A streak of accuracy
Eric W. Schneider, MD, shares a case of a 52-year-old patient with a prior medical history of pseudoxanthoma elasticum, hypertension, and hyperlipidemia. “In his color fundus photographs, we observed interesting-looking vitelliform lesions, alongside dependent vitelliform debris present inferiorly in both maculae with associated RPE changes,” recalls Dr. Schneider. “There were also circumpapillary angioid streaks with radiations extending from the nerve.” Investigating the vitelliform lesions further using structural ocular coherence tomography (OCT), Dr. Schneider observed a classic pseudohypopyon appearance of a hyporeflective cavity superiorly in conjunction with dependent pooling of hyperreflective vitelliform lesion material.
This patient had been referred to Dr. Schneider’s practice for ongoing management of refractory choroidal neovascularization (CNV), OU—but was this accurate? “It can be difficult to diagnose CNV in patients with angioid streaks and vitelliform maculopathy because the hyporeflective degenerating cavity can be mistaken for exudative subretinal fluid,” explains Dr. Schneider. The modality that helped him to make this distinction himself was OCT-angiography (OCTA) . “Using the CIRRUS with the outer retina to choriocapillaris (ORCC) slab (Figure 1), we saw very clear CNV present in the inferonasal aspect of the right eye’s macula, corresponding to an area of increased flow on the cross-sectional image with flow overlay,” highlights Dr. Schneider. “However, in the left eye, there was neither CNV nor evidence of abnormal flow in the outer retina.”
Figure 1. OCT-A ZEISS CIRRUS with ORCC Slab
This finding was further confirmed when this patient didn’t attend treatment appointments for four months. A lack of bevacizumab injections resulted in an increase in the retinal thickness of the hypo-affected areas, OD—which had previously reduced substantially after three months of prior treatment. However, this same absence, OS, resulted in no change. “Using the challenge, dechallenge, rechallenge paradigm, we can confidently say this patient has CNV,” Dr. Schneider explains. “Many individuals not familiar with OCTA sometimes struggle to trust their findings; a case like this drives home this technology’s accuracy.”
In, not on
If you’re worried a patient may have proliferative diabetic retinopathy (PDR), how would you clear up your suspicions? OCTA can be key to this determination, too. When an 83-year-old patient, with a medical history of type II diabetes and hypertension, presented for a primary open-angle glaucoma follow-up, Dr. Majcher noted something off during the clinical examination. “I picked up on some abnormal blood vessels in the patient’s superonasal peripapillary region,” she explains. “Given that she had diabetes, my concern was that it might be neovascularization in the disc—sometimes we see ‘featureless retina’ patients that have minimal background DR findings, but still have neovascularization.”
As part of this assessment, Dr. Majcher took a nerve fiber layer (NFL) OCT scan in which, alongside the glaucomatous NFL loss, she observed a section of superonasal NFL loss, corresponding to the location of the abnormal vessels. “We don’t commonly expect to see glaucomatous NFL loss superonasally,” highlights Dr. Majcher; to visualize these vessels further, she turned to OCTA (Figure 2). “I saw retinal telangiectasias alongside areas of retinal capillary dropout, more suggestive of a branch retinal vein occlusion (BRVO).” Using the slice navigator to examine the cross-section of the suspicious blood vessels confirmed this. “These vessels were intraretinally located instead of on top of the retina, as we’d expect to see if it was preretinal neovascularization on the disc,” Dr. Majcher explains. “This gave me confidence that this patient had a superonasal BRVO, presumably related to hypertension and hypertensive retinopathy.”
Figure 2. OCTA Revealed Superionasal BRVO
Although Dr. Majcher didn’t ultimately diagnose this patient as having DR, are there structural OCT changes that could point to peripheral nonperfusion in your patients? Responding to this very question, she says longstanding nonperfusion is typically associated with inner retinal layer atrophy—although this can be difficult to image and cross-section in the peripheral retina. “Anytime there’s retinal thinning, I ask my students or residents whether it’s inner or outer thinning, because this can help differentiate the underlying cause,” she explains. “In DR, it’s typically inner retinal thinning, which can sometimes be isolated out via the ganglion cell complex (GCC). However, things become complicated with DR patients that are also glaucoma suspects. Here, it’s a challenge to determine whether GCC or ganglion cell analysis loss is due to DR or glaucoma.”
Yasha S. Modi, MD, MHS, also warns that it’s easy to mis-stage DR if you only use OCT. “If you’re seeing lots of areas of inner retinal thinning and you’re thinking a patient may have moderate NPDR, you may be underestimating the disease severity,” he highlights. “It’s a great opportunity to consider FA or montage OCTAs to look for areas of nonperfusion outside the macula—major risk factors for progression to proliferative disease. Doing so will tell you if you have the right diagnosis and what exactly to worry about.”
A tale in time
But sometimes the impact of imagery isn’t found in a singular moment but, instead, in its ability to assess change—and inform multiple ocular subspecialties—over time. The case Shalini Sood, MD, shares is of a 25-year-old patient referred to the uveitis team in 2025. Over the prior five years, starting from her first presentation in the emergency department in 2020 with an intraocular pressure (IOP) of 50 mmHg, OD, the patient had received several procedures—including pars plana vitrectomy, Ahmed tube shunt, endolaser, and cyclophotocoagulation (CPC)—aiming to control her IOP. Alongside this were several medication changes, aiming to strike the balance between addressing her cystoid macular edema (CME) and associated inflammation, and looking to quell steroid-associated IOP increases.
“Following CPC, some mild subretinal fluid was noted, OS, so topical prednisolone was increased, but the patient developed a steroid response, causing her IOP to reach the 40s—leading us to start her on Diamox,” recalls Dr. Sood. “Over the next while, we went on a back-and-forth clinical course whereby her CME would improve when put on a more potent steroid—like Durezol—alongside which, we gave oral CAIs. We’d try to taper off of the steroid, but any time we did, her pressure would increase, and the inflammation would return.”
Selective laser trabeculoplasty is regularly discussed in the setting of steroids, but what value does it have in a case like this? “The problem with the steroid response is that it frequently generates high pressures, so the laser might not be quick enough; it doesn’t work immediately,” answers Michael V. Boland, MD, PhD. “Because of that, it’s not always the first thing I try. If the pressure isn’t that bad, it can be reasonable to consider a laser because it can work—the fundamental issue is meshwork dysfunction. But if the pressure is very high after something like a Kenalog injection, you might not have the luxury of waiting six weeks for the laser to actually do its thing.” But that doesn’t mean that there aren’t interventions that can be beneficial in these cases. “Of course, we should adjust the drops and move to lower-potency steroids if we can, but with the availability of much safer, less-invasive surgical options like MIGS, my threshold is now pretty low for taking a patient to the OR to lower IOP,” Dr. Sood explains. “In patients that require long-term steroids, we need to think about how we’ll treat IOP long-term.”
So, how was this patient managed after referral to the uveitis team? She was first examined and imaged again to compare her current ocular landscape to its previous states. Through this, Dr. Sood observed a healthy optic nerve, OS, without the signs of ischemia or PDR present, OD. There was some persistent subretinal fluid identified, OS, using OCTA; with FA also demonstrating petaloid and peripheral vascular leakage, OS, alongside optic nerve hyperfluorescence. With this, Dr. Sood made multiple adjustments to the patient’s medications and, because the patient was relatively young and likely to require some sort of chronic therapy, offered her a tube shunt—which she refused. Instead, she received MicroPulse, OS, and later on, a second CPC diode with a Kenalog injection, OS, to curtail increases in IOP.
“At her most recent examination, her vision was 20/60 and 20/20, OD and OS, respectively,” says Dr. Sood. “Her pressure is currently controlled, at 5 and 13 mmHg; she’s been off oral CAIs since her last CPC; and maintaining Durezol, BID has kept her CME under control.” But, as Dr. Sood says, reaching this point required effective inter-specialty collaboration—and impactful imaging.
