Should I be referring patients with retinal holes, especially without subretinal fluid, for treatment?
There are many things to consider here. The first consideration is that the general break features are indicative of a high risk for progression to rhegmatogenous retinal detachment. During clinical assessment or with OCT, you want to determine whether there’s a subretinal fluid cuff, and, if so, the extent. You should also assess whether there’s vitreous retinal traction on the margin of the break; when there's motion, the vitreous attached to the tear flap will experience a consistent pull, promoting the flow of fluid that then accumulates in the subretinal space.
The clinical case as a whole should also be assessed to determine whether there are other rhegmatogenous retinal detachment risk factors present, and thus, whether to refer. These risk factors include whether:
- The patient is a high myope
- There is a history of trauma—trauma-related breaks should always be referred to retina specialists for potential barrage laser.
- There is any intraocular surgery history (e.g., cataract or Nd:YAG capsulotomy surgery)
- There is a history of rhegmatogenous retinal detachment in the other eye, or a family history of a rhegmatogenous retinal detachment in a first-degree relative. Additionally, certain genetic disorders like Stickler syndrome also increase the risk of developing rhegmatogenous retinal detachment.
There’s also a table from the American Academy of Ophthalmology preferred practice patterns for posterior vitreous detachment, retinal breaks, and lattice degeneration that you can refer to.1 This table summarizes each type of lesion and the step that you need to take, whether it be potential referral to a retina specialist for treatment, or in-house management and monitoring.
What are some other reasons why time in range (TIR) is now chosen over A1C, and why not use them both?
Both are important, but TIR provides a really valuable perspective on the variability of glycemic control compared to A1C, which is just an average.
Imagine you have two patients, both with 6% hemoglobin A1Cs. From this alone, both cases seem pretty good; however, one patient may be consistently maintaining the same glucose level, while the other patients could be constantly fluctuating—but still result in the same average. It's similar to glaucoma: two patients may have the same mean intraocular pressure (IOP), but if one patient’s IOP is really stable, it’ll be less damaging to the optic nerve head compared to another who experiences large IOP fluctuations.
It's likely that such variability damages blood vessels with glycemic index in patients with diabetic retinopathy. If a patient does have a continuous glucose monitor, asking them about TIR is very important,but also knowing the average A1C is useful.
How can you treat macular edema based on OCT?
OCT is really valuable when determining diabetic macular edema (DME) classification—and the way we manage each case depends on the etiology. For DME patients, anti-VEGF agents are typically used as first-line therapy, although focal and grid macular photocoagulation are used in some rare cases when extra or non-center-involved macular edema is identified as a point source of leakage.
Many retina specialists follow DRCR.net Protocol V—in this study, the natural prognosis of center-involved edema patients was evaluated to determine whether to treat such patients early.2 The researchers observed no significant difference in vision loss between patients with 20/25 vision or better in whom treatment was deferred until their visual acuity declined to 20/30 or worse, and those treated from the get-go. Some retina specialists may wait until a patient’s vision declines to treat center-involved diabetic macular edema, but I don't think that's our call to make as optometrists. We should refer all patients with center-involved edema for consideration of anti-VEGF therapy.
There are also other macular edema causes:
- Retinal venous occlusive disease—whether central or branched, first line therapy is anti-VEGF injections. Other potential therapies include intravitreal injections or sustained release steroids.
- Post-pseudophakia (formerly Irvine-Gass syndrome) is typically treated with topical NSAIDs and steroids ~four times a day.
- Uveitic macular edema—chronic and especially intermediate uveitis can have associated macular edema and a little disc edema. Treatment here includes topical steroids and cycloplegic agents, and if necessary, subconjunctival, sub-Tenon’s, or intravitreal steroids.
- Inherited retinal diseases (e.g., retinitis pigmentosa). Typically treated with topical carbonic anhydrase inhibitors.
- The side effects of anti-cancer medications and the medication toxicities that come with them.
How do you view the role of AREDS 2 vitamins in patients with geographic atrophy (GA)? Although they weren’t tracked in the complement inhibitor trials, some studies have shown that AREDS 2 alone reduces GA progression, but others report that the zinc content can worsen GA in some patients.
The study, which assessed AREDS 2 benefits in GA patients, found that this supplementation reduced progression towards the center of the fovea, alongside slowing general progression and enlargement in non-central GA patients.3 I definitely recommend AREDS 2 in GA patients—especially the non-central subtype—with useful vision. Regarding zinc concerns, there are formulations with reduced zinc; the AREDS 2 study supported the idea that we can lower zinc concentration and still see benefits in our patients.4
But we also have other emerging options to further flesh out our management pathway for very early GA patients. This includes photobiomodulation, which not only reduces the onset of GA development but also improves vision in the intermediate stage of AMD. The LIGHTSITE III study, a two-year trial that led to the FDA approval of photobiomodulation in 2024, demonstrated a mean difference between sham versus treatment groups of approximately four to five letters—about one line on an ETDRS visual acuity chart.5
Additionally, in their post hoc analysis, the researchers observed that photobiomodulation decreased the incidence of new onset GA at month four. One in four sham group members developed GA over two years compared to only around 7% of the photobiomodulation group. It highlights that we can help patients with intermediate-stage AMD at high risk for progression using AREDS 2 supplementation and photobiomodulation, and once patients develop significant GA, complement inhibition therapies then come into play to slow any central foveal GA progression.
Dr. Majcher’s full responses to these and additional questions can be found in the video on demand of the live Q&A session.
