurring; treatment is rarely necessary.⁴

Horseshoe Tear

A horseshoe tear represents a full-thickness break of neurosensory retina that occurs from vitreous traction, often as the result of a recent PVD. Risk factors for a retinal tear include age, myopic refractive error, lattice degeneration, and trauma. Although flashes of light and floaters are common symptoms of a horseshoe tear, patients can also be asymptomatic. The literature estimates that, without proper intervention, at least half of symptomatic horseshoe or flap tears will lead to a clinical RRD.^1,4 To prevent this, all patients should promptly be referred for laser retinopexy after diagnosis.³

Retinal Break

Roughly 65% of patients 65 years of age or older develop a PVD with no adverse ocular sequelae.4 However, up to 15% of patients who present with an acute symptomatic PVD have concomitant retinal breaks.⁴ Therefore, when evaluating a patient who presents with symptoms of flashes and floaters and signs of an acute PVD (ie, a new Weiss ring), it is important to assess them for the presence of a Shafer sign. A Shafer sign, which is often called tobacco dust, is associated with the presence of brown pigmented cells in the anterior vitreous.⁵ It is widely thought that these cells arise from the shearing force of the break in the retinal pigment epithelium.⁵

It is also important to look for a vitreous hemorrhage in a patient who presents with flashes and floaters. A vitreous hemorrhage that accompanies an acute PVD can also signify the presence of a retinal break. In a recent study of 9,636 eyes with acute PVDs, among those that had a vitreous hemorrhage at the time of presentation, 42% had a concurrent or delayed retinal break.⁶

CLINICAL PEARL

PVDs occur frequently in clinical practice and are usually harmless. Following up is important, however, because there a retinal break may develop. Our patient was asymptomatic at her 1-month follow-up, yet a fundus examination showed an acute horseshoe tear. Given that the horseshoe tear occurred in the same anatomic location as the operculated retinal hole with a cuff of edema, we felt it prudent to refer her for laser retinopexy. Additionally, it is important to remember that, although many asymptomatic horseshoe tears remain uncomplicated, approximately 5% can progress to an RD.^4,7 Quick recognition of peripheral retinal tears and a prompt referral for treatment can ultimately help preserve patients’ vision and quality of life.