What is the risk of worsening background diabetic retinopathy in patients that have just a few peripheral hemorrhages?
There’s some research suggesting that patients with predominantly peripheral retinopathy have an increased risk of progression to proliferative disease compared to individuals in whom the majority of the hemorrhaging is located in the posterior pole.1
Peripheral retinopathy is best detected with either binocular indirect ophthalmoscopy examination or ultra-widefield color fundus photography, which is why I perform ultra-widefield imaging on nearly all diabetic retinopathy patients. It's hard to determine the exact percent risk that a patient with several peripheral hemorrhages progresses, but, as a known risk factor, it’s definitely something that should prompt close monitoring. Electroretinography also aids this determination.
I’ve lately observed a small, flat nevus that's been growing very slowly over time—the past eight to 10 years. It’s very benign in appearance; without a prior photo, I would have never referred. What are your thoughts?
Anytime you’re observing the growth of a pigmented choroidal tumor, it’s absolutely worth referring the patient for a second opinion. A lot of tumors in the periphery are really hard to assess if all you have is a description or a hand fundus drawing, so get photos and use the caliper tools to measure the longest diameter. Additionally, measure the anterior-posterior thickness and its change over time to determine if a tumor is acoustically hollow. Your cutoff point for suspicion should be approximately 2 mm when using ultrasound and half of this for OCT.
Leveraging your ultra-widefield imaging to assess changes over time can be invaluable—especially for those occurring in the retinal periphery. Wide-field fundus autofluorescence, in particular, allows us to assess for lipofuscin deposition that could be subtle on clinical examination but will show up with a very bright white intensity due to its natural fluorescence.
There’s a graph in one of Dr. Carol Shield's studies that demonstrates changes to patient risk profiles based on the number and type of risk factors.2 However, not all are created equal—orange pigment alone is indicative of a 37% risk of growth over the next five years. Another indication of high risk is fluid, especially subretinal, overlying tumors.
In today's modern optometry practice, how critical is OCTA, considering that we may typically refer these retinal cases to ophthalmology?
I‘d argue very critical. OCTA enables neovascularization detection at the earliest point possible, whether in patients with macular degeneration or non-exudative choroidal neovascular membranes. We can locate choroidal NEO before any fluid actually leaks out, and then, knowing that these patients are at high risk of exudative conversion, closely monitor them to catch them as soon as they convert and start treating them to preserve good vision. Detecting the earliest proliferative retinopathy in diabetic retinopathy patients is also a huge clinical application of OCTA. Because it provides really high microvascular resolution of the retina, we can observe subtle retinal abnormalities such as intraretinal microvascular abnormalities (IRMA), retinal non-perfusion, and potential neovascularization—and also go a step further and definitively differentiate between IRMA and neovascularization elsewhere (NVE), and thus non-proliferative and proliferative diabetic retinopathy (PDR).
I saw a patient who, based upon their clinical exam, appeared to have intraretinal hemorrhaging in all four quadrants. There seemed to be some IRMA present, alongside cotton wool spots and some exudate—but nothing indicative of neovascularization on the disc or elsewhere; there was no pre-retinal or vitreous hemorrhage. However, OCTA highlighted that this patient actually had a tiny area of neovascularization in the inferior temporal arcade that I hadn’t been able to see during my clinical examination. Without OCTA, I would've misclassified this patient as having severe NPDR when, in actuality, they had low-risk PDR. Such clarifications occur almost on a weekly basis. We also can’t visualize issues such as macular ischemia with a clinical exam or structural macular cube OCT; without some form of angiography, a visual prognosis may be limited in patients with diabetic retinopathy or retinal venous occlusive disease.
What's the go-to protocol for central serous chorioretinopathy treatment? And what's your take on topical NSAID usage in active central serous?
Fortunately, most central serous chorioretinopathy resolves on its own—it’s my experience that in about 90% of cases this occurs within six months. Although we don’t need to intervene during this time, we do need to determine whether there’s a choroidal neovascular membrane present. OCTA is great for this. Also important is asking about risk factors such as pregnancy, steroid use, obstructive sleep apnea, a patient’s job, and their work schedule—patients such as airline attendants or those who work nights are more likely to suffer from central serous chorioretinopathy. Although there may be nothing you can do about some of these risk factors, it's essential to have this information to address as many as possible to aid resolution.
I wouldn't refer a patient to a retinal specialist until the fluid has been there for at least three months without improvement, at which point the subretinal fluid present could potentially cause photoreceptor atrophy and RPE scarring. In that three-month timeframe, I may put patients on topical NSAID therapies, although I admittedly haven't personally seen a patient in whom I felt as though these therapies worked yet. However, I currently don’t think they hurt as long as they’re not used for so long that the corneal integrity is compromised or significant superficial punctate keratitis is caused. Typically, a period of use of four to five weeks is most appropriate. I also recommend that patients consider taking melatonin, as there are some case reports that potentially support its use. There are potential off-label options such as mineral corticoids, but I personally don’t prescribe them as they have a lot of associated side effects.
If I do ultimately refer a patient to the retina specialist, I may also consider micropulse laser photocoagulation and photodynamic therapy, which are both common therapies that tend to work really well. Macular photocoagulation can also be of benefit to these patients. And if the OCTA or fluorescein angiography highlights a choroidal neovascular membrane, anti-VEGF therapy may potentially be instituted in these patients.
Dr. Majcher’s full responses to these and additional questions can be found in the VOD of the live Q&A session.
