||Volume 16, Number 2
THE DESK OF THE EDITOR
Since 2017, the Optometric Retina Society has sponsored an annual case report contest for residents in memory of Dr. Larry Alexander, a field pioneer and a past president within the ORS. The winning case report, focused on vitreoretinal disease, is featured in Review of Optometry and receives an $1,000 award. Each year the number and quality of case report submissions has increased making it more difficult for the chair, Dr. Julie Rodman, to pick the winner. This year with the generous support of our industry sponsors, we are pleased to announce two winners: Drs. Sophia Leung (Oklahoma Medical Eye Group) and Paul Krabill (James A. Haley VA).
The contest is a great opportunity for residents to showcase their hard work. While unfortunately, we can’t acknowledge all of the great submissions, I’d like to feature some of the other great cases and images within this newsletter forum. You’ll notice the case featured in this edition’s What’s Your Diagnosis section is from a case report submission from resident, Dr. Ashley Bailey. Congratulations to all of these bright and talented residents who will be wrapping up their residency year shortly.
It has sure been a challenging year for our residents and students alike. We have all been affected by COVID-19 whether by a disrupted education, graduation, research, or clinical practice. I have been impressed by our field and the rush of support created for clinical education activities, financial/business guidance, seminars on telehealth and so forth. Our stress levels are high with an uncertain future. For now, I continue to try and just keep my head up. As Dory from “Finding Nemo” would say, “just keep swimming.” And yes, in the past 12 weeks, I have watched far too many Disney movies with my children. But still, an excellent mantra to live by in the current environment!
Anna Bedwell, OD, FAAO
I hope that everyone is healthy and safe in these crazy times that we live in right now. As the stay at home orders are being lifted and businesses are beginning to open, I think it’s necessary that we all take the appropriate precautions, but also get back to business and life as normal as possible. I think we have learned a few things from the past three months of dealing with the ever-changing guidelines and news on the coronavirus that can be applied to eye care and life in general.
We have learned who the most vulnerable to coronavirus are in our society and what we could have done to better protect them. Likewise, we know who the most vulnerable are to the ravages of the most common vision-threatening retinal disease: macular degeneration. We also know things that they can do to better protect themselves from vision loss. Are we all counseling our elderly patients who are at higher risk for macular degeneration on the things that they can do to minimize that risk?
It has become very clear from the current “quarantines” that socialization is very important in maintaining normal mental health in human beings. With normal social interaction having been necessarily prevented over the past three months, many people are very anxiously awaiting a return to normalization. Much of our normal social interaction revolves around vision. I recently walked right by one of my very good friends as I was making my way through a hardware store and didn’t recognize him due to the mask he was wearing. He was able to partially recognize me and furtively called my name thereby allowing us to have a nice conversation. If I can’t recognize my friend walking right next to me, I have lost the opportunity to greet him and maintain that valued relationship. This same loss of facial recognition comes with macular degenerations’ loss of central vision. I am daily grateful for good vision and also grateful every day that I’m in a profession wherein I can help others to preserve their precious vision. My sincere hope is that we can all get back to our normal lifestyle as quickly as safely possible and that we, as eye doctors, can seek out the most vulnerable in our practices and help them to prevent eye disease and loss of vision.
Jeffrey Austin, OD, FAAO
MAKE THE DIAGNOSIS
Answer appears later in newsletter.
Answer appears later in newsletter.
Which of the following fundus autofluorescence images represents adult-onset vitelliform dystrophy?
Answer appears later in the newsletter.
Multimodal Evaluation of Central and Peripheral Alterations in Stargardt Disease: A Pilot Study
Stargardt disease, a hereditary retinal dystrophy, is characterized by impairment to the macula. Peripheral involvement can also be present but varies widely. This study sought to use ultrawide field (UWF) to classify peripheral subtypes and compare that to macular findings.
The study recruited 40 patients with genetically confirmed Stargardt disease—35 met criteria, and 70 healthy controls were included in a pilot, observational, cross-sectional design. Peripheral retinal testing included UWF color and autofluorescence and macular testing with OCT and OCTA. The duration of those with Stargardt disease was 17±10 years. Assessing the UWF peripheral findings in the Stargardt group, 34 eyes (49%) fell into type I pattern with no peripheral alterations. There were 24 eyes (34%) with type II pattern, presence of retinal flecks and atrophic changes. The remaining 12 eyes (17%) were categorized as type III pattern, characterized by extensive peripheral alterations. All cases were symmetrical between the eyes in UWF pattern.
The results aligned with previous studies alluding to the presence of three different phenotypes of peripheral retinal involvement rather than disease progression itself. They found each phenotype had variable damage on OCT and OCTA. In particular, type III correlated with the worst visual acuity and more damage on OCT and OCTA analysis. Further study is indicated to compare the peripheral manifestations of Stargardt disease with the maculopathy.
Arrigo A, Grazioli A, Romano F, et al. Multimodal evaluation of central and peripheral alterations in Stargardt disease: a pilot study. Br J Ophthalmol. 2019; Nov 20. [Epub ahead of print].
Outcomes of Rhegmatogenous Retinal Detachment Repair After Failed Pneumatic Retinopexy
In the treatment of rhegmatogenous retinal detachment (RRD), pneumatic retinopexy (PR) entails injecting a gas bubble into the vitreous and then positioning the patient’s head to place the bubble at the best location to seal a break. It offers an often successful and less invasive alternative to scleral buckle or vitrectomy. But what is the outcome for those in which PR doesn’t work? This retrospective review investigated the outcomes of those who had a failed pneumatic retinopexy (PR) in initial treatment to repair RRD.
Records were analyzed on 114 eyes in those who had a primary RRD treated by PR (with cryotherapy in 109 cases) who subsequently had persistent RD or needed further treatment (within the first six weeks post PR) to reattach the retina. Of those failed cases, 92 eyes were single breaks, 16 were two breaks and six eyes were three breaks. Multiple breaks were all clustered within 1.5 clock-hours. Only seven of the failed PR cases were treating breaks in the inferior retina, a situation where PR is not generally utilized.
In most cases, 79.8%, re-treatment was successful with just one additional procedure at the surgeon’s discretion. Most often this was pars plana vitrectomy (PPV) with gas tamponade in 50%, scleral buckle in 18% and PPV with silicone oil in 15%. Before PR, visual acuity averaged 0.73 ± 0.78 logMAR, and with failed PR, remained similar at 0.77 ± 0.73 logMAR. In the 91 eyes that had just one additional treatment, the final visual acuity improved to 0.39 ± 0.51 logMAR. The VA in those with multiple surgeries fared worse, as expected. Interestingly, in the seven eyes with inferior breaks and PR failure, none required multiple interventions (all reattached with PPV and either gas or oil).
With regard to visual acuity, the authors found it was not harmful to those who failed an initial treatment of PR. The vast majority (79%) of those who failed PR went on to have a successful outcome. As a primary procedure, PR is not as successful as other interventions (PPV or scleral buckle), which may make it less enticing. But the authors suggested that, though failures are more common with PR, it is still a worthwhile option, as the failures still mostly go on to have a successful outcome with a single additional procedure. While this study had its limitations, mostly with regard to the retrospective nature, it provided a different perspective. Rather than just looking at the successful PR cases, how do the failure PR cases actually end up?
Vidne-Hay O, Abumanhal M, Elkader AA, et at. Outcomes of rhegmatogenous retinal detachment repair after failed pneumatic retinopexy. Retina. 2020; May;40(5):805-10.
Correlation Between Obstructive Sleep Apnea and Central Retinal Vein Occlusion
Obstructive sleep apnea (OSA) is a sleep-related breathing disorder characterized by episodes of upper airway obstruction throughout the night. It has been associated with many systemic diseases such as atherosclerosis, hypertension, diabetes mellitus and stroke. The goal of this study was to investigate the relationship between obstructive sleep apnea and central retinal vein occlusion (CRVO). Thirty patients that had a CRVO within the last three months were included in the study as well as age- and gender-matched control subjects. Patients with comorbidities such as diabetes mellitus, stroke, or coronary artery disease were excluded from the study because those are well-known risk factors for a CRVO. All subjects underwent sleep testing, and OSA severity was classified based on apnea-hypopnea index (AHI), which is defined as the number of apnea and hypopnea events per hour of sleep. Oxygen desaturation index (ODI), or the number of times the blood's oxygen level drops by a certain degree from baseline per hour of sleep, was also recorded. Results showed that 73.33% of patients with a CRVO had OSA, which was significantly higher than control subjects found to have OSA (40%). They also found that AHI was positively correlated with body mass index and ODI. Although the sample size was small, the authors concluded that OSA is likely a risk factor for a CRVO, so it is important for optometrists to order appropriate sleep testing for patients presenting with a CRVO.
Wand YH, Zhang P, Chen L, et al. Correlation between obstructive sleep apnea and central retinal vein occlusion. Int J Ophthalmol. 2019;12(10): 1634-6.
A Review and Update on the Ophthalmic Implications of Susac Syndrome
Susac syndrome is a rare condition presumed to be caused by immune-mediated damage to the endothelial cells of the brain, inner ear and retina. Occlusion of small arteries in these areas result in a pathognomonic triad of encephalopathy, hearing loss and branch retinal artery occlusions (BRAO). One study found that 24% of these patients present with visual disturbances as their initial symptoms. Ocular symptoms can include visual field defects that correspond to BRAOs such as altitudinal defects or central and paracentral scotomas. Neurological symptoms are usually non-specific and include migraine-like headaches, impaired cognition, ataxia, and mood and personality changes. Auditory symptoms include tinnitus, hearing loss and vertigo. Physical examination may show a BRAO or vasculitis, peripheral aterio-arterial collateral vessels, and Gass plaques or yellow refractile lesions similar to emboli but which can occur at any location along the arteries. Fundus fluorescein angiography (FA) is key to diagnosing and monitoring for treatment and will show arterial wall hyperfluorescence (AWH) in areas away from the occluded arteriole or even in normal vessels. OCT shows patchy atrophy of inner retinal layers, often in a bitemporal pattern. Outer retinal layers appear normal. Unfortunately, there are no serologic tests to confirm Susac syndrome, but MRI can be helpful in distinguishing it from other differential diagnoses such as multiple sclerosis or acute disseminated encephalomyelitis. Early diagnosis and treatment is important in preventing permanent deafness, blindness, dementia or other neurological defects. Initial treatment usually includes high-dose steroids although no randomized control trials exist for the treatment of Susac syndrome. Although thought to be self-limiting, there have been reports of recurrence even after 18 years in remission. Observation with FA in the acute phase and long-term is recommended, as Susac syndrome is more sensitive than brain MRI in monitoring disease activity. Although rare, optometrists can play an important part in helping to diagnose and monitor patients with Susac syndrome.
Heng LZ, Bailey C, Lee R, et al. A review and update on the ophthalmic implications of Susac syndrome. Surv Ophthalmol 2019; 64:477-485.
Safety of 6000 Intravitreal Dexamethasone Implants
Macular edema is one of the most common causes of vision loss and can occur in a variety of diseases including central retinal vein occlusion, diabetic macular edema, post-surgical macular edema and uveitis. One treatment for macular edema includes a sustained-release intravitreal steroid device, with a dexamethasone implant being the most widely used. This retrospective study of 6,015 dexamethasone implants aimed to evaluate the device’s safety profile and is the largest study to do so to date. Included patients underwent a dexamethasone implant for any indication and were followed for at least six months after the last injection. Side effects included cataract progression, and about one-third of phakic patients required extraction surgery. Progression increased in eyes receiving a higher number of dexamethasone injections. Another main side effect was an elevation in intraocular pressure (defined as an IOP>25 mmHg), affecting about one-fourth of patients. However, over 90% of these eyes were able to be managed with a topical anti-glaucoma medication and only 0.5% required filtering surgery. More serious side effects including vitreous hemorrhage, retinal detachment and endophthalmitis were rare, occurring in less than 0.1% of all cases. Interestingly, there was no statistically significant change in visual acuity and central macular thickness at the last follow-up visit, although it was significant in the subsets of patients with diabetic macular edema and retinal venous occlusion. Due to its retrospective nature, this study lacked uniformity in treatment and follow-up protocols; however, it showed that dexamethasone implants were safe and that the most common side effects are treatable.
Rajesh B, Zarranz-Ventura J, Fund AT, et al. Safety of 6000 intravitreal dexamethasone implants. Br J Ophthalmol 2020;104:39-46.
Ghost Cell Glaucoma after Intravitreous Injection of Ranibizumab in Proliferative Diabetic Retinopathy
Ghost cell glaucoma occurs in eyes with vitreous hemorrhage when degraded red blood cells make their way to the anterior chamber in sufficient quantity to elevate intraocular pressure. In eyes with proliferative diabetic retinopathy (PDR)-induced vitreous hemorrhage, intravitreal injections of anti-VEGF medications are sometimes administered prior to vitrectomy in an attempt to help stabilize the retinopathy and improve outcomes. This retrospective study from China examined the records of 71 eyes with PDR induced vitreous hemorrhage that had received intravitreal injection prior to planned vitrectomy. The authors postulated that intravitreal injections in this scenario may increase the risk of developing ghost cell glaucoma. Of the 71 eyes, eight developed ghost cell glaucoma. This rate was higher than had been previously published (11% vs. 3%). The ghost cell glaucoma developed within two days of the injection in all cases, most commonly within one day. Factors found to increase the risk of ghost cell glaucoma in this setting were the presence of tractional retinal detachment, or the presence of a fibrovascular membrane involving the optic disc. In all cases, subsequent vitrectomy led to resolution of the ghost cell glaucoma without the need for ongoing IOP management.
Xu J, Zhao M, Li JP, et al. Ghost cell glaucoma after intravitreous injection of ranibizumab in proliferative diabetic retinopathy. BMC Ophthalmology. 2020;20:149.
Thrombolytic Therapy for Acute Central Retinal Artery Occlusion
Central retinal artery occlusion (CRAO) is a devastating ocular condition for which there is no accepted standard of care treatment. Attempts at treatment may include the use of hyperbaric oxygen therapy or intravenous thrombolysis. While intravenous thrombolysis is not an accepted standard of care, it is offered as a treatment option in over half of academic centers, though it is the primary treatment offered in only approximately one-third of them. There are several barriers to the routine use of thrombolysis in the management of CRAO. In order to be effective, it needs to be delivered within 4.5 hours of symptom onset. It is often very difficult to accomplish this, especially when the patient notices the vision loss upon awaking, thus making the true time of the onset of vison loss unknown. In addition, thrombolysis carries with it the small risk of death due to hemorrhaging. This risk is much lower, however, with newer thrombolytic agents than it is with the older agents that were used in prior studies of thrombolytic CRAO therapy. After reviewing the available literature and pathophysiology of non-arteritic CRAO, and making recommendations regarding the need for future clinical trials (while admitting how difficult those would be), the authors of this paper recommended broader adoption of the use of thombolytic agents for the treatment of CRAO. This recommendation, however, came with the caveat that the protocol should be the same one used for the treatment for acute cerebral ischemic stroke.
Mac Grory B, Lavin P, Kirshner H, et al. Thrombolytic therapy for acute central retinal artery occlusion. Stroke.2020;51(2):687-95.
TO "YOU MAKE THE DIAGNOSIS"
Chronic Localized Bilateral Chorioretinal Folds with Clinical and Multimodal Imaging
INTRODUCTION: Chorioretinal folds (CRFs) are folds of the anterior choroid, Bruch’s membrane, RPE and entire sensory retina. Clinically, they have a distinct presentation of alternating light and dark bands. CRFs are commonly within the posterior pole oriented in a parallel fashion, but can be in a variety of orientations depending on the cause. The light and dark bands are caused by changes in RPE density. The light bands are where RPE is stretched at a peak. The dark bands are where RPE is compressed at the trough of the undulation. The RPE itself does not undergo a structural change contributing to the colored pattern.1 There is a long list of conditions associated with CRF including tumors, hypotony, CNVM, papilledema, etc. Depending on the cause, the patient may or may not present clinically with symptoms. In those cases with acute onset, the patient may complain of decreased vision or metamorphopsia due to the distortion of photoreceptors.1-6 However, if the onset is gradual, the patient will likely be asymptomatic.1,4 As with many retinal conditions, fundus imaging can be helpful in assessing patients with CRF.
CASE REPORT: A 65-year-old male, established patient, presented to clinic for a chorioretinal folds (CRF) follow-up. He had a history of bilateral strabismus surgery when he was approximately four years old, with a resulting alternating esotropia, right eye preference. At age 40, he had an isolated episode of central serous chorioretinopathy (CSCR) OD. He was diagnosed with CRF OD at the age of 58 and OS at the age of 61. At each time he was examined, he did not report any symptoms of decreased vision, diplopia, ocular pain, entopic phenomenon or metamorphopsia in the affected eye. He had a negative history of trauma, intraocular surgery, optic neuropathy, thyroid imbalance, autoimmune or inflammatory conditions. In addition, he had been documented to be a hepatitis B carrier. His current medications included Ammonium Lactate lotion, Cetirizine HCL, Diclofenac cream, Entecavir, Flunisolide, Hydrochlorothiazide and Omeprazole.
At this follow-up, the patient’s best-corrected visual acuity was 20/20 and 20/20-1 OD and OS, respectively. The manifest refraction was +4.00-1.25x097 OD and +4.75-1.00x095 OS. Upon diagnosis of the CRF, his refraction was +2.75 DS OD in 2013 and +5.00-0.75x095 OS in 2016. Over the course of the patient’s follow-up visits, his refractive error became consistently more hyperopic, although no changes greater than 0.50 diopter occurred at any time between baseline and the subsequent appearance of CRF in either eye. Intraocular pressure was 19mmHg and 20mmHg, respectively.
Entrance testing and slit lamp examination of the anterior segment was unremarkable. Fundus examination revealed CRF present almost circumferentially around the posterior pole located in a concentric pattern in the superior and inferior arcades of both eyes, more prominent OS, and not in the macula (Figure 1). Mild RPE mottling just superonasal to the macula and a significant epiretinal membrane (ERM) superonasal and nasal to macula OD were also noted.
Axial scans measured normal axial lengths of 23.55mm and 22.85mm, respectively. No mass, posterior scleral thickening, flattening of the posterior pole or detachment was found with B scan. The CRF were documented with color fundus photos (Figure 1), MColor (Figure 2), FAF, OCT (Figure 3), EDI, OCT-A and en face analysis.
When the patient’s CRF were diagnosed in each eye, he had unremarkable visual field testing without enlarged blind spots. An extensive review of past lab work, including complete blood count and basic metabolic panel, confirmed the absence of any autoimmune disorders. Upon further questioning, the patient denied headaches, diplopia, transient vision loss, periorbital paresthesia, pulsatile tinnitus or ocular pain. Signs of globe displacement, restricted eye motility, ptosis, conjunctival swelling or optic disc swelling were absent. Ordering further invasive tests such as lumbar puncture, MRI or orbital CT scans was not indicated. Suspicion of elevated intracranial pressure or orbital mass was low.
DISCUSSION: The precise pathogenesis of CRF is still elusive. The folds are thought to be caused by scleral thickening, shrinkage, or compression causing the choroid to buckle on itself due to a decrease in scleral area.1,8-11 If caused by compression, the folds are usually perpendicular to the direction of the applied compression.7 Others hypothesize that the folds are caused by choroidal expansion due to hyperpermeable choroidal vasculature.9,12 Because the sclera is a more rigid tissue, this expansion of the choroid puts pressure on the less structurally rigid Bruch’s membrane causing it to fold.1,7,9
Since there is an extensive list of conditions commonly associated with CRF, the workup will vary between patients, depending on their presentation and case history. Overall, each case should include a detailed medical history to determine any inflammatory, neoplastic, infectious or infiltrative disorders.9 Idiopathic causes of CRF tend to occur in middle-aged males with acquired hyperopia, but without pathologic associations.2,3 An acquired hyperopic shift is the most common associated finding with CRF. The hyperopic shift is generally caused by a mass or thickening of the posterior sclera pushing the retina anteriorly, which decreases the axial length.1-3,11 According to other case studies, hyperopic shifts usually range from 1.00 to 6.00 diopters at the time of diagnosis.3-5 Kalina and Mills suggest that cases of acquired hyperopia with choroidal folds and without other clinical signs do not require anything other than noninvasive investigative exams and should have periodic observation.3
Multimodal imaging can be useful in formal diagnosis of CRF and in assessing for ocular conditions contributing to CRF formation. Color fundus photography (CFP) is excellent for demonstrating the classic clinical appearance of the light and dark bands seen with CRF. Multicolor fundus images are superior to CFP in terms of quality and extractable diagnostic information by using three monochromatic laser sources at specific wavelengths that capture details at differing retinal depths.13 FAF produces images that reveal the status of the RPE. CRF cause bands of hyper- and hypo-autofluorescence on FAF. SD-OCT of CRF will show a uniform retinal thickness throughout the area of folds, with ripple-like waves of the choroid and all retinal layers.
En face is useful to evaluate changes in choroidal elevation. Within the en face analysis, there are seven discrete images extracted from the scan showing differing retinal layers. Since CRFs affect both the choroid and all retinal layers, the classic ripples will be seen in all map analyses, but may become less evident in the more anterior retinal scans, especially the vitreoretinal interface map. With the invention of OCT angiography (OCTA), blood flow in the choriocapillaris and choroid can now be analyzed in addition to retinal structure simultaneously and noninvasively. OCTA findings from CRFs show disruption of choriocapillaris flow along each fold. This disruption could be caused by the distressing effects of repeated swelling, stretching or expanding of choriocapillaris layer. Conversely, the signal reduction may be due to increased pigment or pigment compression along the troughs.14
CONCLUSION: There is a long list of conditions associated with CRFs, and the presence of concerning or questionable clinical findings often indicates the need for further work-up. Multimodal imaging in cases of CRFs can be instrumental in making a definitive diagnosis and in ruling out other ocular signs that indicate potential sight- or life-threatening.
Ashley Bailey, OD
Resident, American Lake VA
|Figure 1 (top of newsletter). Fundus photos showing alternating bands of light and dark circumferential-like chorioretinal folds in the superior and inferior arcades, both temporal and nasal to the optic nerve head OD (left image) and OS (right image) sparing the maculas, using the Zeiss Clarus 500 Fundus Camera.
|Figure 2. Multicolor scanning laser imaging showing a combined scan of Infrared (820nm), green (515nm) and blue (488nm) reflectance scans as well as each laser scan individually using Spectralis Heidelberg OCT. The chorioretinal folds can be seen in the superior arcades OD (top image) and OS (bottom image) viewed with the 30-degree default lens attachment. An old central serous chorioretinopathy scar and epiretinal membrane are also visible OD.
|Figure 3. Heidelberg Spectralis OCT showing chorioretinal folds, obvious by the undulations of the choroid affecting all retinal layers in the superior arcades OD (top image) and OS (bottom image). Note the thickness of the retinal layers above the choroid remain unchanged with exception of blood vessel thickness changes.
1. Gasperini J, Elliot D MD, E.T. Cunningham Jr. ET. How to recognize and treat chorioretinal folds. Rev of Ophthalmology. 2006 Nov;13:11.
2. Dailey RA, Mills RP, Stimac, GK, et al. The natural history and CT appearance of acquired hyperopia with choroidal folds. Ophthalmology. 1986 Oct;93(10):1336-42.
3. Kalina RE, Mills RP. Acquired hyperopia with choroidal folds. Ophthalmology. 1980 Jan;87(1):44-50.
4. Jacobsen AG, Toft PB, Prause JU, et al. Long term follow-up of persistent choroidal folds and hyperopic shift after complete removal of retrobulbar mass. BMC Res Notes. 2015 Nov;8:678.
5. Murdoch D, Merriman M. Acquired hyperopia with choroidal folds. Clin Exp Ophthalmol. 2002 Aug;30(4):292-4.
6. Olsen TW, Palejwala NV, Lee LB, et al. Chorioretinal folds: associated disorders and a related maculopathy. Am J Ophthalmol. 2014 May;157(5):1038-47.
7. Jaworski A, Wolffsohn JS, Napper GA. Aetiology and management of choroidal folds. Clin Exp Optom. 1999 Sep-Oct;82(5):169-176.
8. Bagnis A, Cutolo CA, Corallo G, et al. Chorioretinal folds: a proposed diagnostic Algorithm. Int Ophthalmol. 2019 Nov;39(11):2667-2673.
9. Xirou T, Kabanarou SA, Gkizis I, et al. Chronic Central serous chorioretinopathy-like maculopathy as atypical presentation of chorioretinal folds. Case Rep Ophthalmol. 2017 Dec 14;8(3):568-73.
10. Leahey AB, Brucker AJ, Wyszynski RE., et al. Chorioretinal folds. A comparison of unilateral and bilateral cases. Arch Ophthalmol. 1993 Mar;111(3):357–9.
11. De La Paz MA, Boniuk M. Fundus manifestations of orbital disease and treatment of orbital disease. Surv Ophthalmol. 1995 Jul-Aug;40(1):3-21.
12. Corvi F, Capuano V, Benatti L, et al. Atypical presentation of chorioretinal folds-related maculopathy. Optom Vis Sci. 2016 Oct;93(10):1304-14.
13. He L, Chen C, Yi Z, et al. Clinical application of multicolor imaging in central serous chorioretinopathy. Retina. 2018 Dec 31.
14. Del Turco C, Rabiolo A, Carnevali A, et al. Optical coherence tomography angiography features of chorioretinal folds: a case series. Eur J Ophthalmol. 2017 Mar 10;27(2):e35-8.
Group Calls for Suspension of Prior Authorizations by Insurance Companies
The American Academy of Ophthalmology (AAO) wrote a letter to all health plans in an attempt to stop the prior authorization and step therapy process during the COVID-19 pandemic. Other national physician organizations have followed suit.
The letter argues against the “cosmic absurdity” of the health plans’ policies in a time where both insurance companies and medical practices have limited staff to be available for receiving or making phone calls. Doctors returning to work will be providing long-delayed services, and the AAO states these authorizations only further delay medically necessary services.
Ophthalmology Takes Lead in Patient Volume Loss During COVID-19
Ophthalmology saw an 81% decline in services compared to a similar 2019 time period —the most by any discipline—according to an analysis by Strata Decision Technology. Cataract surgery fell by 97%, which also led all other surgical procedures. Glaucoma surgery numbers were only slightly better at an 88% reduction.
Not surprisingly, the report noted a significant decline in access to clinical care for life-threatening conditions such as congestive heart failure, heart attacks and stroke. Access for chronic conditions such as diabetes and hypertension also dipped. The number of uninsured or self-pay patients increased as well, which they attributed to the rise in the national unemployment rate. Optometry was not included in the analysis.
Icare Rebounds with New Retinal Imaging Device
The “No Drops, No Puff Tonometer” company Icare USA announced the release of the Centervue DRSplus confocal imaging system. The fully automated system utilizes the entire visible spectrum through white LED illumination to produce sharp, true color images. Confocal imaging reduces or suppresses scattered or reflected light outside the focal plane, according to the product description. Using the mosaic function increases the image field from 45 to 80 degrees. The company touts an under 10 second acquisition time for both eyes with the push of a single button.
||AI-Supported Test May Bring Earlier Glaucoma Progression Out of the DARC
Detection of apoptosing retinal cells, or DARC, could detect glaucoma progression 18 months before clinical signs appear, according to a sponsored clinical trial by the University College London. Because specialists often differ when reading the same scan, the technology incorporated an artificial intelligence (AI) algorithm.
For DARC, researchers inject a fluorescent dye through venipuncture. As it travels through the bloodstream, the dye attaches to retinal cells and illuminates those that are in the process of apoptosis, appearing bright white. The DARC count is the cumulative number of damaged cells. Eighteen months after the initial phase II trial period, all patients over a certain DARC threshold were found to have progressive glaucoma.
|| Efficacy On-Par with Ranibizumab, But with Inflammatory Differences
Neovascular age-related macular degeneration patients may soon have another treatment option with abicipar pegol (Allergan/Molecular Partners), which is expected to receive FDA approval this year. The drug represents a new class of designed ankyrin repeat proteins (DARPins). Results of the Phase III CEDAR and SEQUOIA trials showed noninferiority of eight- and 12-week regimens of abicipar 2mg compared with four-week treatment with ranibizumab. Because of this, abicipar patients averaged 10 injections over the two-year study, vs. 25 for ranibizumab. First-year intraocular inflammation rates reached 15 percent vs. 0.6 percent for ranibizumab, with second-year abicipar rates decreasing to 1.9 percent
|| OD-OS Brings Retinal Laser Training to the iPad
The makers of the Navilas® retina laser recently unveiled the Navigate App—an online tool for implementing a better approach to retinal laser treatment. The app uses preloaded or custom images from multimodal imaging (FA, OCT, OCTA) to develop laser treatment strategies in various cases. The app is free and offers medical decision-making and treatment strategies in a controlled environment prior to live patient experience.
|| Retina-Specific Physician Management Service Adds Fifth
Retina Consultants of America (RCA), formed earlier this year by Webster Equity Partners, recently added its fifth practice—California Retina Consultants. The physician management services organization seeks to partner with leading retinal specialists. With its capital resources and expertise, RCA invests in the practice and positions it for continued growth. The business model shares best practices and executive management support while enabling doctors to retain ownership and autonomy.
IMAGE QUIZ ANSWER
The correct answer, image B, shows the characteristic fundus autofluorescence (FAF) findings in adult-onset vitelliform dystrophy. Considered one of the pattern dystrophies, findings typically begin in middle age with bilateral, yellow lesions localized at the fovea. The later age of onset and smaller size (1/3-1/2 DD) of the lesions help to differentiate adult-onset vitelliform dystrophy from Best’s disease. The vitelliform material is hyperfluorescent on FAF, as seen in the image, due to a buildup of lipofuscin. On OCT, the lesions are hyper-reflective and lie between the ellipsoid zone and the retinal pigment epithelium. Generally, patients with adult vitelliform dystrophy maintain good visual acuity. However, there is risk for development of choroidal neovascularization.
A: cone-rod dystrophy
C: Best’s dystrophy (atrophic stage)
D: central serous chorioretinopathy
MEET THE FELLOWS
Brian Bucca, OD, FAAO, received his bachelor’s degree in biology/chemistry from the University of Southern Mississippi in 1997 and obtained his doctorate in optometry from the University of Alabama Birmingham in 2001. After completion of his residency in primary care/ocular disease at the Northern Navajo Medical Center in Shiprock, NM, he joined the United States Public Health Service (USPHS) and remained stationed in Shiprock to direct the Diabetes Eye Care Program and hold adjunct faculty status at the Southern California College of Optometry. During his tenure with USPHS, Dr. Bucca achieved the rank of lieutenant commander, became deputy chief of eye clinic, and directed both the optometry externship and residency programs at the Northern Navajo Medical Center.
Since 2007, Dr. Bucca has been director of eye clinic at the Barbara Davis Center for Diabetes located on the University of Colorado Anschutz Medical Campus in Aurora, CO, where he is an associate professor in both the departments of pediatrics and ophthalmology. He obtained training in ETDRS grading in 2007 at the University of Wisconsin Ocular Epidemiology Research Group and has weaved this unique skillset into patient care as a tool for assessing retinopathy progression on the most sensitive scale. In addition to patient care, Dr. Bucca is active within the pediatric ocular disease optometry residency program at Children’s Hospital Colorado, he teaches in the classroom setting within the University of Colorado Physical Assistant Program and serves as a contractor for obtaining fundus photography and ETDRS grading in many local, industry-sponsored and multicenter randomized clinical trials.
WHY BECOME AN ORS FELLOW?
By Bill Denton, O.D., F.A.A.O.
Chair, Membership Committee
At some point in your career, you realize you just may be coasting. Your knowledge has been limited to the journals you receive and attempt to read, and the conferences that may not be as fulfilling as they once were. You simply need a challenge that will add an extra dimension to your professional learning.
Fellowship in the Optometric Retina Society (ORS) can provide several benefits in addition to the initial challenge of qualifying for this honor. Plenty of perks accompany your induction, but the coolest part is being associated with a body of knowledge and resources which can help you in many other ways. It is not uncommon to receive weekly thought-provoking emails about challenging cases and treatment dilemmas. Some fellows like to share their awesome cases they have diagnosed, while others post their cases with hopes that other Fellows will suggest an alternative differential diagnosis. At times it is like a round-table of brainstorming, but through the use of modern technology. Fellowship has little obligation with a huge opportunity for professional growth.
If you are up to the challenge of becoming a Fellow of the ORS, feel free to peruse the details and application at www.optometricretinasociety.org. Advice can be given to assist you in your quest. Feel free to contact us.
Anna K. Bedwell, OD, FAAO
Brad Sutton, OD, FAAO
Larissa Krenk, OD
Jim Williamson, OD, FAAO
Senior Graphic Designer
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