REVIEW OF OPTOMETRY ■

EARN 2 CE CREDITS: Positive Visual Phenomena—Etiologies Beyond the Eye, PAGE 58 VOL. 155 NO. 1 ■

January 15, 2018 www.reviewofoptometry.comwww.reviewofoptometry.com

ANNUAL CORNEA REPORT JANUARY 15, 2018 ■

CXL ■ EPITHELIAL DEFECTS ■

How to Heal Persistent Epithelial Defects PAGE 38 TRANSPLANTS ■ Corneal Transplants: The OD’s Role PAGE 44

INFILTRATES Diagnosing Corneal Infiltrative Disease PAGE 50 ■

POSITIVE VISUAL PHENOMENA CXL: Your Top 12 Questions —Answered! PAGE 30

001_ro0118_fc.indd 1 1/5/18 4:34 PM ĊčĞĉėĆęĊĉĆĒēĎĔęĎĈĒĊĒćėĆēĊċĔėĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊĘ ĊđĎĊċĎēĘĎČčę ċċĊĈęĎěĊ  Ȉ ‡–ƒ‹•–Š‡‰”‘™–Šˆƒ –‘”•ˆ‘—†‹ƒ–—”ƒŽƒ‹‘–‹ ‡„”ƒ‡1 Ȉ ‡–ƒ‹•‘”‡‘ˆ–Š‡•‡‰”‘™–Šˆƒ –‘”•–Šƒ‘–Š‡” †‡Š›†”ƒ–‡†ƒ‹‘–‹ ‡„”ƒ‡’”‘†— –1 ĊđđǦęĔđĊėĆęĊĉ  Ȉ ‘–ƒ’‡–ƒ”•‘””Šƒ’Š›”‡“—‹”‡†  Ȉ ‹‹‹œ‡†ˆ‘”‡‹‰„‘†›•‡•ƒ–‹‘ ĎĒĕđĊĎēǦĔċċĎĈĊĕėĔĈĊĉĚėĊ  Ȉƒ•‹Ž›ƒ’’Ž‹‡†–‘ƒ†”› ‘”‡ƒ  Ȉ‘˜‡”‡†™‹–Šƒ„ƒ†ƒ‰‡ ‘–ƒ –Ž‡• ĔēěĊēĎĊēę  Ȉ͝›‡ƒ”•Š‡ŽˆŽ‹ˆ‡  Ȉ–‘”‡†ƒ–”‘‘–‡’‡”ƒ–—”‡  Ȉ‘ˆ”‡‡œ‡”‘”•’‡ ‹ƒŽ•Š‹’’‹‰ƬŠƒ†Ž‹‰”‡“—‹”‡†

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RO0118_Katena.indd 1 1/2/18 10:34 AM News Review

VOL. 155 NO. 1 ■ JANUARY 15, 2018

IN THE NEWS Accelerated CXL Shows The FDA recently approved Luxturna (voretigene neparvovec-rzyl, Spark Promise—and Caution Therapeutics), a directly administered gene therapy that targets biallelic This new technology is already advancing, but not without RPE65 mutation-associated retinal dystrophy. The therapy is designed to some bumps in the road. deliver a normal copy of the gene to By Rebecca Hepp, Managing Editor retinal cells to restore vision loss. While the approval provides hope for patients, wo new studies highlight the resulted in infection—while tradi- the $425,000 per eye price tag stands as pros and cons of accelerated tional C-CXL has a reported inci- a signifi cant hurdle. Tcorneal crosslinking (A- dence of 0.0017%.2 The researchers Scutti S. Gene therapy for rare retinal disorder to cost CXL). Researchers in Switzerland examined possible contributory fac- $425,000 per eye. CNN. www.cnn.com/2018/01/03/ health/luxturna-price-blindness-drug-bn/index.html. studied the outcomes of conven- tors in those seven cases and found Accessed January 4, 2018. tional (C-CXL) and accelerated young age, a pre-existing immuno- corneal crosslinking (A-CXL) in compromized state, poor hygiene A study 167 patients with suspected a pediatric population and found at the operation site and in post-op bacterial endophthalmitis after cataract A-CXL was equally effective after environments, long-term steroid surgery found intravitreal dexametha- one year.1 use and poor post-op education sone provided no improved visual “The potential advantages in- and management were all concerns. acuity. Patients were treated twice with clude reduced exposure time, better Although the study was limited to intravitreal injections of 0.2mg vanco- patient compliance and possibly one clinical site, it highlights the mycin and 0.05mg gentamicin, followed lower infection risk (more patient importance of patient education by either 400µg dexamethasone sodium and doctor friendly),” says S. Barry and careful post-op follow up with diphosphate or placebo. The four-week, Eiden, OD, president and medical this new procedure. 10-week, six-month and 12-month fol- director at North Suburban Vision These studies further highlight low ups showed no signifi cant difference Consultants, Ltd., and president not just the evolving nature of treat- in best-corrected visual acuity. and cofounder of the International ment, but “what we at the IKA call Manning S, Ugahary LC, Lindstedt EW, et al. A Keratoconus Academy (IKA). ‘the changing paradigm of kera- prospective multicentre randomized placebo-controlled superiority trial in patients with suspected bacterial en- The study included 78 eyes of toconus management,’” Dr. Eiden dophthalmitis after cataract surgery on the adjuvant use 58 pediatric patients with progres- says. With access to a treatment of intravitreal dexamethasone to intravitreal antibiotics. Acta Ophthalmol. December 7, 2017. [Epub]. sive keratoconus. Half of the eyes that can halt progression and pos- underwent C-CXL and half had A- sibly prevent vision loss, clinicians New research suggests a desktop CXL. One year post-procedure, the have a duty to diagnose patients humidifi er may help patients with researchers noted no difference in as early as possible and identify dry eye symptoms during continuous outcomes between the two groups, those at high risk of progression. computer use. Investigators measured including uncorrected visual acuity, Improved diagnostic technologies noninvasive tear break-up time (NTBUT) best-corrected visual acuity and would be welcome additions to the in patients who did and did not use a kmax values. The treatment failure evolving treatment options, such desktop humidifi er for an hour of com- rate was slightly lower for A-CXL, as A-CXL, for patients at risk for puter use and found improved NTBUT in at 15.4% compared with 23.1% of keratoconus, Dr. Eiden concludes. the humidifi er users compared with those the C-CXL group. 1. Baenninger PB, Bachmann LM, Wienecke L, et al. Pediatric without a humidifi er. However, a second study took corneal cross-linking: comparison of visual and topographic outcomes between conventional and accelerated treatment. Am Wang MT, Chan E, Ea L, et al. Randomized trial of a closer look at other A-CXL J Ophthalmol. 2017 Nov;183:11-16. desktop humidifi er for dry eye relief in computer users. outcomes such as infection rates 2. Maharana PK, Sahay P, Pranita, Sujeeth M, et al. Microbial Optom Vis Sci. 2017;94(11):1052-7. keratitis after accelerated corneal collagen cross-linking in and found 1.3% (seven of 532 eyes) keratoconus. Cornea. November 2, 2017. [Epub ahead of print].

REVIEW OF OPTOMETRY JANUARY 15, 2018 3

0003_ro0118_news(v2).indd03_ro0118_news(v2).indd 3 11/5/18/5/18 2:122:12 PMPM News Review

Beware of ISNT Rule Exceptions, Study Says

linicians who rely on the Photos: Jarett Mazzarella, OD ISNT rule when assessing Cthe optic nerve—for signs of early glaucoma, for example— should remember it doesn’t neces- sarily apply to all patients. While the rule states optic nerves typically show a larger rim width inferior, superior, nasal and then temporal, a new study highlights just how often patients deviate from this: within Optic nerves come in all shapes and sizes, making the ISNT rule tough to follow. Can this particular study population, you tell which are normal, anomalous but non-glaucomatous and glaucomatous? only 37.0% of rim assessments and 43.8% of retinal nerve fi ber layer most signifi cant causes of devia- for early signs of glaucoma, Dr. (RNFL) measurements follow the tion, with 10.9% of subjects having Mazzarella says the fi ndings serve rule, according to the researchers. a wider nasal rim than inferior, as a stark reminder of the impor- “As we know, there is a wide 29.4% with a wider nasal rim than tance of obtaining baseline readings, variance of normal nerve anatomy, superior, 14.7% with a narrower following for change over time and which makes diagnosing early glau- nasal rim than temporal and 42.9% “not getting stuck in the mindset of coma diffi cult in some patients,” having thinner nasal RNFLs com- always following traditional rules.” says Jarett Mazzarella, OD, who pared with the temporal quadrant. “Early disease is the confounding practices in the VA Health Care Sys- “We know glaucoma patients factor between identifying abnor- tem in Salisbury, NC. “Although a tend to lose neuroretinal rim on the mal structure vs. a normal variant. number of patients in the study did superior and inferior rims, and in For example, we see this often with not conform to the standard rule, this study, excluding the nasal rim our OCT technology when a patient in my opinion it does not invalidate to modify the rule to the IST or IS fl ags as abnormal on OCT RNFL the ISNT rule since the areas of made it apply to roughly 70%,” or ganglion cell compared with the rim we are concerned with in says Justin Cole, OD, of the VA the normative data values,” Dr. early glaucoma are the inferior or Health Care System in Salisbury, Mazzarella says. “Many of these superior rim.” NC. “So the rule still applies, but I patients never change or progress, Researchers looked at 110 nor- also think we have really been using which usually indicates a variant mal subjects and found a larger or it as the ‘IS’ rule all along.” of normal anatomy. It comes down smaller nasal sector was one of the For clinicians assessing patients to establishing a baseline for that individual patient and watching Hot Tea’s Impact on Glaucoma for any indication of structural or Tea drinkers have one more reason to brew another pot this functional progression over time, winter. A new study found drinking hot, caffeinated tea may especially for the normal nerve that be associated with a lower risk of glaucoma. Data from the does not look so ‘typical.’” 2005-2006 National Health and Nutrition Examination Survey “Each clinician must use their indicates hot tea-drinkers were 74% less likely to have own judgment in identifying normal glaucoma. The same was not true for coffee (caffeinated or from abnormal cup-to-disc ratios decaffeinated) decaffeinated tea, iced tea or soft drinks. and appearances, while also having While the survey had a small number of patients diagnosed with glaucoma and didn’t take the wherewithal to know that ana- into account other factors such as cup size, tea type or brewing time, the researchers speculate tomical differences are common,” the tea’s antioxidants and anti-infl ammatory and neuroprotective chemicals may play a role. concludes Dr. Cole. Poon LYC, Valle DSD, Turalba AV, et al. The ISNT rule: how often Wu CM, Wu AM, Tseng VL, et al. Frequency of a diagnosis of glaucoma in individuals who consume coffee, tea and/or soft does it apply to disc photographs and retinal nerve fi ber layer drinks. British J Ophthalmol. December 14, 2017. [Epub ahead of print]. measurements in the normal population? Am J Ophthalmol. 2017;184:19-27.

4 REVIEW OF OPTOMETRY JANUARY 15, 2018

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Exccessive Exercise May Raise Men’s AMD Risk Photo: Andrew Rixon, OD new study suggests exercis- Still, no strong biological rationale ing fi ve or more times a exists for this fi nding yet. Aweek may increase a man’s “However, the authors were cau- risk of neovascular age-related tious about the results and recom- macular degeneration (AMD). mended additional studies,” says Researchers in Japan looked at Sherrol Reynolds, OD, an associate 211,960 patients ages 45 to 79 at professor of optometry at Nova baseline and then seven to 10 years Southeastern University College of later and found men ages 45 to 64 Vigorous exercise may increase a man’s Optometry. “Before clinical recom- who exercised vigorously had a risk of neovascular AMD, as seen here. mendations are made about limiting 54% increased risk of neovascular physical activity or discussing AMD compared with men in the While neither previous research caution with rigorous activity and non-exercise group. They did not nor this study provide further neovascular AMD, more research is fi nd the same association in women. insight into the possible reasons necessary.” These results come after adjusting behind the association, the investi- Rim TH, Kim HK, Kim JW, et al. A nationwide cohort study on the association between past physical activity and neovascular for factors such as age, medical his- gators speculate excessive exercise age-related macular degeneration in an East Asian population. tory and body mass index. may affect the patient’s choroid. JAMA Ophthalmol. December 14, 2017. [Epub]. Macular Damage Mechanism Discovered

esearchers at the University in the pathogenesis of GA.” vide insight into the understanding of Virginia School of Medi- While cGAS is well known for its of the mechanisms of cell damage Rcine have uncovered one of role in detecting foreign DNA and and death in patients with geo- the fi rst triggers of infl ammation in initiating the immune response to graphic atrophy,” says Dr. Weid- macular degeneration, a common infections, researchers were sur- mayer. “Watching so many patients enzyme called cyclic GMP-AMP prised to discover its impact on dry progressively lose their vision due to synthase (cGAS). age-related macular degeneration. GA, with very little to offer in the “This research found that, in hu- Without any foreign invasion to way of treatment, is disheartening; man cell cultures and mice in vivo, activate cGAS, elevated levels in the the prospect of someday being able certain proteins including the DNA RPE of eyes with GA suggests the to employ a treatment to block an sensing enzyme cGAS, played a role enzyme may play a bigger part in enzyme which drives the disease is in activating an infl ammatory im- the body’s response to noninfectious certainly exciting for the entire eye mune response that ultimately leads human disease. care community.” to retinal pigmented epithelium “These fi ndings continue to pro- “This research may prompt the

(RPE) cell death,” says Sara Weid- Photo: Sara Wedmayer, OD development of medications to mayer, OD, who works at the VA block or inhibit cGAS, which Ann Arbor Healthcare System in could ultimately change the trajec- Ann Arbor, Mich., and is a clinical tory of visual outcomes for GA assistant professor at the Kellogg patients,” Dr. Weidmayer adds. Eye Center, Department of Oph- “Hopefully this research will serve thalmology and Visual Sciences at as a step on the path to the goal of the University of Michigan. individualized, precision medi- “These proteins were found in cine.” ■ higher levels in patients with geo- Patient with AMD may one day have a new Kerur N, Fukuda S, Banerjee D, et al. cGAS drives nonca- graphic atrophy (GA), so the fi nd- treatment option to combat geographic nonical-infl ammasome activation in age-related macular ings suggest that they are involved atrophy, as seen here. degeneration. Nature Medicine. November 27, 2017. [Epub].

6 REVIEW OF OPTOMETRY JANUARY 15, 2018

003_ro0118_news(v2).indd 6 1/5/18 2:13 PM T:8” S:7”

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For more information about VYZULTA, visit vyzultanow.com INDICATION For more information about VYZULTA,• Macular visit edema, vyzultanow.com including cystoid macular VYZULTA™ (latanoprostene bunod ophthalmic edema, has been reported during treatment with solution), 0.024% is indicated for the reduction of prostaglandin analogs. Use with caution in aphakic INDICATION • Macular edema, including cystoid macular intraocular pressure (IOP) in patients with open-angle patients, in pseudophakic patients with a torn VYZULTA™ (latanoprostene bunod ophthalmic edema, has been reported during treatment with glaucoma or ocular hypertension. posterior lens capsule, or in patients with known solution), 0.024% is indicated for the reduction of prostaglandin analogs. Use with caution in aphakic risk factors for macular edema intraocularIMPORTANT pressure SAFETY (IOP) INFORMATION in patients with open-angle patients, in pseudophakic patients with a torn glaucoma• Increased or pigmentation ocular hypertension. of the iris and periorbital • posterior There have lens been capsule, reports or in of patients bacterial with keratitis known tissue (eyelid) can occur. Iris pigmentation is likely riskassociated factors with for macularthe use of edema multiple-dose containers of IMPORTANT SAFETY INFORMATION risk factors for macular edema to be permanent topical ophthalmic products that were inadvertently • Increased pigmentation of the iris and periorbital • There have been reports of bacterial keratitis contaminated by patients • tissueGradual (eyelid) changes can to occur. eyelashes, Iris pigmentation including increased is likely associated with the use of multiple-dose containers of tolength, be permanent increased thickness, and number of • Contact topical ophthalmic lenses should products be removed that were prior inadvertently to the eyelashes, may occur. These changes are usually administrationcontaminated by of patientsVYZULTA and may be reinserted • Gradual changes to eyelashes, including increased contaminated by patients reversible upon treatment discontinuation 15 minutes after administration length, increased thickness, and number of • Contact lenses should be removed prior to the • eyelashes,Use with caution may occur. in patients These with changes a history are usually of • administrationMost common ocularof VYZULTA adverse and reactions may be withreinserted reversibleintraocular upon infl ammation treatment (iritis/uveitis). discontinuation VYZULTA 15incidence minutes • after2% are administration conjunctival hyperemia (6%), should generally not be used in patients with active eye irritation (4%), eye pain (3%), and instillation • Use with caution in patients with a history of • Most common ocular adverse reactions with intraocular infl ammation site pain (2%) intraocular infl ammation (iritis/uveitis). VYZULTA incidence •2% are conjunctival hyperemia (6%), should generally not be used in patients with active REFERENCEeye irritation (4%), eye pain (3%), and instillation intraocular infl ammation 1. siteVYZULTA pain Prescribing (2%) Information. Bausch & Lomb Incorporated. 2017.

ForREFERENCE more information, please see Brief Summary VYZULTA and the V design are trademarks of Bausch & Lomb Incorporated or its affi liates. 1. VYZULTA Prescribing Information. Bausch & Lomb Incorporated. 2017. ©2017 Bausch & Lomb Incorporated. All rights reserved. VYZ.0351.USA.17 of1. VYZULTA Prescribing Prescribing Information Information. Bausch on next & Lomb page. Incorporated. 2017. For more information, please see Brief Summary VYZULTA and the V design are trademarks of Bausch & Lomb Incorporated or its affi liates. ©2017 Bausch & Lomb Incorporated. All rights reserved. VYZ.0351.USA.17 of Prescribing Information on next page.

RP0118_BauschVyzulta.indd 1 12/22/17 11:55 AM BRIEF SUMMARY OF PRESCRIBING INFORMATION Doses ≥ 20 μg/kg/day (23 times the clinical dose) produced 100% embryofetal lethality. Structural abnormalities observed in rabbit fetuses included anomalies of the great This Brief Summary does not include all the information needed to use VYZULTA vessels and aortic arch vessels, domed head, sternebral and vertebral skeletal anomalies, safely and effectively. See full Prescribing Information for VYZULTA. limb hyperextension and malrotation, abdominal distension and edema. Latanoprostene ™ VYZULTA (latanoprostene bunod ophthalmic solution), 0.024%, for topical bunod was not teratogenic in the rat when administered IV at 150 mcg/kg/day (87 times ophthalmic use. the clinical dose) [see Data]. Initial U.S. Approval: 2017 The background risk of major birth defects and miscarriage for the indicated population 1 INDICATIONS AND USAGE is unknown. However, the background risk in the U.S. general population of major birth defects is 2 to 4%, and of miscarriage is 15 to 20%, of clinically recognized pregnancies. VYZULTA™ (latanoprostene bunod ophthalmic solution) 0.024% is indicated for the reduction of intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension. Data 4 CONTRAINDICATIONS Animal Data None Embryofetal studies were conducted in pregnant rabbits administered latanoprostene bunod daily by intravenous injection on gestation days 7 through 19, to target the period 5 WARNINGS AND PRECAUTIONS of organogenesis. The doses administered ranged from 0.24 to 80 mcg/kg/day. Abortion 5.1 Pigmentation occurred at doses ≥ 0.24 mcg/kg/day latanoprostene bunod (0.28 times the clinical VYZULTA™ (latanoprostene bunod ophthalmic solution), 0.024% may cause changes to dose, on a body surface area basis, assuming 100% absorption). Embryofetal lethality pigmented tissues. The most frequently reported changes with prostaglandin analogs (resorption) was increased in latanoprostene bunod treatment groups, as evidenced have been increased pigmentation of the iris and periorbital tissue (eyelid). by increases in early resorptions at doses ≥ 0.24 mcg/kg/day and late resorptions at doses ≥ 6 mcg/kg/day (approximately 7 times the clinical dose). No fetuses survived Pigmentation is expected to increase as long as latanoprostene bunod ophthalmic in any rabbit pregnancy at doses of 20 mcg/kg/day (23 times the clinical dose) or greater. solution is administered. The pigmentation change is due to increased melanin content Latanoprostene bunod produced structural abnormalities at doses ≥ 0.24 mcg/kg/day in the melanocytes rather than to an increase in the number of melanocytes. After (0.28 times the clinical dose). Malformations included anomalies of sternum, coarctation discontinuation of VYZULTA, pigmentation of the iris is likely to be permanent, while of the aorta with pulmonary trunk dilation, retroesophageal subclavian artery with pigmentation of the periorbital tissue and eyelash changes are likely to be reversible in absent brachiocephalic artery, domed head, forepaw hyperextension and hindlimb most patients. Patients who receive prostaglandin analogs, including VYZULTA, should be malrotation, abdominal distention/edema, and missing/fused caudal vertebrae. informed of the possibility of increased pigmentation, including permanent changes. The long-term effects of increased pigmentation are not known. An embryofetal study was conducted in pregnant rats administered latanoprostene bunod daily by intravenous injection on gestation days 7 through 17, to target the Iris color change may not be noticeable for several months to years. Typically, the period of organogenesis. The doses administered ranged from 150 to 1500 mcg/kg/day. brown pigmentation around the pupil spreads concentrically towards the periphery of Maternal toxicity was produced at 1500 mcg/kg/day (870 times the clinical dose, on the iris and the entire iris or parts of the iris become more brownish. Neither nevi nor a body surface area basis, assuming 100% absorption), as evidenced by reduced freckles of the iris appear to be affected by treatment. While treatment with VYZULTA™ maternal weight gain. Embryofetal lethality (resorption and fetal death) and structural (latanoprostene bunod ophthalmic solution), 0.024% can be continued in patients who anomalies were produced at doses ≥ 300 mcg/kg/day (174 times the clinical dose). develop noticeably increased iris pigmentation, these patients should be examined Malformations included anomalies of the sternum, domed head, forepaw hyperextension regularly [see Patient Counseling Information (17) in full Prescribing Information]. and hindlimb malrotation, vertebral anomalies and delayed ossification of distal limb 5.2 Eyelash Changes bones. A no observed adverse effect level (NOAEL) was established at 150 mcg/kg/day (87 times the clinical dose) in this study. VYZULTA may gradually change eyelashes and vellus hair in the treated eye. These changes include increased length, thickness, and the number of lashes or hairs. Eyelash 8.2 Lactation changes are usually reversible upon discontinuation of treatment. Risk Summary 5.3 Intraocular Inflammation There are no data on the presence of VYZULTA in human milk, the effects on the VYZULTA should be used with caution in patients with a history of intraocular breastfed infant, or the effects on milk production. The developmental and health inflammation (iritis/uveitis) and should generally not be used in patients with active benefits of breastfeeding should be considered, along with the mother’s clinical need intraocular inflammation as it may exacerbate this condition. for VYZULTA, and any potential adverse effects on the breastfed infant from VYZULTA. 5.4 Macular Edema 8.4 Pediatric Use Macular edema, including cystoid macular edema, has been reported during treatment Use in pediatric patients aged 16 years and younger is not recommended because of potential with prostaglandin analogs. VYZULTA should be used with caution in aphakic patients, in safety concerns related to increased pigmentation following long-term chronic use. pseudophakic patients with a torn posterior lens capsule, or in patients with known risk 8.5 Geriatric Use factors for macular edema. No overall clinical differences in safety or effectiveness have been observed between 5.5 Bacterial Keratitis elderly and other adult patients. There have been reports of bacterial keratitis associated with the use of multiple-dose 13 NONCLINICAL TOXICOLOGY containers of topical ophthalmic products. These containers had been inadvertently contaminated by patients who, in most cases, had a concurrent corneal disease or a 13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility disruption of the ocular epithelial surface. Latanoprostene bunod was not mutagenic in bacteria and did not induce micronuclei 5.6 Use with Contact Lens formation in the in vivo rat bone marrow micronucleus assay. Chromosomal aberrations were observed in vitro with human lymphocytes in the absence of metabolic activation. Contact lenses should be removed prior to the administration of VYZULTA because this product contains benzalkonium chloride. Lenses may be reinserted 15 minutes after Latanoprostene bunod has not been tested for carcinogenic activity in long-term animal administration. studies. Latanoprost acid is a main metabolite of latanoprostene bunod. Exposure of rats and mice to latanoprost acid, resulting from oral dosing with latanoprost in lifetime 6 ADVERSE REACTIONS rodent bioassays, was not carcinogenic. The following adverse reactions are described in the Warnings and Precautions section: Fertility studies have not been conducted with latanoprostene bunod. The potential to pigmentation (5.1), eyelash changes (5.2), intraocular inflammation (5.3), macular impact fertility can be partially characterized by exposure to latanoprost acid, a common edema (5.4), bacterial keratitis (5.5), use with contact lens (5.6). metabolite of both latanoprostene bunod and latanoprost. Latanoprost acid has not been 6.1 Clinical Trials Experience found to have any effect on male or female fertility in animal studies. Because clinical trials are conducted under widely varying conditions, adverse reaction 13.2 Animal Toxicology and/or Pharmacology rates observed in the clinical trials of a drug cannot be directly compared to rates in the A 9-month toxicology study administered topical ocular doses of latanoprostene bunod clinical trials of another drug and may not reflect the rates observed in practice. to one eye of cynomolgus monkeys: control (vehicle only), one drop of 0.024% bid, one VYZULTA was evaluated in 811 patients in 2 controlled clinical trials of up to 12 months drop of 0.04% bid and two drops of 0.04% per dose, bid. The systemic exposures are duration. The most common ocular adverse reactions observed in patients treated equivalent to 4.2-fold, 7.9-fold, and 13.5-fold the clinical dose, respectively, on a body with latanoprostene bunod were: conjunctival hyperemia (6%), eye irritation (4%), eye surface area basis (assuming 100% absorption). Microscopic evaluation of the lungs pain (3%), and instillation site pain (2%). Approximately 0.6% of patients discontinued after 9 months observed pleural/subpleural chronic fibrosis/inflammation in the 0.04% therapy due to ocular adverse reactions including ocular hyperemia, conjunctival dose male groups, with increasing incidence and severity compared to controls. Lung irritation, eye irritation, eye pain, conjunctival edema, vision blurred, punctate keratitis toxicity was not observed at the 0.024% dose. and foreign body sensation. Distributed by: 8 USE IN SPECIFIC POPULATIONS Bausch + Lomb, a division of 8.1 Pregnancy Valeant Pharmaceuticals North America LLC Risk Summary Bridgewater, NJ 08807 USA There are no available human data for the use of VYZULTA during pregnancy to inform U.S. Patent Numbers: 6,211,233; 7,273,946; 7,629,345; 7,910,767; 8,058,467. any drug associated risks. VYZULTA is a trademark of Bausch & Lomb Incorporated or its affiliates. Latanoprostene bunod has caused miscarriages, abortion, and fetal harm in rabbits. Latanoprostene bunod was shown to be abortifacient and teratogenic when administered © Bausch & Lomb Incorporated intravenously (IV) to pregnant rabbits at exposures ≥ 0.28 times the clinical dose. Based on 9464800 11/2017 VYZ.0055.USA.16 Issued: 11/2017

RRP0118_BauschVyzultaPI.inddP0118_BauschVyzultaPI.indd 1 112/22/172/22/17 11:5811:58 AMAM Contents ANNUAL CORNEA REPORT Review of Optometry January 15, 2018

Your Top 12 Crosslinking Fixing a Hole: How to Heal 30Questions—Answered! 38 Persistent Epithelial Defects New to corneal collagen crosslinking? This Q&A guide Clinicians have a robust arsenal for treating this reccurring from Wills Eye Hospital will help prepare you to manage condition. Knowing where to start and when to switch it up is keratoconus patients in the new era. By Clark Chang, OD, key. By Alan Kwok, OD MSA, MSc, and Christopher J. Rapuano, MD

An OD’s Guide to Intruder Alert: Diagnosing 44Corneal Transplant Options 50 Corneal Infiltrative Disease Optometrists can play a significant role in preparing patients The age-old question, “is this sterile or infectious?” may be an for these procedures and safeguarding against complications. oversimplification. This review will help you find the underlying By Mitch Ibach, OD, and Scott Hauswirth, OD cause of your patient’s issue. By Suzanne Sherman, OD, and Fiza Shuja, OD

Earn 2 CE Credit: 58 Positive Visual Phenomena: Etiologies Beyond the Eye Prepare to investigate the many non-ocular events that cause patients to see flashes or bright lights. By Sara Weidmayer, OD

REVIEW OF OPTOMETRY JANUARY 15, 2018 9

009_ro0118_toc.indd 9 1/8/18 5:39 PM Departments Review of Optometry January 15, 2018

3 News Review

14 Outlook Smart Phone, Dumb App

JACK PERSICO BUSINESS OFFICES 11 CAMPUS BLVD., SUITE 100 16 Through My Eyes NEWTOWN SQUARE, PA 19073 2018: What’s in View for You CEO, INFORMATION SERVICES GROUP MARC FERRARA PAUL M. KARPECKI, OD (212) 274-7062 • [email protected]

PUBLISHER 18 Chairside JAMES HENNE Quiet Down! 20 (610) 492-1017 • [email protected] MONTGOMERY VICKERS, OD REGIONAL SALES MANAGER MICHELE BARRETT (610) 492-1014 • [email protected] 20 Clinical Quandaries REGIONAL SALES MANAGER Dry Eye Gone Awry MICHAEL HOSTER PAUL C. AJAMIAN, OD (610) 492-1028 • [email protected]

VICE PRESIDENT, OPERATIONS CASEY FOSTER 22 The Essentials (610) 492-1007 • [email protected] The Purpose of Prostaglandins VICE PRESIDENT, CLINICAL CONTENT BISANT A. LABIB, OD PAUL M. KARPECKI, OD, FAAO [email protected] 26 Coding Connection PRODUCTION MANAGER What Are You Worth? SCOTT TOBIN (610) 492-1011 • [email protected] JOHN RUMPAKIS, OD, MBA 69 SENIOR CIRCULATION MANAGER HAMILTON MAHER 69 Cornea + Contact Lens Q&A (212) 219-7870 • [email protected] Heroes and Shields CLASSIFIED ADVERTISING JOSEPH P. SHOVLIN, OD (888) 498-1460

SUBSCRIPTIONS $56 A YEAR, $88 (US) IN CANADA, 70 Review of Systems $209 (US) IN ALL OTHER COUNTRIES. Streaks of Concern SUBSCRIPTION INQUIRIES CARLO J. PELINO, OD, AND (877) 529-1746 (US ONLY) JOSEPH J. PIZZIMENTI, OD OUTSIDE US CALL: (845) 267-3065

CIRCULATION PO BOX 81 74 Retina Quiz CONGERS, NY 10920 Leak Investigation TEL: (TOLL FREE): (877) 529-1746 OUTSIDE US: (845) 267-3065 MARK T. DUNBAR, OD 70 76 Therapeutic Review Spot the Dot ALAN G. KABAT, OD, AND CEO, INFORMATION SERVICES GROUP MARC FERRARA JOSEPH W. SOWKA, OD SENIOR VICE PRESIDENT, OPERATIONS JEFF LEVITZ 77 Advertisers Index VICE PRESIDENT, HUMAN RESOURCES TAMMY GARCIA 78 Classifieds VICE PRESIDENT, CREATIVE SERVICES & PRODUCTION MONICA TETTAMANZI 81 Meetings + Conferences CORPORATE PRODUCTION DIRECTOR JOHN ANTHONY CAGGIANO

82 Diagnostic Quiz VICE PRESIDENT, CIRCULATION Ram On 82 EMELDA BAREA ANDREW S. GURWOOD, OD

10 REVIEW OF OPTOMETRY JANUARY 15, 2018

009_ro0118_toc.indd 10 1/9/18 10:06 AM CP1217_Bruder.indd 1 12/7/17 10:47 AM CONTRIBUTING EDITORS A. PAUL CHOUS, MA, OD, TACOMA, WASH. PAUL C. AJAMIAN, OD, ATLANTA ROBERT M. COLE, III, OD, BRIDGETON, NJ AARON BRONNER, OD, KENNEWICK, WASH. GLENN S. CORBIN, OD, WYOMISSING, PA. MILE BRUJIC, OD, BOWLING GREEN, OHIO ANTHONY S. DIECIDUE, OD, STROUDSBURG, PA. DEREK N. CUNNINGHAM, OD, AUSTIN, TEXAS S. BARRY EIDEN, OD, DEERFIELD, ILL. MARK T. DUNBAR, OD, MIAMI STEVEN FERRUCCI, OD, SEPULVEDA, CALIF. ARTHUR B. EPSTEIN, OD, PHOENIX MURRAY FINGERET, OD, HEWLETT, NY JAMES L. FANELLI, OD, WILMINGTON, NC IAN BEN GADDIE, OD, LOUISVILLE, KY. FRANK FONTANA, OD, ST. LOUIS PAUL HARRIS, OD, MEMPHIS, TN GARY S. GERBER, OD, HAWTHORNE, NJ MILTON HOM, OD, AZUSA, CALIF. ANDREW S. GURWOOD, OD, PHILADELPHIA BLAIR B. LONSBERRY, MS, OD, MED, PORTLAND, ORE. ALAN G. KABAT, OD, MEMPHIS, TENN. THOMAS L. LEWIS, OD, PHD, PHILADELPHIA DAVID KADING, OD, SEATTLE DOMINICK MAINO, OD, MED, CHICAGO PAUL M. KARPECKI, OD, LEXINGTON, KY. KELLY A. MALLOY, OD, PHILADELPHIA JEROME A. LEGERTON, OD, MBA, SAN DIEGO RICHARD B. MANGAN, OD, LEXINGTON, KY. JASON R. MILLER, OD, MBA, POWELL, OHIO RON MELTON, OD, CHARLOTTE, NC CHERYL G. MURPHY, OD, BABYLON, NY PAMELA J. MILLER, OD, JD, HIGHLAND, CALIF. CARLO J. PELINO, OD, JENKINTOWN, PA. BRUCE MUCHNICK, OD, COATESVILLE, PA. JOSEPH PIZZIMENTI, OD, SAN ANTONIO, TEXAS MARC MYERS, OD, COATESVILLE, PA. JOHN RUMPAKIS, OD, MBA, PORTLAND, ORE. WILLIAM B. POTTER, OD, FREEHOLD, NJ DIANA L. SHECHTMAN, OD, FORT LAUDERDALE, FLA. CHRISTOPHER J. QUINN, OD, ISELIN, NJ JEROME SHERMAN, OD, NEW YORK MICHAEL C. RADOIU, OD, STAUNTON, VA. JOSEPH P. SHOVLIN, OD, SCRANTON, PA. MOHAMMAD RAFIEETARY, OD, MEMPHIS, TN JOSEPH W. SOWKA, OD, FORT LAUDERDALE, FLA. JOHN L. SCHACHET, OD, ENGLEWOOD, COLO. MONTGOMERY VICKERS, OD, LEWISVILLE, TEXAS JACK SCHAEFFER, OD, BIRMINGHAM, ALA. WALTER O. WHITLEY, OD, MBA, VIRGINIA BEACH, VA. LEO P. SEMES, OD, BIRMINGHAM, ALA. LEONID SKORIN, JR., OD, DO, ROCHESTER, MINN. EDITORIAL REVIEW BOARD JOSEPH W. SOWKA, OD, FORT LAUDERDALE, FLA. JEFFREY R. ANSHEL, OD, ENCINITAS, CALIF. SRUTHI SRINIVASAN, PhD, BS OPTOM, WATERLOO, ONT. JILL AUTRY, OD, RPH, HOUSTON BRAD M. SUTTON, OD, INDIANAPOLIS SHERRY J. BASS, OD, NEW YORK LORETTA B. SZCZOTKA, OD, PHD, CLEVELAND EDWARD S. BENNETT, OD, ST. LOUIS MARC TAUB, OD, MEMPHIS, TN MARC R. BLOOMENSTEIN, OD, SCOTTSDALE, ARIZ. TAMMY P. THAN, MS, OD, BIRMINGHAM, ALA. CHRIS J. CAKANAC, OD, MURRYSVILLE, PA. RANDALL THOMAS, OD, CONCORD, NC JERRY CAVALLERANO, OD, PHD, BOSTON SARA WEIDMAYER, OD, ANN ARBOR, MI WALTER L. CHOATE, OD, MADISON, TENN. KATHY C. WILLIAMS, OD, SEATTLE BRIAN CHOU, OD, SAN DIEGO KAREN YEUNG, OD, LOS ANGELES

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REVIEW OF OPTOMETRY® 2018 EDUCATIONAL MEETINGS OF CLINICAL EXCELLENCE MEETINGS FEBRUARY 16-20, 2018 Winter Ophthalmic Conference ASPEN, CO Westin Snowmass Conference Center Program Chairs: Murray Fingeret, OD & Leo Semes, OD www.skivision.com

APRIL 6-8, 2018 NASHVILLE, TN Nashville Marriott at Vanderbilt Program Chair: Paul Karpecki, OD www.reviewofoptometry.com/nashville2018

APRIL 26-29, 2018 SAN DIEGO, CA** San Diego Marriott Del Mar Progrom Chair: Paul Karpecki, OD www.reviewofoptometry.com/sandiego2018

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NOVEMBER 2-4, 2018 ARLINGTON, VA The Westin Arlington Gateway Program Chair: Paul Karpecki, OD www.reviewofoptometry.com/arlington2018

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Administered by OPTOMETRIC CORNEA, CATARACT AND REFRACTIVE SOCIETY ® Review of Optometry *Approval pending **15th Annual Education Symposium Joint Meeting with NT&T in Eye Care Review of Optometry® partners with Salus University for those ODs who are licensed in states that require university credit. See Review website for any meeting schedule changes or updates. Outlook By Jack Persico, Editor-in-Chief PRINTED IN USA

FOUNDING EDITOR, FREDERICK BOGER 1891-1913

EDITORIAL OFFICES Smart Phone, Dumb App 11 CAMPUS BLVD., SUITE 100 NEWTOWN SQUARE, PA 19073 Valuing convenience and cost savings over expertise and WEBSITE • WWW.REVIEWOFOPTOMETRY.COM results enables bad habits that could prove harmful. SUBSCRIPTION INQUIRIES 1-877-529-1746 CONTINUING EDUCATION INQUIRIES arby Parker dove into the Homer does about aluminum J-chan- 1-800-825-4696 online refraction market nels. If this app and others like it don’t last year with an iPhone qualify as The Half-Assed Approach EDITOR-IN-CHIEF • JACK PERSICO W (610) 492-1006 • [email protected] app called Prescription Check that, to Eye Care, I don’t know what does. MANAGING EDITOR • REBECCA HEPP as others do, looks to skim the After the breezy medical screening, (610) 492-1005 • [email protected] SENIOR EDITOR • BILL KEKEVIAN easiest Rx refills off the top of the the app got me to simulate an exam (610) 492-1003 • [email protected] market. Only healthy myopes need lane using my laptop. It made no ASSOCIATE EDITOR • MICHAEL IANNUCCI apply. Earlier this month, the app stipulations about lighting conditions (610) 492-1043 • [email protected] kicked up some controversy when it or the viewing angle and height of the SPECIAL PROJECTS MANAGER • JILL HOFFMAN (610) 492-1037 • [email protected] was the top-featured item in Apple’s screen—you know, minor stuff. Next ART DIRECTOR • JARED ARAUJO app store, with the cheeky ad line, it asked if I “have any complaints (610) 492-1032 • [email protected] “Dr. Warby will see you now.” about the prescription” I’m currently DIRECTOR OF CE ADMINISTRATION • REGINA COMBS (212) 274-7160 • [email protected] So I downloaded the app to size wearing and gave me a yes/no reply up Dr. Warby. It starts with a dis- and the option to leave a note for the EDITORIAL BOARD claimer that the app isn’t a substitute doctor. (Nice chairside manner, Dr. CHIEF CLINICAL EDITOR • PAUL M. KARPECKI, OD ASSOCIATE CLINICAL EDITORS • JOSEPH P. SHOVLIN, OD; for an eye exam. (Then why per- Warby.) It asked for a copy of my cur- ALAN G. KABAT, OD; CHRISTINE W. SINDT, OD sonify a bare-bones vision test with a rent Rx—as if people keep that handy. DIRECTOR OPTOMETRIC PROGRAMS • ARTHUR EPSTEIN, OD cutesy fake-doctor persona?) I scribbled a fake one and plowed on. CLINICAL & EDUCATION CONFERENCE ADVISOR First I fielded questions about Finally, it walked me through a few PAUL M. KARPECKI, OD CASE REPORTS COORDINATOR • ANDREW S. GURWOOD, OD amblyopia, nystagmus, flashes and simple acuity tests. The results will CLINICAL CODING EDITOR • JOHN RUMPAKIS, OD, MBA floaters, glaucoma and other com- be checked by a doctor, the company CONSULTING EDITOR • FRANK FONTANA, OD plex eye health issues. By the time it says, and there’s no charge if it recom-

COLUMNISTS asked if I have family members with mends a comprehensive eye exam. But CHAIRSIDE • MONTGOMERY VICKERS, OD “hereditary retinal problems like reti- if the mysterious Dr. Warby deems CLINICAL QUANDARIES • PAUL C. AJAMIAN, OD nitis pigmentosa,” all I could think that your Rx didn’t change and can be CODING CONNECTION • JOHN RUMPAKIS, OD of was Troy McClure, the beloved refilled online, you get charged $40— CORNEA & CONTACT LENS Q+A • JOSEPH P. SHOVLIN, OD Simpsons character, a washed-up and, I’m sure, are steered right into DIAGNOSTIC QUIZ • ANDREW S. GURWOOD, OD actor who would take any job, no the Warby Parker frame selection app. THE ESSENTIALS • BISANT A. LABIB, OD FOCUS ON REFRACTION • MARC TAUB, OD; matter how small or undignified. In My Dr. Warby experience was PAUL HARRIS, OD a 1992 episode, Homer buys a do-it- lousy. But, hey, it was “convenient.” GLAUCOMA GRAND ROUNDS • JAMES L. FANELLI, OD yourself video narrated by McClure Why should that justify it? Listen, I NEURO CLINIC • MICHAEL TROTTINI, OD; called The Half-Assed Approach to wish the public knew about RP and MICHAEL DELGIODICE, OD OCULAR SURFACE REVIEW • PAUL M. KARPECKI, OD Foundation Repair in a foolhardy glaucoma and everything else so they RETINA QUIZ • MARK T. DUNBAR, OD effort to save a few bucks, thinking could make better-informed decisions REVIEW OF SYSTEMS • CARLO J. PELINO, OD; he can tackle such a complex project about their care. But apps like this JOSEPH J. PIZZIMENTI, OD himself instead of hiring a profes- encourage irresponsibility and cloak SURGICAL MINUTE • DEREK N. CUNNINGHAM, OD; WALTER O. WHITLEY, OD, MBA sional. Homer quickly gets flustered it in the guise of convenience and THERAPEUTIC REVIEW • JOSEPH W. SOWKA, OD; by Troy’s complicated, jargon-heavy empowerment, which is worse than ALAN G. KABAT, OD instructions (“Assemble the alumi- the benign neglect that keeps most THROUGH MY EYES • PAUL M. KARPECKI, OD num J-channel using self-furring people out of doctors’ offices. Don’t URGENT CARE • RICHARD B. MANGAN, OD screws”) and realizes foundation let eye health be another victim of JOBSON MEDICAL INFORMATION LLC repair is not a DIY project. this era’s war on expertise. Tell your I’m guessing most people know as patients: Be Lisa Simpson, not Homer. much about retinitis pigmentosa as Brains beat buffoonery every time. ■

14 REVIEW OF OPTOMETRY JANUARY 15, 2018

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2018: What’s in View for You A new year is an exciting time to contemplate what lies ahead. Many key technologies could greatly affect how we practice. By Paul M. Karpecki, OD, Chief Clinical Editor

fter shelling out what seems Outside the office, tear neurostim- Genetics. Spark Therapeutics like a month’s pay for gifts, ulation will advance, and artificial just debuted one of the first ocular Aholiday parties and cham- tears containing new agents such as disease gene therapies, Luxturna, pagne, no one makes a New Year’s trehalose are on the way. Hyaluronic which uses an adeno-associated viral resolution to “spend more money.” acid–based products will gain further vector to transmit the proper genetic But with so many new things coming indications in surface healing. Punc- code necessary to treat rare retinal in 2018, your resolution should be tal plugs with six months’ duration dystrophies. Avellino Labs is working “invest in my practice.” Here’s a look may become a mainstay in the field. on a genetic test for keratoconus that at some promising new products. In 2018 meibography may become could allow for earlier treatment and Ocular surface issues. One of “OCT for dry eye,” and noninvasive stave off progression. today’s great opportunities is optom- testing (especially tear break-up time) Retina. This year, we may see etry’s move toward the ‘dental model’ will play a major role in care, given progress in treatments for other approach of routine preventative its accuracy, sensitivity and specificity. conditions once considered untreat- care. In-office procedures such as Point-of-care testing with the ability able, such as AMD with geographic thermal meibomian gland treat- to know within minutes if the patient atrophy or ischemic optic neuropathy ments, intense-pulsed light therapy has dry eye, plus the level of inflam- (Quark Pharmaceuticals). Further and microblepharoexfoliation will mation and antibody biomarkers advances in OCT, ultra-widefield advance patient-pay dry eye care. present, will change how we practice. imaging and ultrasound technologies A just-approved product likely to will keep ODs a part of the manage- How to Fit it All In? take off this year is Lumify (Bausch ment team for retinal diseases signifi- With so many new options out there, it’s hard + Lomb). This six- to eight-hour cantly longer in the disease course to know where to start. eye drop is designed to whiten eyes before there’s a need to refer out. First, find what interests you—whether 300% more than traditional vaso- Vision care. Last month’s approval or not it’s in your comfort zone. Some of the constrictors without the risks of of RxSight’s light-adjustable IOL greatest opportunities for growth occur when rebound hyperemia or tachyphylax- places optometry as the key doctor in we’re willing to embrace new things. is—a new option for patients who determining what, if any, prescription Second, you may need to set aside more always want to be ‘selfie-ready.’ change is required post-procedure. time this year to focus your practice on these Glaucoma. Not one but two new Presbyopia will have a new foe in new opportunities. One way to carve out time drops are on their way. The recently 2018 if the Visability scleral insert is to outsource management aspects such as FDA-approved Vyzulta (Bausch + (Refocus) gains approval. Eye align- human resources, payroll and frame board Lomb) is a prostaglandin analog ment/prism correction will see a management. Optometric Medical Solutions that increases uveoscleral outflow major boost with the NeuroLens and allows a doctor to outsource medical logistics plus a nitric oxide donor that works SightSync (eyeBrain) technologies. like credentialing, accounts receivable, directly on the trabecular meshwork There’s no shortage of new tech- insurance verification and staff training. (TM) to increase outflow. Also newly nologies, treatments and business Finally, stay online to protect your patients approved is the first rho-kinase management resources to help make and your business. Companies like Click inhibitor for glaucoma, Rhopressa 2018 your best year yet. Any num- Optical work directly with the practice at (netarsudil, Aerie), which has a multi- ber of them can better position your no cost, allowing ODs to compete in online pronged mechanism of action that practice and address patients’ vision contact lens sales. Consider telemedicine combines uveoscleral outflow, effects care needs and ocular health. ■ where appropriate, such as EyeCare Live, on the TM and lowering of the epi- Note: Dr. Karpecki is a consultant which is optometry dedicated. scleral venous pressure. for many companies mentioned here.

16 REVIEW OF OPTOMETRY JANUARY 15, 2018

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CP1217_Eyecheck.indd 1 12/7/17 10:48 AM Chair Side

Quiet Down! This year, I’m going to shut my mouth. Or, more likely, I’ll forget and use these words more often. By Montgomery Vickers, OD

veryone knows I am the quiet- means the first night the patient out and say, “Have a nice day, Mrs. est person in my family. I still goes to bed without their lenses Jones.” HIPAA violation. Enever shut up, so just imagine for the first time in 27 years, some 8. Have a nice day. They’ll bend the rest of the family. Since I am Staph. bug just hanging around at your ear telling why they won’t. the quietest person only when my the base of an eyelash will do all he 9. Blonde fundus. Many patients siblings are around, my New Year’s can to prove who’s boss. will find that personally offensive. Resolution is to become the quiet- 3. Always. If you tell two parents 10. Bifocal age. Instead, say, est person always and forever. Of who are, respectively, -9.00D and “your glasses should be more ver- course, I have now made 64 resolu- -11.00D, and every family mem- satile.” It will take them roughly 21 tions and only successfully kept one: ber for 70 generations has been days to realize what you meant, and to become potty trained by first nearsighted, that their kids will by then you will be on vacation. grade—and that wasn’t exactly a be nearsighted too, you just magi- 11. Mesozeaxanthin. You will smooth ride. cally created an emmetrope. Just be pull a muscle in your mouth. I just The first step is quieting patient quiet and let genes prevail. Another hurt my finger typing it. and staff interactions. I often say option, of course, is to prophylac- 12. Congratulations, this is the too much with patients, as I want tically treat with myopia control best time to be over 40! One of my them to: (a) totally understand their techniques and take the credit. in-office reading cards says that, ocular conditions and visual status 4. Curse words. Avoid these— and I am actively searching for the and (b) know every trivial thing unless, of course, the patient is your 27-year-old marketing guru who I have ever done. Sometimes this mom, who just bought new glasses came up with that piece of crap. makes for a very long exam; or, I online. Then, go for it. There are so many more, but just reschedule the exam and part 5. Problem. The road to practice I have to start somewhere. After two of my life story. hell is paved with docs who say to all, “this is the best time to be in Because of my blabbering, I have their parting patient, “Let me know optometry!” ■ learned a lot of words should be if you have any problems.” avoided when talking to patients: 6. Cataract surgery is really no 1. Stupid. This should only be big deal. The patient will kindly used in sentences that directly refer- think, “wait until it’s your eye, ence the patient’s previous, obvi- doc.” They will also find a post- ously stupid, optical experience. operative complication like, “My Example: “Why did my surgeon toilet flushed just fine until I had leave me so farsighted after cataract cataract surgery.” surgery?” You know the answer. 7. Names. 2. Never. If you tell a patient who Never walk switches to daily disposables after the patient wearing monthly lenses continu- ously for six months that they will never develop a corneal ulcer, you are doomed. Did you know most strains of Staph. have tiny ears? This, combined with the bacteria’s black-hearted sense of humor,

18 REVIEW OF OPTOMETRY JANUARY 15, 2018

018_ro0118_chairside.indd 18 1/5/18 2:16 PM Innovative Materials, Individualized Recommendations

By Roy A. Kline, OD Senior Partner, Drs. Kline & Boyd, PLLC Glenn Falls, New York

lot of things have changed since Confidence, comfort, I offered her Bausch + Lomb ULTRA® for AI first opened up my practice in and clarity Astigmatism contact lenses, and then I let 1986. Back then, I opened the her experience firsthand what they could Even before Bausch + Lomb ULTRA® for office with a receptionist, optician, and do for her. She did not even wait a full Astigmatism contact lenses were on the myself. Today we have 4 doctors and 14 week before she expressed to my staff that market, I already had a list of 40 patients highly trained staff who love working with she could already feel a difference. Within for whom I thought the lenses would people and deliver excellent care at every just 2 or 3 days, she was able to keep be a good fit. Of those 40 patients, 38 touchpoint. With a patient base of 50,000, these lenses in comfortably all day while purchased these lenses within the first our practice is one of the largest in the area. enjoying excellent clarity. 2 weeks that we began offering them! I credit much of our success to the very Many patients told me, “These contact The family is complete personalized care we give to our patients. lenses are so comfortable, and my vision Between the thin, tapered edges, the As a practitioner, I am always on the hunt is incredibly sharp.” My patients are stability of OpticAlign™ design, and for the best vision I can provide to my impressed that they are able to maintain the moisture maintenance provided by patients. I was a biochemist before I became both comfort and clarity of vision MoistureSeal® technology, it is an easy an optometrist, and I am intrigued by throughout the day. decision to reach into my drawer for the innovation that goes into contact lens Bausch + Lomb ULTRA® for Astigmatism technology. Today we have better materials, For my patients with contact lenses. You just know the comfort, better design, and more choices than ever astigmatism who have tried to clarity, and ease of fit will be there. My before for patients who wear contact lenses, wear contact lenses and failed, patients notice the confidence I have including patients with astigmatism. I like to show them what in the product, which helps them be Despite innovations in technology, many a vast difference the right comfortable and confident. people still believe that astigmatism and contact lenses can make.” With the Bausch + Lomb contact lens soft contact lenses do not mix. Some portfolio completed, today we can have been told that because they have One of my patients, a nurse in her mid- reach out to more patients, put them in astigmatism, they cannot wear contact 30s, recently came in wearing a different innovative lenses, and give them more lenses. Others may have tried them before brand of frequent-replacement toric choices than ever before. but did not have a comfortable experience. contact lenses. She said, “I’d really like For my patients with astigmatism who have to get more wear time out of my lenses. tried to wear contact lenses and failed, I I’m just not getting what I’d like to have. I like to show them what a vast difference the put up with them during the day, but it’s right contact lenses can make. After I fit a kind of a struggle.” Of course, we know patient with Bausch + Lomb ULTRA® for that patients who experience this type of Astigmatism contact lenses, they sometimes discomfort with their lenses often stop look at me and smile, like, “OK, Doc, I think wearing contacts altogether, so we need to you’re on the right track here.” Those smiles take the situation seriously. can be more valuable than words.

®/™ are trademarks of Bausch & Lomb Incorporated or its affiliates. Any other brand/product names and/or logos are trademarks of the respective owners. © 2017 Bausch & Lomb Incorporated. UFA.0243.USA.17 SPONSORED BY BAUSCH + LOMB

RO0118_BL Ultra.indd 1 1/3/18 9:58 AM Clinical Quandaries

Dry Eye Gone Awry When you try every topical therapy in the book and still can’t get resolution, you may need a systemic agent—and an ally in another field. Edited by Paul C. Ajamian, OD Photo: Alan G. Kabat, OD Q I have a Sjögren’s disease patient autologous drops formulated from a with a dry eye flare up and com- 50% concentration. After using the plications. No topical treatments have combination every two hours for a helped. What’s next? period of three weeks in both eyes, “I saw this patient for irritation the patient felt much better, initially. A and burning in both eyes about “Her punctate changes were much a year ago,” says Brian Den Beste, improved and she was much more OD, of LASIK Pro Eye Consultants comfortable,” says Dr. Den Beste. Sjögren’s patients often present with in Orlando. The patient, a 62-year- A week later, however, the patient inflammatory dry eye, shown here. old Caucasian female who Dr. Den came back with a large abrasion on Beste had seen on and off for signifi- the inferior cornea of her right eye. inflammatory pathways.” According cant dry eye and narrow angles, had “The surrounding anterior stroma to Dr. Den Beste, large sterile ulcers a long-standing history of Sjögren’s demonstrated white blood cell migra- that occur in the periphery can lead disease and chronic fatigue syndrome. tion, so I prescribed a topical fluo- to extreme corneal thinning and per- At the time of the aforementioned roquinolone,” says Dr. Den Beste. forations, typically in patients already visit, the patient had stopped wear- Again the patient’s infiltrate resolved on medications for serious autoim- ing her soft contact lenses based on and she went home with a bandage mune conditions, such as Sjögren’s. instructions from her primary care lens. One more week later, though, “This case was unusual, however, optometrist, but was using artificial she came back with yet another large because the patient was under the tears 10 times a day. “I suggested a epithelial abrasion. Also, her previous care of a rheumatologist and was mild steroid and added oral doxy- inferior lesion showed stromal thin- thought to be doing fine systemi- cycline, as she demonstrated mild ning. “After four months of steroids, cally,” says Dr. Den Beste. “It wasn’t facial rosacea and chronic lid margin bland ointment, autologous drops, until she broke down from an oph- changes characteristic of posterior amniotic membranes, moisture cham- thalmic standpoint that we recog- blepharitis,” says Dr. Den Beste. “I ber goggles and bandage contacts, I nized she needed oral medication for thought her complaints were more sent her to her rheumatologist and her rheumatologic disease.” inflammatory in nature rather than suggested she be given a biologic According to Dr. Den Beste, cor- arising from a lack of tears.” response modifier or a traditional neal involvement in patients with When she returned a week later disease-modifying antirheumatic drug severe autoimmune diseases such as with a 3mm oval abrasion above (DMARD),” says Dr. Den Beste. rheumatoid arthritis can typically fixation in the right eye, Dr. Den be managed with topical medica- Beste stopped the steroids and placed The Fix tions and, occasionally, oral steroids. a bandage soft lens on the eye. After Per Dr. Den Beste’s request, the rheu- However, sometimes they require a two-week period of follow-up and matologist gave the patient 200mg ongoing treatment with a DMARD several different bandage lenses, not of Plaquenil (hydroxychloroquine, or a biologic response modifier such much had changed. Instead, Dr. Den Sanofi-Aventis). Within two weeks, as Humira (adalimumab, AbbVie). Beste tried a Prokera (Bio-Tissue) her condition changed dramatically; “As ODs, we often call on rheu- amniotic graft. While the abrasion the abrasions resolved and her com- matologists when dealing with severe shrunk significantly over the next fort returned. “Plaquenil is an older uveitis or scleritis,” says Dr. Den five days, the surrounding epithelium DMARD but it is still used, especially Beste. “The lesson here is to consider began to show intense staining. for patients with lupus,” says Dr. Den that same referral when dealing At this point, Dr. Den Beste Beste. “It is not clear how the drug with recalcitrant dry eye and corneal went with a bland ointment and works, but it is thought to block pro- inflammation.” ■

20 REVIEW OF OPTOMETRY JANUARY 15, 2018

020_ro0118_CQ.indd 20 1/5/18 2:17 PM 12HRS CONSISTENT & CONTINUOUS SYMPTOM RELIEF

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RP0717_Mentholatum.indd 1 6/20/17 2:23 PM The EssentialsEssentials

The Purpose of Prostaglandins Two decades ago, these drugs revolutionized glaucoma therapy. Use this refresher on how they work to understand what makes the newest entrant fit in. By Bisant A. Labib, OD

ince their introduction in PGA Tour 1996, prostaglandin analogs Topical drugs that mimic the func- S(PGAs) have been the main- tion of naturally occurring PGs are stay of glaucoma treatment due called prostaglandin analogs, given to their efficacy, once-daily dosing their pharmacodynamic similarities and limited adverse effect profile.1 to some PG-mediated processes. The aim of all medical and surgical PGAs are stand-ins for PGs, but not glaucoma interventions is to reduce identical in form or function. intraocular pressure (IOP), to date Traditionally, eye doctors have the only modifiable factor. Since relied on four topical PGAs: latano- most eye care practitioners gravitate Trichomegaly resulting from prolonged prost, bimatoprost, travoprost and towards the use of these drugs as use of PGA for cosmesis. preservative-free tafluprost oph- first-line glaucoma treatment—and thalmic solutions.2 While all these a new one has just arrived—it’s smooth muscle, adipocyte differen- agents are classified as prodrugs of important to understand exactly tiation and remodeling of the extra- PGF2, only latanoprost, travoprost, what a PGA is and how it works to cellular matrices found throughout and tafluprost are prostanoids. lower IOP. the body.3-5 It is the latter—a This means that following topical PG’s role in extracellular matrix instillation, enzymes on the cor- What is a Prostaglandin? remodeling—that yields its primary neal surface hydrolyze the drug Pro-inflammatory molecules that mechanism in increasing aqueous into a biologically active form. bind to receptors throughout the outflow to reduce IOP in glaucoma Bimatoprost, on the other hand, is entire body, including ocular struc- patients. PGs also elicit their known classified as a prostamide. This dif- tures, prostaglandins (PGs) elicit effect on smooth muscle by binding ference in its chemical makeup has several effects. There are approxi- to the PG receptors located in the led to studies questioning whether mately nine types of PGs in the ciliary muscle, causing relaxation this is in fact a true prodrug of body, but only the PGF2 subtypes and, subsequently, increased aque- prostaglandins, as the drug remains are currently targeted in glaucoma ous outflow.1,6 mostly unchanged following topical treatment because they are located Also, at the site of the ciliary administration.1 directly on aqueous outflow struc- muscle, the iris root and sclera, In November 2017, a new PGA tures and activation of this specific PGs induce matrix metallopro- combination drug gained FDA receptor affects aqueous humor teinase (MMP) expression, a approval. Vyzulta (latanoprostene dynamics.2 critical component in connective bunod ophthalmic solution 0.24%, PGs are generally produced tissue remodeling. As a result, the Valeant Pharmaceuticals) contains a through the arachidonic acid path- extracellular matrix is modified to PGA as well as a nitric oxide (NO) way, in which the latter substance reduce outflow resistance and lower metabolite. Besides the mechanisms is released from the plasma mem- IOP. More recent histological stud- of PGAs described above, NO has brane and metabolized by the cyclo- ies support a similar mechanism been added to further increase oxygenase enzymes. As such, they of tissue remodeling at the level of aqueous outflow through the play an important role in immune Schlemm’s canal, providing evi- conventional pathway, by directly system regulation and inflamma- dence that PGAs act on the conven- working on the trabecular mesh- tion.1 Additionally, PGs function in tional pathway as well, although to work and causing relaxation and the constriction and relaxation of a lesser degree.3,6 outflow. This dual-action drug has

22 REVIEW OF OPTOMETRY JANUARY 15, 2018

022_ro0118_essentials.indd 22 1/5/18 2:21 PM Earn up to NEW TECHNOLOGIES 18 CE 2018 & TREATMENTS IN Credits* Eye Care

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Administered by ® Review of Optometry *Approval pending The Essentials

been shown more efficacious than conjunctival hyperemia or inflam- PGAs in Practice a PGA alone in clinical trials, with mation.5 Clinicians should exercise Without PGAs, our ability to a mean decrease of 9mm Hg after caution when using topical PGAs in control IOP would be markedly 28 days of use in the Vyzulta group patients with inflammatory ocular reduced. While other glaucoma vs. a mean decrease of 7.77mm Hg conditions such as postoperative drug classes serve us well, a PGA’s with latanoprost 0.005% alone.7 cystoid macular edema or uveitis.4,10 ability to improve aqueous out- Latanoprostene bunod is nearly Researchers looked at PG levels in flow gives clinicians one more identical to the molecular struc- dry eye disease and concluded that lever to pull in managing the deli- ture of latanoprost, except that it ocular injection, pain and discom- cate balance of forces that govern contains a terminal NO group.8 fort from dryness (as well as PGA IOP—and, by extension, glaucoma Because of this similarity, the side use) may be due to significantly progression. effects are the same as the current elevated levels of PGs on the ocu- Natural prostaglandins perform topical PGAs on the market.9 lar surface, which correlated with several functions; our understand- patient symptoms.11 ing of these illuminates the mecha- Side Effects of Treatment PGs also have an effect on adipo- nisms of IOP lowering as well as the Given the integral role PGs play in genesis—the differentiation of cells side effects and contraindications the initiation of the acute inflam- into adipocytes, or fat cells. Studies we discuss with our patients. Of the matory pathway, the most com- show that PGAs inhibit this process, nine PG subtypes, only one is cur- mon side effect of topical PGAs is and topical use decreased dermato- rently targeted in glaucoma. Other chalasis and cause deepening of the receptors may one day serve as Review of Outflow Pathways upper lid sulcus.4,10 potential treatment sites for patients IOP is maintained through a balance of The synthesis of MMPs and the who require additional therapy. ■

aqueous humor production and drainage. extracellular matrix remodeling 1. Winkler NS, Fautsch MP. Effects of prostaglandin analogues In most glaucoma cases, it is impaired effect of PGAs also occurs at the on aqueous humor outflow pathways. J Ocular Pharmacol Thera. drainage that results in elevated IOP and 2014;30(11):102-9. level of the cornea, with one study 2. Doucette LP, Walter MA. Prostaglandins in the eye: Function, subsequent optic nerve damage. Aqueous concluding that the use of latano- expression, and roles in glaucoma. Ophthalmic Genetics. drainage from the anterior chamber is prost resulted in an increase in cor- 2016;38(2):108-16. 3 3. Bolivar G, Sánchez-Barahoma C, Teus M, et al. Effect of permissible through two mechanisms: neal hysteresis. topical prostaglandin analogues on corneal hysteresis. Acta the conventional outflow pathway and the Cosmetically, the use of topical Opthalmologica. 2015;93:e495-8. 1 4. Kim JW. Topical prostaglandin analogue drugs inhibit adipo- unconventional pathway. PGAs results in iris hyperpigmenta- cyte differentiation. Korean J Opthalmol. 2014;28(3):257-64. The conventional outflow pathway, tion and trichomegaly, or eyelash 5. Ricciotti E, Fitzgerald GA. Prostaglandins and inflammation. Arteriocler Thromb Vasc Biol. 2011;31(5):986-1000. responsible for 60% to 80% of aqueous growth. The mechanism of induced 6. Toris CB, Gabelt BT Kaufman PL. Update on the mechanism of drainage, mainly involves filtration through iris hyperpigmentation is not well action of topical prostaglandins for intraocular pressure reduc- tion. Surv Ophthalmol. 2008;53(11):S107-20. the trabecular meshwork and Schlemm’s understood, but appears to be sec- 7. Weinreb RN, Ong T, Scassellati B, et al. A randomised, canal, which results in the aqueous ondary to PG stimulation of iris controlled comparison of latanoprostene bunod and latanoprost 0.005% in the treatment of ocular hypertension and open angle ultimately exiting through the episcleral melanocytes resulting in melanin glaucoma: the VOYAGER study. Br J Ophthalmol. 2015;99:738-45. venous system. In contrast, the remaining production and melanocyte migra- 8. Garcia GA, Ngai P, Mosaed S, et al. Critical evaluation of 20% to 40% of aqueous that is produced latanoprostene bunod in the treatment of glaucoma. Clin tion. These effects are often experi- Opthalmology. 2016;10:2035-50. drains through the unconventional, or enced following three to six months 9. Shannon A. Bausch + Lomb and Nicox announce FDA uveoscleral, pathway by diffusing through of treatment and most commonly approval of Vyzulta. Valeant Pharmaceuticals International, Inc. 12 2017(11):1-6. the interstitial spaces of the ciliary muscle affect hazel-colored irides. 10. Shah M, Lee G, Lefebvre DR, et al. A cross-sectional and ultimately the suprachoroidal space.1 Trichomegaly occurs through PG survey of the association between bilateral topical prostaglan- din analogue use and ocular adnexal features. PLOS ONE. These pathways often become resistant stimulation of melanocytes in the 2013;8(5):1-7. to drainage in glaucoma patients, making hair follicle, as well as stimulation 11. Shim J, Park C, Lee HS, et al. Change in prostaglandin expression levels and synthesizing activities in dry eye disease. them key targets for drug therapies. While of follicles into the anagen, or active Ophthalmology. 2012;119(11):2211-9. PGAs have been thought to work mainly on growth, phase.13 The effect of these 12. Stjernschantz JW, Albert DM, Hu DN, et al. Mechanism and clinical significance of prostaglandin-induced iris pigmentation. the unconventional pathway, more recent induced processes is greater lash fre- Surv Opththalmol. 2002;47(1):S162-75. evidence supports their role in increasing quency, thickness and length. This 13. Kaur S, Mahajan BB. Eyelash trichomegaly. Indian J Dematol. 2015;60(4):378-80. outflow through the conventional pathway mechanism forms the basis of the 14. Johnstone MA. Prostaglandin induced hair growth: a pro- as well.1,2 FDA approval of a topical PGA for posed site and mechanism of action. Invest Ophthalmol Vis Sci. eyelash lengthening.14 2010;51(13).

24 REVIEW OF OPTOMETRY JANUARY 15, 2018

0022_ro0118_essentials.indd22_ro0118_essentials.indd 2244 11/5/18/5/18 2:212:21 PMPM RO0118_Keeler Tono.indd 1 1/3/18 10:00 AM Coding Connection

What Are You Worth? Timely fee analysis and periodic restructuring is essential to practice success. By John Rumpakis, OD, MBA, Clinical Coding Editor n the world of compliance and and a conversion factor (CF) to One Code, One Fee reimbursement, we often focus ultimately convert a geographically- Remember, the golden rule is one Ion medical record compliance adjusted CPT RVU value into fee charged per CPT code. That to survive an audit. However, how dollars. Using this system, CMS means if I set my fee for 92004 you establish a fee schedule is just established the following formula at $150.00, I must charge every- as important—but rarely discussed. for their physician fee schedule: one who gets a 92004 the same The schedule must be structured in price without bias or discrimina- an objective fashion that ensures 2018 non-facility pricing amount = tion—that includes my non-insured you are paid fairly for the services [(work RVU x work GPCI) + (non- patients. Clinicians must respect you perform. facility PE RVU x PE GPCI) + (MP the rules and regulations regarding The first of the year is a great RVU x MP GPCI)] x CF time of service or prompt pay dis- time to review your processes and counts; ignoring these may put you make adjustments to boost your Understandably, most people in jeopardy with your carriers. With practice’s success in the coming look at this complicated math insured patients, if the charged rate year. Let’s start off by discussing equation and turn a blind eye— exceeds the contracted reimbursed how you might look at your fees in continuing to set their fees without rate from a specific carrier, the dif- a new light. understanding the implications of ference is generally adjusted off and this system. not billed to the patient. It’s Just Math, However, this methodology is the Not Rocket Science key to uncovering a fair amount Vigilance = Profit Analyzing and setting your fees of stealth reimbursement for your Just as with most things, when you should be an analytical, objective practice. Automated tools exist to pay attention to something your process that is done at least twice a help you manage this math, and performance generally increases. year. However, many physicians are some allow you to compare your Even small changes to your fee unsure how to properly handle the fee with CMS’s maximum allow- schedule can add up to significantly fee restructuring process and fall able reimbursement and with the better cash flow and profitability back on setting fees in a haphazard range of reimbursements from your over a year. Don’t let complacency fashion such as calling other doc- contracted medical carriers. Armed affect your bottom line. If the math tors to price shop or, worse yet, not with this information, you can then seems daunting, use an automated performing any analysis at all. set your fee appropriately.2 tool to help you manage this very The reimbursement methodology important, but often overlooked, used today has been in place since CMS Isn’t the Only area within your practice. 1992 with the initial rollout of the Game in Town Paying proper attention to the resource-based relative value sys- Many make the assumption that value of your intellectual property tem.1 This introduced the concept CMS is the highest paying carrier can start 2018 off on the right foot, of each CPT code having a relative in their area and simply set their and diligent monitoring can lead to value unit (RVU) composed of three fees as a percentage of the Medicare better business decisions for a long areas: work, practice expense (PE) maximum allowable. By not includ- time to come. ■ and malpractice (MP).1 ing your other contracted carriers Send questions and comments to It also takes into account cost in your analysis, you may be leav- [email protected]. of living differences based on geo- ing significant dollars on the table, 1. American Medical Association. RBRVS Overview. www. graphic location. It uses the geo- considering their reimbursed rates ama-assn.org/rbrvs-overview. Accessed November 21, 2017. 2. Practice Resource Management Inc. CodeSAFEPLUS.com. graphic practice cost index (GPCI) may be higher than Medicare. Accessed November 21, 2017.

26 REVIEW OF OPTOMETRY JANUARY 15, 2018

026_ro0118_coding.indd 26 1/5/18 2:22 PM 8.4 base curve now available!

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RO0817_Menicon.indd 1 7/27/17 10:57 AM Advertorial THE WAIT IS OVER. NEW New MyDay® toric lenses New MyDay® toric contact lenses incorporate CooperVision’s proven toric lens design and most advanced material

WHY DO YOU REACH “MYDAY® TORIC IS It’s the best of both worlds: the FOR MYDAY® TORIC? A GAME CHANGER.” world-renowned design features WHAT WOULD YOU TELL ® of Biofi nity toric combined with YOUR COLLEAGUES ABOUT DAWN BIRCHER, O.D. the Smart Silicone™ chemistry of MyDay®. And it’s here. CooperVision THIS LENS? has unveiled MyDay® toric, the McIntyre: With the shift toward Koepke: The best features of MyDay® long-awaited addition to its fi tting 1-day contact lenses, the toric are its stability and reliability. premium silicone hydrogel 1-day introduction of MyDay® toric is very It’s been very easy to fi t; it settles lens family. timely. CooperVision is known for quickly. It’s stable, even as the patient is looking from left to right. Take the For your patients who wake up its toric contact lenses, and they’ve prescription, pick that lens, put it on, each morning viewing the day as made really good torics throughout and it’s likely going to work. Rarely an opportunity. For those patients my very lengthy career. But there ® have I had to make any adjustments who are the most discerning of is nothing better than this. MyDay for axis or power changes. And your consumers, demanding superior toric has the water content, the patients are going to be happy with performance from every brand they Dk, the comfort, the vision—it has it. I’ve been really satisfi ed with the choose. They’re conquering life, and everything you want in a toric, let outcomes. It has been spot on. MyDay® is their contact lens. alone a 1-day toric. I would tell my colleagues, “Just try them. You’re Browning: MyDay® toric is ® Early adopters of MyDay toric going to love them.” CooperVision’s best lens to date. It are sharing their experiences with has been a great lens. We’ve always Bircher: I would tell my colleagues the lens, and it is everything they wanted Biofi nity® toric in a daily that MyDay® toric is a game had hoped for. All-day comfort. disposable. Now we have a great changer. Whether patients are using Stability. Familiar fi t. Healthier lens that is going to be very clear, it to supplement their current supply, modality and material. Find out consistent, and extremely comfortable or transitioning to the 1-day modality more about why practitioners are to wear all day long. MyDay® toric has full time, we fi nally have a lens that reaching for them, why patients already become my fi rst choice and will make them very happy with the love them, and why some are my favorite for fi tting daily disposable vision and comfort. And the doctor is saying that MyDay® toric is torics. We get the benefi ts of the all- going to be happy with the health of CooperVision’s best toric contact day comfort of Biofi nity®, now with the the eye. lens yet. advantages of daily disposables to have that fresh, clean lens on the eye every day.

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RO0118_Coopervision Adv.indd 2 1/2/18 10:51 AM “MYDAY TORIC IS COOPERVISION’S BEST LENS TO DATE.” DAVID BROWNING, O.D.

HOW SIMILAR IS THE HOW HAVE YOUR PATIENTS Don’t wait to give your PERFORMANCE OF MYDAY® RESPONDED TO MYDAY® patients with astigmatism an TORIC TO BIOFINITY® TORIC? TORIC? unprecedented 1-day contact Browning: Biofi nity® has been the Koepke: My patients tell me that lens wearing experience with ® gold standard for all toric lenses. MyDay® toric is a homerun when it MyDay toric. It’s been fantastic as far as not comes to comfort. It’s been really soft , It features the same Optimized rotating, very good vision, very good it’s easy for them to handle and get in Toric Lens Geometry™ found comfort. In my practice, we compare and out, and they’re getting great all- ® everything we have to Biofi nity®. day wear. in Biofi nity toric, the most prescribed toric lens in the Most daily disposables rotate more, Browning: The number one complaint so patients will experience more for all contact lens wearers that I have United States. This proven vision fl uctuation, and that’s why seen is end-of-day comfort. They can toric design provides uniform they end up going back to monthly put on almost any lens and be good for horizontal ISO thickness, an lenses—for more stable vision. But an hour or two, but to be able to sit in optimized ballast band design, then they complain that they’re not as front of a computer or to do daily tasks, large toric optic zone, and a comfortable. Now you don’t have to they’re just done. By the time it’s 5:00 smooth, continuous surface to worry. With MyDay® toric, you have or 6:00 p.m., patients want to remove make it an easy-to-fi t, stable the stability of Biofi nity® with the contact lenses, and we’ve found that toric lens. advantages of a daily disposable. It with MyDay® toric, patients have done has been a great lens for us. so much better. They can put on the And with MyDay® toric’s McIntyre: We fi t a lot of Biofi nity® lens and not think about their contacts extensive power range, you torics, so we were interested to see all day long. can fi t an even greater number ® how MyDay toric would perform Bircher: Seeing patients’ reactions is of patients in CooperVision’s ® vis-à-vis the Biofi nity toric. They ® what I’ve enjoyed most about MyDay soft est ever 1-day silicone have been very similar in the fi tting, toric. I’ve had a patient for over a hydrogel lens—so they can the speed of the adjustment, the decade, who has always had long-term get back to tackling life. comfort. In every way we could complaints about her vision and comfort ® ® monitor, Biofi nity toric and MyDay in toric lenses. When I fi rst received toric performed equally. MyDay® toric, I instantly thought of her. Prescribe the contact Koepke: For my patients going from When we dispensed the fi rst lenses, you lens of conquerors. Biofi nity® toric, which is a great toric could tell she was very hesitant. She For more information, visit lens, putting them into the MyDay® shrugged her shoulders and said, “We’ll PrescribeMyDay.com/toric/RO toric was actually very easy. They see.” Within a week we got a phone fi t very similarly. They’re both very call from her, telling us this was the comfortable, and the stability has game changer for her. She had all-day, been great. end-of-day comfort with MyDay® toric, in addition to crisp, sharp vision. With MyDay® toric, I feel confi dent telling my patients that they will have the same comfort in 8-10 hours as they do at initial insertion.

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RO0118_Coopervision Adv.indd 3 1/2/18 10:51 AM CXL Questions

Your Top 12 Crosslinking Questions–Answered!

New to corneal collagen crosslinking? This Q&A guide from Wills Eye Hospital will help prepare you to manage keratoconus patients in the new era. By Clark Chang, OD, MSA, MSc, and Christopher J. Rapuano, MD

or many eye care providers patients with community clinicians. and patients, keratoconus As with any new treatment pro- (KCN) management can feel cedure, a learning curve exists for Flike maintaining an undesir- clinicians to refine patient education able status quo. Due to advance- and selection process, as well as ments in specialty contact lens other perioperative management- technologies, corneal grafts are now related protocols. An open chan- only necessary for 10% to 20% of nel of communication allows our KCN patients.1 Notwithstanding, Corneal Service to help comanaging these patients still scored similarly clinicians to gain clinical comfort to those with advanced macular with CXL in their KCN practices. degeneration on the National Eye Here are 12 common questions our Institute’s visual function question- partner doctors ask; the answers can naire in CLEK Study (Collaborative help you decide on how to best edu- Longitudinal Evaluation of Kera- cate your KCN patients on CXL. toconus Study).2-5 Another report by the same group found that self- 1. What is CXL and how does perceived quality-of-life scores for it work? KCN patients continue to decline Fig. 1. Christopher Rapuano, MD, performs Crosslinking is a polymerization over time.6 With postulated KCN standard a corneal crosslinking protocol process that rearranges monomers prevalence reaching one in every 375 with the FDA-approved KXL System. into a three-dimensional network individuals, disease stabilization and of polymers to increase the sound- quality of life improvement or main- (FDA) approval in 2016 (Avedro’s ness of a molecular structure. This tenance are top priorities.7 KXL System and two photoenhanc- process naturally occurs in our bod- Since its development in 2003, ers, Photrexa and Photrexa viscous), ies as connective tissues gradually corneal crosslinking (CXL) has we have been able to offer CXL stiffen over time. Facilitated by the quickly become the treatment of treatments to patients for many endogenous enzyme lysyl oxidase choice for KCN progression con- years at Wills Eye Hospital under in launching the required oxida- trol.8 Although CXL only received the auspices of clinical trials. As a tive reactions, additional covalent US Food and Drug Administration result, we comanage many of these bonds (or tissue “crosslinks”) are

30 REVIEW OF OPTOMETRY JANUARY 15, 2018

030_ro0118_f1.indd 30 1/5/18 2:27 PM COMBO CHAIRS & STANDS formed between and within collagen efficacy with good safety profiles in fibrils—yielding increased tissue bio- KCN patients using the same CXL mechanical strength.9 protocol involving epithelial removal Typically, the cumulative effects (Figure 1).10-13 of natural crosslinking reactions are slow to manifest. In the late 1990s, 2. What is riboflavin’s role researchers from the University of during CXL? Optimise Dresden in Germany determined Since the bioavailable oxygen mole- that the photochemical induction cules in the cornea cannot be activat- space and process was the most clinically via- ed by UV light directly, a photosen- ble method for boosting induction functionality. of crosslinks in the cornea, bring- ing about CXL.8 This study used 0.1% riboflavin (with 20% dextran in solution) as the photosensitizer to absorb a carefully calibrated ultraviolet (UV) energy dose, thus converting available tissue oxygen into singlet oxygen molecules. The resultant reactive oxygen species possesses sufficient energy to activate the lysyl oxidase enzymatic pathway, leading to formation of new covalent bonds within the corneal stroma. The study from Dresden reported that all of the 23 progressive KCN eyes treated were stabilized, with 70% showing maximal keratometry flattening by 2.01D. Since then, many studies have achieved similar

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Figs. 2a and 2b. Above, saturation of riboflavin seen in the corneal stroma after riboflavin loading. Below, after 30 minutes of riboflavin loading at two-minute intervals, clinicians must check for aqueous riboflavin staining.

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sitizing substance must act as an fort and allow for faster, more intermediate agent. Riboflavin homogenous stromal saturation catalyzes CXL’s photochemical of Photrexa viscous (riboflavin reactions by transferring UV 5’-phosphate in 20% dextran energy (specifically, UVA from ophthalmic solution) during 365nm to 370nm) to stromal CXL. This phase lasts for 30 oxygen molecules, thereby con- minutes with riboflavin instilla- verting stable oxygen molecules tion in two-minute intervals.10 into a more reactive singlet After 30 minutes, patients are form. These reactive oxygen examined under the slit lamp species then initiate intrastromal to ensure the riboflavin has oxidative reactions. saturated the intended treat- Assuming UV energy is not ment area and that it is present the limiting resource, continu- Fig. 3. Crosshair guidance is projected from KXL within the aqueous (Figures 2a ous oxygen replenishment and device onto treatment site. and 2b). Per FDA approved active riboflavin molecules are indications, clinicians must essential in maintaining the with high antioxidant properties perform pachymetry after ribo- energy transfer required to perpetu- such as ascorbate and tryptophan flavin application to make sure the ate the CXL process. residues, which can prevent UV corneal thickness is at least 400µm. Additionally, saturating the penetrance and scavenge reactive If it is less than 400µm, hypotonic cornea with riboflavin creates a oxygen species. Moreover, the pres- Photrexa riboflavin should be “shielding effect” in which the ence of an epithelial barrier slows administered every five to 10 sec- respective UV energy levels reaching the rate of oxygen replenishment onds until the cornea is rehydrated the endothelium, lens and retina are during CXL procedures, thus reduc- to 400µm or greater.10 titrated to a much lower intensity ing the total amount of new cellular Once the appropriate pachym- than the actual cellular damage crosslinks that can be created. Con- etry level is verified, clinicians use thresholds. In fact, if a riboflavin- sequently, when the same standard the KXL UV device (Avedro) for saturated cornea is at least 400µm CXL protocol is carried out with the second phase of CXL treat- in thickness, the UV irradiance an intact corneal surface, the proce- ment, where 30 minutes of UV transmitted to the endothelium is dure’s overall efficacy will be lower irradiance (3mW/cm2) yields a total only 0.18mW/cm2, whereas the than anticipated. On the other hand, energy dose of 5.4J/cm2.8 During actual endothelial damage thresh- due to non-homogenous riboflavin the UV emission period, Photrexa old is approximately 0.35mW/cm2. saturation and reduced riboflavin viscous is instilled in two-minute Thereafter, the energy level pro- shielding effects, UV transmissions intervals while proper centration jected to reach the crystalline lens delivered to the endothelium and and device-eye distance are main- and retina is even lower compared deeper ocular tissues may be higher tained by the operator. The proper with the respective damage thresh- than previously calculated.16,17 KXL device position can be guided olds of these tissue layers.14,15 Clinicians should not assume by the crosshair image projections CXL is only effective when accom- (Figure 3), which aid the delivery 3. What is the purpose of panied by epithelial debridement. of an optimum illumination beam epithelial removal in the Although transepithelial CXL (TE- profile to the treated cornea. standard CXL protocol? CXL) applications do not currently Excess riboflavin can be rinsed The lipophilic nature of the corneal have FDA approval, modified treat- off with a balanced salt solution epithelium and the small pore size ment techniques are under investiga- at the end of a treatment session. of its tight junctions make this layer tion to enhance TE-CXL efficacy. A bandage contact lens (BCL) is essentially impervious to riboflavin inserted after instillation of topi- molecules. These epithelial barrier 4. How is the standard CXL cal antibiotic and corticosteroid characteristics prevent efficient and protocol performed? agents. The BCL should be kept homogenous riboflavin saturation in Topical anesthesia is used when on the treated eye for three to five the targeted stromal tissue.16 removing the central 9mm of days or until epithelial closure (Fig- Epithelium also contains enzymes epithelium to ensure patient com- ures 4a and 4b).

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030_ro0118_f1.indd 32 1/5/18 2:27 PM COMBO SELECT YOUR CHAIR 5. What are the patient selection recommendations? In 2016, the standard CXL protocol received labeled indications in the United States to treat patients 14 years of age or older with progres- sive KCN or corneal ectasia follow- 1000-CH ing refractive surgeries. However, when left untreated, disease severity Examination Chair and rate of progression are known to be more aggressive in younger Fig. 4a. Here, a bandage soft contact patients. Therefore, the KXL system lens is on the eye immediately after CXL and Photrexa/Photrexa viscous can treatment on a patient where corneal be considered for off-label use in riboflavin saturation is still evident. younger patients with minimum cor- neal thickness of 400µm or greater. KCN patients as young as eight have been reported by clinical trials, but special informed consents must be 1800-CH obtained from the patients and their Manual Recline guardians in these cases.18 Although the FDA has not speci- fied any contraindications, clinicians should exercise judgment before Fig. 4b. Epithelial wound closure is offering CXL to lactating mothers mostly complete on the same patient and patients older than 65 years only three days after treatment with CXL. of age. Also, researchers strongly recommend avoiding CXL during progression are just two potential the course of a pregnancy. A recent clinical examples.19,21 study found topographic, pachy- According to the conventional metric and biomechanical evidence KCN care model, some amount of KCN progression in 100% of its of meaningful changes in clinical 2000-CH pregnant patient cohort.19 This led parameters must manifest prior to researchers to recommend discuss- initiating a new treatment course. Cradle Tilt ing prophylactic CXL with female However, significant progression patients prior to family planning. frequently occurs before action is Some European countries have taken due to the lack of consensus begun to proactively offer CXL to on the exact clinical indicator and female KCN patients who are plan- corresponding magnitude of change ning for pregnancy despite lack of that constitutes disease progression. disease progression.20 Many CXL studies define KCN pro- gression as changes over a 12-month 6. Is KCN progression period in the any of the following necessary to recommend CXL? measurements: 1D or more in maxi- 2500-CH Although KCN progression is part mum keratometry; 0.5D or more in of the on-label indication for CXL myopia; 1D or more in astigmatism; Motorized treatment, certain circumstances or 10µm or more loss in thinnest Recline do not require progression before a pachymetric point.10-12,20,22 However, CXL consult. Female KCN patients with the limited accuracy of tradi- who are planning to become preg- tional topographers when imaging nant and patients at a high risk for the irregular corneal surface and

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the refractive variability of KCN found 24% of the 186 eyes newly After standard CXL, keratometry, patients, these guidelines may result diagnosed with KCN belonged to pachymetry and transient CXL haze in a higher rate of false positives. patients aged 40 or older.23 measurements also follow a similar Alternatively, one expert panel In addition, given that post-surgi- temporal pattern, with further steep- recently recommended that the pres- cal ectasia can occur at a later point ening, thinning and reduction in ences of at least two of three criteria in life than a typical KCN patient, corneal transparency during the first can establish progression: steepening clinical consensus has not defined an month. These trends typically reverse in anterior corneal curvature; steep- age range for when ectasia typically over the following two months, at ening of posterior corneal curvature; occurs and when progression may which point patients slowly return to or thinning when comparing pachy- slow down. Thus, clinicians should baseline characteristics. Sometimes metric distribution profile from refrain from using age as an absolute these patients even experience mild periphery to thinnest point.21 While contraindication for CXL candidacy. improvements before reaching a pla- useful, these guidelines require access teau of stabilization (Figure 5).10-12 to corneal tomography capable of 8. What are the general CXL It’s important to refrain from tracking changes over time, present- postoperative findings and misconstruing these immediate post- ing a possible challenge for some expectations? operative trends as worsening in comanaging clinicians. The initial phase of recovery from KCN disease or CXL failure. Over- Given these clinical hurdles, the standard CXL is much like any all, despite an epi-off CXL protocol, expert panel assembled from four procedure involving corneal epithe- only a short period exists during supranational corneal societies con- lial removal. Although BCLs offer the immediate postoperative recov- cluded that CXL recommendations therapeutic protection and enhanced ery where patients may feel visu- can be made to KCN patients with patient comfort, most patients still ally compromised. This is because high-risk profiles, even if progression experience some ocular discomfort patients are refit in contact lenses or has not been documented.21 or pain until the epithelial defect can resume contact lens wear before closes, which usually occurs in three they reach post-CXL stabilization. 7. Should I consider CXL for to five days.24 patients older than 40? After epithelial closure, visual acu- 9. Can CXL patients expect any The short answer is yes. KCN ity generally worsens or greatly fluc- refractive changes? patients tend to display a slower rate tuates throughout the first month Studies have reported variable results of progression or even stabilization before slowly returning to baseline for sphere, cylinder and spherical in their fourth or fifth decade of by the third month. Patients may equivalent at 12 months post-CXL life—likely a byproduct of age-asso- experience a mild improvement in treatment. Some show statistically ciated crosslinking. However, KCN vision between months three and significant refractive changes, while expression is highly variable, and age six or months six and 12. Addition- others recorded no notable differ- alone is not always a well-defined ally, a stabilization trend typically ences.25-27 Researchers have reported end point for KCN. A retrospective emerges as the new baseline between improvements in total higher-order chart review from Wills Eye Hospital months six and 12.10-12 aberration, spherical aberration and coma as well as average topographic flattening of 1.6D.10,28 Still, the liter- ature provides no consistent correla- tions between changes in these clini- cal parameters and CXL treatment. Consequently, KCN stabilization should remain the primary objec- tive of currently available CXL protocols. Before recommending Fig. 5. An example of topographic flattening seen as early as three months after CXL, patients should be informed standard (epi-off) corneal crosslinking protocol. The left map shows the patient’s pre- that contact lenses or glasses will operative axial topography. The center map is the postoperative topography at month still be required after CXL, and this three, and the right map provides a difference calculation revealing the topographic management approach may improve improvement at month three. patients’ quality of life by reducing

34 REVIEW OF OPTOMETRY JANUARY 15, 2018

030_ro0118_f1.indd 34 1/5/18 2:27 PM COMBO COMBINE WITH OUR Photo: Aaron Bronner, OD the frustration often associated UNIQUE STAND with frequent optical changes when KCN is left untreated. 10. Is CXL haze a concern? Transient CXL haze can appear Eff ortless similar to post-PRK corneal haze. With experience, however, clini- instrument cians can differentiate the two entities under the slit lamp. CXL Fig. 6. The demarcation lines are visualized positioning haze creates a dust-like tissue with optic section in a patient who received change in the anterior to mid- off-label treatment of CXL and Intacs stromal levels, whereas PRK haze corneal implant (AJL Ophthalmic). manifests in a reticulated fibrotic proliferation pattern that is local- topical steroids do not mitigate CXL ized to the subepithelial to anterior haze and their long-term use is not stromal layers. Given the different necessary after standard CXL. How- anatomic appearances and the self- ever, one study proposed that topical resolving nature of CXL haze, it is steroids may be justified if persistent unlikely to carry the same visual haze or stromal scarring is observed implications as PRK haze.24 after the one-year mark.24,29 Immediately after CXL treatment, confocal microscopy will reveal ker- 11. Can you perform CXL atocyte apoptosis and lacunar edema without removing the in the anterior to mid-stromal area. epithelium? As areas of CXL haze and stromal Standard epi-off CXL is minimally edema start to show improvement invasive and highly effective in halt- by the end of the first month, clini- ing KCN progression. Additionally, cians will see zones of optical discon- adverse events are uncommon tinuity—or demarcation lines—with after standard CXL.10-13 However, an optic section during slit lamp researchers continue to investigate examination (Figure 6).24 delivery methods to increase com- Although glare disability is a fort during and after the procedure, Advanced possibility during the first six to shorten visual recovery time and eight weeks, transient CXL haze reduce risks of potential infection. ergonomics and demarcation line depth are Keeping the epithelium intact often used as indicators to reflect reduces diffusion rates of riboflavin, treatment penetration and resul- UV light and oxygen, all of which tant stromal collagen remodeling. are essential to the photochemical As keratocytes slowly repopulate, reactions during CXL. Researchers the backscattering of light starts to have been able to bypass the epi- resolve and the areas of CXL haze thelial barrier function by disrupt- begin to fade between three and six ing tight junctions with chemical months. The haze will often become enhancers such as benzalkonium unnoticeable by one-year post-CXL. chloride (BAK) and ethylenediami- Topical steroids are often discontin- netetraacetic acid (EDTA). These ued after the first few weeks follow- corneal enhancers are incorpo- ing the procedure, yet most cases rated into the riboflavin solution of CXL haze self-resolve over time to assist penetrance into corneal without further therapeutic inter- stroma. However, some studies have ventions; thus, researchers suggest reported shallower demarcation lines

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2008;145(4):611-7. and reduced corneal stiffening effects their contact lenses may be expected 7. Godefrooij DA, de Wit GA, Uiterwaal CS, et al. Age-specific after TE-CXL.30,31 over the next six to 12 months. incidence and prevalence of keratoconus: a nationwide registra- tion study. Am J Ophthalmol. 2017;175:169-72. Although several studies reported 8. Wollensak G, Spoerl E, Seiler T. Riboflavin/ultraviolet-a-induced collagen crosslinking for the treatment of keratoconus. Am J higher regression rates with TE- The emergence of CXL has Ophthalmol 2003;135(5):620-7. CXL, its rates of adverse events are ushered in a new era of KCN 9. Schumacher S, Mrochen M, Wernli J, et al. Optimization model for UV-riboflavin corneal cross-linking. Invest Ophthalmol also lower than those of standard management in which clinicians Vis Sci. 2012;53(2):762-9. 10. Chang CY, Hersh PS. Corneal collagen cross-linking: a review epi-off CXL. Additionally, the shal- no longer have to assume a passive of 1-year outcomes. Eye Contact Lens. 2014;40(6):345-52. lower CXL treatment depth may be reactive management approach 11. Hersh PS, Stulting RD, Muller D, et al. United States multi- center clinical trial of corneal collagen crosslinking for keratoco- advantageous in eyes with thinner and offer patients only a forced nus treatment. Ophthalmology. 2017;124(9):1259-70. corneas at baseline. Patients with a choice between contact lenses 12. Hersh PS, Stulting RD, Muller D, et al. US multicenter clinical trial of corneal collagen crosslinking for treatment low risk of progression and those and corneal grafts. With early of corneal ectasia after refractive surgery. Ophthalmology. 2017;124(10):1475-84. who are concerned about visual CXL intervention for appropriate 13. Raiskup F, Theuring A, Pillunat LE, Spoerl E. Corneal collagen recovery time may be reasonable candidates and continual post-CXL crosslinking with riboflavin and ultraviolet-a light in progres- sive keratoconus: ten-year results. J Cataract Refract Surg. candidates for TE-CXL.24,30,31 monitoring, clinicians can help 2015;41(1):41-6. 14. Spoerl E, Mrochen M, Sliney D, Trokel S, Seiler T. Safety Until the efficacy of TE-CXL patients maintain their best visual of UVA-riboflavin cross-linking of the cornea. Cornea. 2007 improves, we will continue to function and maximally defer the May;26(4):385-9. 15. Schumacher S, Mrochen M, Wernli J, et al. Optimization recommend standard epi-off possible needs for keratoplasties. model for UV-riboflavin corneal cross-linking. Invest Ophthalmol Vis Sci. 2012;53(2):762-9. CXL for KCN patients with a Today’s clinical focus should go 16. Bottós KM, Schor P, Dreyfuss JL, et al. Effect of cornea high likelihood of progression or beyond simply refitting contact epithelium on ultraviolet-a and riboflavin absorption. Arq Bras Oftalmol. 2011;74(5):348-51. aggressive clinical progression. lenses as KCN progresses. With 17. Richoz O, Hammer A, Tabibian D, et al. The biomechanical effect of corneal collagen cross-Linking (CXL) with riboflavin and early detection of KCN, access to UV-A is oxygen dependent. Transl Vis Sci Technol. 2013;2(7):6. 12. When should I refit contact CXL and advancements in specialty 18. Padmanabhan P, Rachapalle Reddi S, Rajagopal R, et al. Cor- neal collagen cross-linking for keratoconus in pediatric patients- lenses after CXL? lens designs, clinicians can help long-term results. Cornea. 2017;36(2):138-43. 19. Naderan M, Jahanrad A. Topographic, tomographic A study using confocal microscopy their KCN patients live life to the and biomechanical corneal changes during pregnancy in showed that epithelial thickness fullest. ■ patients with keratoconus: a cohort study. Acta Ophthalmol. 2017;95(4):e291-e296. gradually returns to normal between Dr. Chang is director of Cornea 20. Sandvik GF, Thorsrud A, Råen M, et al. Does corneal collagen cross-linking reduce the need for keratoplasties in patients with three and six months after standard Specialty Lenses at Wills Eye Hos- keratoconus? Cornea. 2015;34(9):991-5. CXL.24 However, many patients pital–Cornea Service and director of 21. Gomes JA, Tan D, Rapuano CJ, et al. Global consensus on keratoconus and ectatic diseases. Cornea. 2015;34(4):359-69. require contact lens rehabilitation to clinical services at TLC Vision. He 22. Nordström M, Schiller M, Fredriksson A, Behndig A. Refrac- tive improvements and safety with topography-guided corneal function and cannot wait six months is an advisory board member for the crosslinking for keratoconus: 1-year results. Br J Ophthalmol. before resuming contact lens wear. International Keratoconus Academy, 2017;101(7):920-5. 23. Yildiz EH, Diehl GF, Cohen EJ, et al. Demographics of patients Our personal approach is to the Gas Permeable Lens Institute older than 50 years with keratoconus. Eye Contact Lens. and the Optometric Cornea, Cata- 2009;35(6):309-11. adopt a lens fitting strategy that 24. Mazzotta C, Hafezi F, Kymionis G, et al. In vivo confocal allows minimal to no interaction ract and Refractive Society. microscopy after corneal collagen crosslinking. Ocul Surf. 2015;13(4):298-314. between the posterior lens surface Dr. Rapuano is chief of Cornea 25. Cınar Y, Kürs¸at Cingü A, Turkcu FM, et al. Accelerated cor- and corneal epithelium, given the Service at Wills Eye Hospital. He has neal collagen cross-linking for progressive keratoconus. Cutan Ocul Toxicol. 2014;33:168-71. possibility of persistent haze with published several books, numerous 26. Kanellopoulos AJ. Long-term results of a prospective randomized bilateral eye comparison trial of higher fluence, delayed epithelial healing or dis- book chapters and over 175 peer- shorter duration ultraviolet a radiation, and riboflavin collagen rupted epithelial remodeling. Various reviewed articles, including having cross linking for progressive keratoconus. Clin Ophthalmol. 2012;6:97-101. lens designs can help accomplish this co-authored The Wills Eye Manual. 27. Cummings AB, McQuaid R, Naughton S, et al. Optimizing corneal cross-linking in the treatment of keratoconus: a com- goal including those with corneal parison of outcomes after standard- and high-intensity protocols. vaulting capacities, such as hybrid, 1. Godefrooij DA, Gans R, Imhof SM, Wisse RP. Nationwide Cornea. 2016;35(6):814-22. reduction in the number of corneal transplantations for keratoco- 28. Vinciguerra P, Albè E, Trazza S, et al. Refractive, topo- scleral, piggyback and even custom nus following the implementation of cross-linking. Acta Ophthal- graphic, tomographic, and aberrometric analysis of keratoconic mol. 2016;94(7):675-8. eyes undergoing corneal cross-linking. Ophthalmology. soft lenses. From clinical experience, 2. Davidson AE, Hayes S, Hardcastle AJ, et al. The pathogenesis 2009;116(3):369-78. we have found the ideal time to con- of keratoconus. Eye (Lond). 2014;28(2):189-95. 29. Kim BZ, Jordan CA, McGhee CN, Patel DV. Natural history 3. Tuft SJ, Moodaley LC, Gregory WM, et al. Prognostic fac- of corneal haze after corneal collagen crosslinking in kerato- sider refitting a lens is approximately tors for the progression of keratoconus. Ophthalmology. conus using Scheimpflug analysis. J Cataract Refract Surg. 1994;101(3):439-47. 2016;42(7):1053-9. four to six weeks after standard 4. Gordon MO, Steger-May K, Szczotka-Flynn L, et al. Baseline 30. Wollensak G, Iomdina E. Biomechanical and histological CXL or two weeks after TE-CXL. factors predictive of incident penetrating keratoplasty in kerato- changes after corneal crosslinking with and without epithelial conus. Am J Ophthalmol. 2006;142(6):923-30. debridement. J Cataract Refract Surg. 2009;35(3):540-6. It’s also prudent to stress to patients, 5. Kymes SM, Walline JJ, Zadnik K, Gordon MO. Quality of life in 31. Caporossi A, Mazzotta C, Paradiso AL, et al. Transepi- keratoconus. Am J Ophthalmol. 2004;138(4):527-35. thelial corneal collagen crosslinking for progressive kerato- particularly after standard CXL, that 6. Kymes SM, Walline JJ, Zadnik K, et al. Changes in the conus: 24-month clinical results. J Cataract Refract Surg. frequent refractive modifications in quality-of-life of people with keratoconus. Am J Ophthalmol. 2013;39(8):1157-63.

36 REVIEW OF OPTOMETRY JANUARY 15, 2018

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RP1017_Akorn Consumer.indd 1 9/20/17 9:55 AM Epithelial Defects

Fixing a Hole: How to Heal Persistent Epithelial Defects Clinicians have a robust arsenal for treating this reccurring condition. Knowing where to start and when to switch it up is key. By Alan Kwok, OD

orneal metabolism The main therapeutic and wound healing goal is to provide an envi- are crucial to prop- ronment conducive for the Cerly maintaining the eye to restart and complete cornea’s integrity and func- the epithelialization process. tionality. When an insult This usually involves pro- occurs to the corneal surface, viding extra lubrication and creating an epithelial defect, supporting the ocular sur- the complex re-epitheli- face to allow for the normal alization process involves proliferation and migration limbal stem cells, cell dif- of differentiated epithelial ferentiation, proliferation, cells to cover the defect. migration and remodeling Early intervention and of the extracellular matrix.1 Fig. 1. Diffuse fluorescein staining with white light reveals resolution is key, as research Researchers believe growth this epithelial defect. shows the length of time a factors involved in the pro- defect is left open is propor- cess include epidermal, keratinocyte, ment, is a significant long-term man- tional to the time it will take for the hepatocyte and basic fibroblast agement problem for ODs.4 defect to be fully repaired.6,7 growth factors.2 In normal, healthy Some risk factors that can con- corneas, supportive therapy can help found corneal epithelial healing Assessment the body resolve an epithelial defect include trauma, diabetic keratopa- When evaluating a persistent epithe- rapidly. However, healing may be thy, limbal stem cell deficiency, dry lial defect, clinicians should carefully delayed or halted altogether in com- eye disease (DED), exposure kera- record both positive and negative promised conditions, leaving the topathy, neurotrophic keratopathy pertinent findings. To properly mon- underlying stroma exposed and vul- after penetrating keratoplasty (PKP) itor the healing process, clinicians nerable to further trauma, infiltrates, and herpetic infections and diabetic should record the size and location infection, scarring or perforation.3 A vitrectomy.5 Each condition can of the defect at each visit and image persistent epithelial defect, defined affect the normal metabolism of the in white light and blue light imme- as a defect that has not resolved epithelium and delay, disrupt or sus- diately after fluorescein instillation after two weeks of standard treat- pend healing of an epithelial insult. (Figures 1 and 2).

38 REVIEW OF OPTOMETRY JANUARY 15, 2018

038_ro0118_f2.indd 38 1/5/18 4:30 PM Clinical experience suggests the glycosides gentamicin size and shape of the defect is most and tobramycin, for conspicuous immediately after example, can cause fluorescein instillation; thus, mea- superficial punctate surements and photos should be keratitis in addition to taken right away. Depending on the delaying corneal heal- depth of the defect, a delay of even ing.12 Similarly, topical five minutes may result in blurred ciprofloxacin and the margins as the fluorescein absorbs topical nonsteroidal into the surrounding epithelium and anti-inflammatory underlying stroma—making the drugs (NSAIDs) diclof- margins harder to discern. enac and ketorolac can In addition, clinicians should also adversely affect Fig. 2. Picture of an epithelial defect taken several monitor for any change in inflam- corneal wound heal- minutes after fluorescein instillation. As the fluorescein mation throughout the management ing.13,14 In addition, absorbs into the stroma, the edges are obscured, making period by noting anterior chamber commonly prescribed it difficult to determine its exact size and shape. reaction for inflammatory cells and glaucoma medications flare. Underlying or associated haze such as latanoprost, travoprost, hour with artificial tears. The adage or infiltrates may be red flags for brinzolamide and dorzolamide cause “you can’t use too much” certainly concurrent infectious activity. If all is low-grade chronic inflammation applies here. Ointment, though it is quiet, the lack of inflammatory cells with prolonged use.9 accompanied by concomitant visual and flare can be recorded as perti- Perhaps more importantly, the symptoms, is the preferred modality nent negative findings to confirm ubiquitous preservative benzal- because of the increased contact time there is no concurrent inflammatory konium chloride (BAK) is a well- with the cornea.3 or infectious activity. known ocular surface irritant. The Punctal occlusion. Another mea- During treatment, the patient wide use of BAK is due largely to its sure to provide a more lubricious should be evaluated frequently, even weak allergenic potential and high environment for the ocular surface is daily initially, to monitor progress. rate of antimicrobial properties. punctal occlusion in the presence of However, research demonstrates its dry eye syndrome. However, punctal Standard Treatments toxic effects on the ocular surface, occlusion may exacerbate any toxic- Many factors will influence your and some studies show significantly ity present from topical medications, treatment regimen, including con- fewer symptoms and signs when and clinicians should be aware of all current conditions, the patient’s patients use preservative-free glau- medications the patient is using to systemic health, medication use and coma medications.15,16 avoid adverse effects.3 response to treatment. Here is a look Whenever possible, clinicians Bandage soft contact lenses. The at the treatment options available should modify a patient’s medication use of a silicone hydrogel contact and when it’s best to use them: use during the treatment period to lens can be effective in protecting Address contributory factors. If decrease the effect of medicamentosa an underlying infiltrate is observed and provide an environment more Etiologies of Persistent with the defect, aggressive measures conducive to corneal healing. Epithelial Defect3 should be taken to treat a presumed Aggressive lubrication. Bathing • Trauma and infection infectious component until negative the cornea in adequate lubrication • Diabetic keratopathy corneal cultures prove otherwise. should be the first line of attack to • Limbal stem cell deficiency The first priority is to treat any infec- initiate the epithelialization pro- • Severe DED tious process to prevent progression cess. Depending on the underlying • Exposure keratopathy to corneal melt and perforation.8 cause of the persistent defect, poor • Neurotrophic keratopathy In addition, many concurrent surface lubricity could be the main - Status post PKP topical medications have known reason for delayed resolution. Oint- - Herpetic infections corneal toxicity and can negatively ment or preservative-free artificial • PKP impact the healing process for epi- tears should be generously applied • Diabetic vitrectomy thelial defects.9-11 The topical amino- every hour for ointment, every half

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038_ro0118_f2.indd 39 1/5/18 4:30 PM Epithelial Defects

the underlying cornea from respond to one night of scleral the shearing forces of the lid lens wear, once healing is initi- that occur with every blink. ated after several nights, the Such protection is particularly healing rate will increase and helpful for newly formed cells full resolution will occur soon attempting to migrate and thereafter. form a new epithelial layer. After resolution of the defect, Because of the risk of infec- researchers postulate that con- tious keratitis, these patients tinuing overnight wear for 24 to should be seen frequently to 48 hours may reduce recurrence monitor the healing process Fig. 3. This patient has a history of neurotrophic of surface breakdown.22 and rule out infection. Con- keratopathy secondary to herpes simplex keratitis. He Amniotic membrane graft- current topical preservative- suffered multiple episodes of surface breakdown that ing. Since their introduction free antibiotics should be ultimately responded to a lateral tarsorrhaphy, which in 1995, amniotic membrane prescribed for prophylaxis. has been kept in place for surface maintenance. grafts have been used for Pressure patching. Though many ocular surface condi- a common treatment option in the cive to corneal surface rehabilitation tions, including persistent epithelial past, evidence suggests pressure by continually bathing the ocular defects.26,27 Two types are available: patching can actually impede the surface and providing a mechani- cryo-preserved and epithelialized. healing process and be a source of cal barrier against the eyelid during The latter of the two needs to be infection.17-20 Several studies show blink related micro-trauma.22,25 maintained at -80°C and dehy- either no additional benefit or The treatment of a persistent epi- drated, unless it is de-epithelialized, delayed healing with pressure patch- thelial defect with scleral lenses or in which case it can be stored at ing compared with use of antibiotic PROSE devices involves overnight room temperature.26 Prokera (Bio- and mydriatic alone.19,21 wear with daily monitoring to track Tissue) cryopreserved amniotic resolution of the defect and check membrane is a commonly-used Secondary Options for any infectious or inflammatory option that can be inserted in-office In spite of many traditional treat- events. Daily wear will provide only with relative ease, though some ment options, some conditions may a partial benefit, as healing improves patients find the ring to be a source prove to be recalcitrant and require much quicker with overnight wear. of discomfort. BioDOptix (BioD) secondary therapies: A drop of preservative-free moxi- and AmbioDisk (Katena) are other Scleral lenses. Research sug- floxacin is applied, either in the amniotic membrane options. gests scleral lenses and PROSE eye prior to lens insertion or into The role of amniotic grafts in re- (for “prosthetic replacement of the the reservoir with preservative-free epithelialization of persistent epithe- ocular surface ecosystem”) devices saline. Vault should be sufficient lial defects may involve a mechanical (BostonSight) can be effective in the to clear the limbus. Based on clini- effect where the basement membrane treatment and resolution of epithe- cal experience, the key is to fit the of the graft serves as a scaffolding lial defects.22-25 PROSE is a medical lens as loose as possible to reduce on which regenerating epithelial cells treatment model developed to treat suction and inflammatory triggers can migrate.26 Researchers speculate complex corneal conditions. Treat- that come from a tight-fitting lens. that the basement membrane also ment involves the customized fit- Typically, a larger diameter lens with reinforces adhesion of basal epi- ting of ocular prosthetic devices to adequate toricity will work better thelial cells and promotes epithelial achieve one or more of the following for overnight wear than a smaller differentiation.28,29 In addition, the goals: improve vision (particularly lens that may have more suction. If growth factors necessary for healing for irregular corneas), improve the patient can tolerate the aware- are present in amniotic membrane.30 comfort (for severe ocular surface ness that comes with edge lift of Autologous serum. This can be disease) and support the ocular sur- the peripheral curve, this would be beneficial to initiating and expedit- face (for pathology of ocular surface acceptable, even preferred, to create ing the healing of an epithelial defect disease). For persistent epithelial a looser fitting lens. because it contains the growth fac- defects, the device may help to pro- Anecdotally, though longstanding tors necessary for re-epithelializa- vide an environment that is condu- persistent epithelial defects may not tion.7,31,32 Clinicians often advocate

40 REVIEW OF OPTOMETRY JANUARY 15, 2018

038_ro0118_f2.indd 40 1/5/18 4:31 PM for frequent instillation, such as one is an effective combination therapy resolution of the epithelial defect drop every two hours, to expedite for persistent epithelial defects.33-35 with a bandage contact lens also healing. One study found an average This protocol combines the mechani- showed less recurrence.33 healing time of 22 days with the use cal protection of a bandage soft However, logistical obstacles to of 50% serum drops.7 contact lens with the nutrients of using autologous serum may limit Recent evidence suggests the use autologous serum eye drops to pro- its utility. The process of attain- of autologous serum eye drops with vide a synergistic effect on healing. ing the drops first requires a blood silicone hydrogel soft contact lenses The use of autologous serum after draw, which may be prohibitive for

Case Example A 38-year-old Caucasian female presented with a history of systemic lupus erythema- tosus and Stevens-Johnson syndrome with severe ocular complications. She suffered an ulcerative keratitis in the left eye that perforated, requiring a therapeutic PKP. Postoperative assessments showed incom- plete re-epithelialization of donor graft that, over a course of a month, did not respond to bandage contact lens treatment and topi- Figs. 1 and 2. After PKP, this patient had active neovascularization to the graft-host cal gentamicin. She was referred for PROSE interface. The fluorescein image highlights the persistent epithelial defect. treatment and resolution of persistent epi- thelial defect. Her entering visual acuity with correc- tion (VAcc) was 20/30 OD, 20/400 OS. Anterior segment evaluation was signifi- cant for cauterized lower puncta OD, OS, conjunctival injection 3+ temporally and inferiorly OS, a decentered 6mm corneal graft with several intact sutures and active corneal neovascularization to the graft Figs. 3 and 4. At left, the fluorescein image after one day of overnight lens wear 360 degrees with corneal vessels at the shows significantly less staining on graft tissue. At right, the patient found resolution graft-host interface infero-nasal (Figure 1). of the epithelial defect after two nights of overnight lens wear. There was a 3mm epithelial defect 10 to 12 o’clock within graft (Figure 2). The PROSE treatment was initiated OS with the following device parameters: Boston XO2 (Dk: 140), 8.5mm BC, +3.50D, 19.0mm diameter and with-the-rule toric peripheral curves. The initial device assessment showed alignment of the peripheral haptics. Prior to insertion, a drop of Vigamox was instilled into the reservoir of the device, along with preservative-free saline solution, for prophylaxis against infectious keratitis. The patient was instructed to not remove the device over- night and to return in the morning for evaluation.

Follow Up The next day, the patient’s VAcc was 20/30 OD, 20/125 OS. The anterior seg- ment evaluation showed slightly reduced conjunctival injection at 2+ OS and Fig. 5. The patient’s left eye two years after treatment. a significantly reduced epithelial defect on the graft (Figure 3). By the next day after another night of overnight wear, the defect was resolved (Figure 4). Overnight wear of the device was discontinued and erythromycin ointment was prescribed prior to bedtime for overnight lubrication. The patient continues to wear the PROSE device on a daily basis and has had no recurrence of epithelial breakdown. At a recent visit, the eye was white and quiet with ghosted corneal vessels that were previously active (Figure 5).

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11. Baudouin C, Labbe A, Liang H, et al. Preservatives in patients with limited access to care Therapies in the Pipeline eyedrops: the good the bad and the ugly. Prog Ret Eye Res. 2010;29(4):312-34. or who are disabled. Other treatments in development are 12. Petroutsos G, Guimarraes R, Giraud J. Antibiotics Limbal stem cell transplanta- promising: and corneal epithelial wound healing. Arch Ophthalmol. 1983;101(11):1775-8. tion. This is an advanced option Matrix regenerating agent. Recently 13. Thompson AM. Ocular toxicity of fluoroquinolones. Clin Exp Ophthalmol. 2007;35(6):566-77. when other standard and secondary available in Europe, this is a large bio- 14. Hersch PS, Rice BA, Baer JC, et al. Topical nonsteroi- polymer that is an analog of glycosami- dal agents and corneal wound healing. Arch Ophthalmol. therapies fail for patients with limbal 1990;108(4):577-83. stem cell deficiency as a complicat- noglycan integral to the structure of the 15. Collin HB. Ultrastructural changes to the corneal endothe- lium due to benzalkonium chloride. Acta Opthalmol (Copenh). ing factor. The procedure involves extracellular matrix. Research demon- 1986;64(2):226-31. 16. Jaenen N, Baudouin C, Pouliquen P, Manni G. Ocular symp- the transplantation of limbal stem strates topical application effectively heals toms and signs with preserved and preservative-free glaucoma cells to the affected eye.36 The source persistent epithelial defects after fortified medications. Eur J Ophthalmol. 2007;17(3):341-9. 17. Campanile TM, St Clair DA, Benaim M. The evaluation of of the grafted tissue can be either an antibiotic treatment of bacterial keratitis.37 eye patching in the treatment of traumatic corneal epithelial defects. J Emerg Med. 1997;15(6):769-74. autograft from the contralateral eye Amniotic membrane extract. 18. Kirkpatrick JN, Hoh HB, Cook SD. No eye pad for corneal or allograft from a donor. Autolo- Research is being conducted on a lyophi- abrasion. Eye (Lond.). 1993;7(Pt 3):468-71. 19. Kaiser PK. A comparison of pressure patching versus no gous transplantation of tissue from lized preparation of amniotic membrane patching for corneal abrasions due to trauma or foreign body 2,36 removal. Opthalmology. 1995;102(12):1936-42. the contralateral eye will ensure no that can be used as an eye drop. The 20. Clemons CS, Cohen EJ, Arentsen JJ, et al. Pseudomonas presence of growth factors in this extract ulcers following patching of corneal abrasions associated with graft rejection, although the grafted contact lens wear. CLAO J. 1987;13(3):161-4. eye may be susceptible to limbal could potentially have similar efficacy in 21. Le Sage N, Verreault R, Rochette L. Efficacy of eye patching 3 for traumatic corneal abrasions: A controlled clinical trial. Ann stem cell deficiency. healing of amniotic membrane in topical Emerg Med. 2001;38(2):129-34. 22. Ciralsky JB, Chapman KO, Rosenblatt MI, et al. Treatment of Tarsorrhaphy. When other form the patient applies at home without refractory persistent corneal epithelial defects: a standardized options are unsuccessful or are the need for in office-application. approach using continuous wear PROSE therapy. Ocul Immunol Inflamm. 2015;23(3):219-24. unavailable, temporary partial or 23. Lim P, Ridges R, Jacobs DS, Rosenthal P. Treatment of persistent corneal epithelial defect with overnight wear of a complete tarsorrhaphies can be hood of recurrence. In most of these prosthetic device for the ocular surface. Am J Ophthalmol. 2013;156(6):1095-101. effective in providing an environ- vulnerable patients, recurrence of 24. Ling JD, Gire A, Pflugfelder SC. PROSE therapy used to ment conducive to healing (Figure surface breakdown may be common minimize corneal trauma in patients with corneal epithelial defects. Am J Ophthalmol. 2013;155(4):615-19. 3). This is a good option when expo- and warrants more frequent exami- 25. Rosenthal P, Cotter JM, Baum J. Treatment of persistent ■ corneal epithelial defect with extended wear of a fluid-ventilated sure keratopathy is either contribu- nations beyond the annual visits. gas-permeable scleral contact lens. Am J Ophthalmol. tory to the formation of the defect or Dr. Kwok is a clinician at Boston- 2000;130(1):33-41. 26. Lee SH, Tseng S. Amniotic membrane transplantation for may complicate healing. Clinicians Sight and was previously a faculty persistent epithelial defects with ulceration. Am J Ophthalmol. 1997;123(3):303-12. should also consider this treatment member of the New England Col- 27. Sabater AL, Perez VL. Amniotic membrane use for manage- modality for patients who are non- lege of Optometry specializing in ment of corneal limbal stem cell deficiency. Curr Opin Ophthal- mol. 2017;28(4):363-9. compliant or are physically unable contact lens education. He is a grad- 28. Khodadoust AA, Silverstein AM, Kenyon KR, Dowling JE. 3 Adhesion of regenerating corneal epithelium: the role of base- to apply lubrication drops. uate of the University of Waterloo ment membrane. Am J Ophthalmol. 1968;65(3):339-48. School of Optometry and completed 29. Guo M, Grinnell F. Basement membrane and human epider- mal differentiation in vitro. J Invest Dermatol. 1989;93(3):372-8. Despite myraid treatment options, a primary care residency at the New 30. Koizumi NH, Inatomi TJ, Sotozono CJ, et al. Growth factor mRNA and protein in preserved human amniotic membrane. persistent epithelial defects remain England College of Optometry. Curr Eye Res. 2000;20(3):173-7. 31. Young AL, Cheng ACO, Ng HK, et al. The use of autologous challenging entities for even the most 1. Ljublimov AV, Saghiizadeh M. Progress in corneal wound serum tears in persistent corneal epithelial defects. Eye (Lond). seasoned clinician, and patience healing. Prog Retin Eye Res. 2015;49:17-45. 2004;18(6):609-14. 2. Choi JA, Jin HN, Jung S, et al. Effects of amniotic membrane 32. Tsubota K, Goto E, Shimmura S, Shimazaki J. Treatment of is a key virtue. Clinicians must be suspension in human corneal wound healing in vitro. Mole Vis. persistent corneal epithelial defect by autologous serum appli- 2009;15:2230-38. cation. Ophthalmology. 1999;106(10):1984-9. vigilant with follow up and see the 3. Jeng BH. Treating the nonhealing epithelial defect. CRST 33. Lee YK, Lin YC, Tsai SH, et al. Therapeutic outcomes of patient daily or every other day until Europe. 2011 Sept:25-8. combined autologous serum eye drops with silicone-hydrogel 4. McCulley JP, Horowitz B, Husseini ZM. Topical fibronectin soft contact lenses in the treatment of corneal persistent resolution, and the timeline depends therapy of persistent corneal epithelial defects. Fibronectin epithelial defects: a preliminary study. Cont Lens Anterior Eye. Study Group. Trans Am Ophthalmol Soc. 1993;91:367-86. 2016;39(6):425-30. on the obstinacy of the disease 5. Wirostoko B, Rafii MJ, Sullivan DA, et al. Novel therapy to 34. Choi JA, Chung SH. Combined application of autologous treat corneal epithelial defects: A hypothesis with growth hor- serum eye drops and silicone hydrogel lenses for the treat- and the effectiveness of the treat- mone. The Ocular Surface. 2015:13(3):204-12. ment of persistent epithelial defects. Eye Contact Lens. ment. Some defects may respond 6. Katzman LR, Jeng BH. Management strategies for per- 2011;37(6):370-3. sistent epithelial defects of the cornea. Saudi J Opthalmol. 35. Wang WY, Lee YK, Tsai SH, et al. Autologous serum eye fairly quickly (i.e., one to two days 2014;28(3):168-72. drops combined with silicone hydrogen lenses for the treatment 7. Jeng BH, Dupps WJ. Autologous serum 50% eyedrops in of postinfectious corneal persistent epithelial defects. Eye Con- with overnight scleral lens wear) the treatment of persistent corneal epithelial defects. Cornea. tact Lens. 2017;43(4):225-9. or may be more prolonged over 2009;28(10):1104-8. 36. Shahriari HA, Tokhmehchi F, Reza M, Hashemi NF. Com- 8. Austin A, Lietman T, Rose-Nussbaumer J. Update parison of the effect of amniotic membrane suspension and several weeks. Once healed, clini- on management of infectious keratitis. Ophthalmology. autologous serum on alkaline corneal epithelial wound healing 2017;124(11):1678-89. in the rabbit model. Cornea. 2008;27(10):1148-50. cians should ensure patients have 9. Fraunfelder FW. Corneal toxicity from topical ocular and sys- 37. Chappelet MA, Bernheim D, Chiquet C, Aptel F. Effect of a sufficient lubrication and manage temic medications. Cornea. 2006;25(10):1133-8. new matrix therapy agent in persistent epithelial defects after 10. Raizman M, Hamrah P, Holland EJ, et al. Drug-induced cor- bacterial keratitis treated with topical fortified antibiotics. Cor- medicamentosa to reduce the likeli- neal epithelial changes. Surv Ophthalmol. 2017;62(3):286-301. nea. 2017;36(9):1061-8.

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0038_ro0118_f2.indd38_ro0118_f2.indd 4242 11/5/18/5/18 4:314:31 PMPM Earn up to NEW TECHNOLOGIES 2018 28 CE & TREATMENTS IN Credits Eye Care (COPE Approval pending) OPTOMETRIC CORNEA, CATARACT REVIEW OF OPTOMETRY® EDUCATIONAL MEETINGS OF CLINICAL EXCELLENCE AND REFRACTIVE SOCIETY SAN DIEGO APRIL 26-29, 2018

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Leading Faculty: San Diego Marriott Del Mar Paul M. Karpecki, OD, FAAO David Friess, OD, FAAO 11966 El Camino Real Review Program Chair President, OCCRS San Diego, California 92130 Phone: 858-523-1700 Three Ways to Register A limited number of rooms have been reserved at $165 per night. Online: www.reviewofoptometry.com/sandiego2018 Please make reservations with the hotel Call: 866-658-1772 • E-mail: [email protected] directly at 858-523-1700. For group rate, mention “New Technologies and Convenient opportunities to register for one or both meetings.* Treatments in Eye Care”.

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*Additional CE fees if attending both meetings. Agenda subject to change. Review of Optometry® partners with Salus University for those See website for details: www.reviewofoptometry.com/SanDiego2018 ODs who are licensed in states that require university credit Graft Management

AN OD’S GUIDE TO Corneal Transplant OPTIONS Optometrists can play a significant role in preparing patients for these procedures and safeguarding against complications. By Mitch Ibach, OD, and Scott Hauswirth, OD

o preserve patients’ vision and ocular health, primary eye care providers need to stand confidently alongside Tophthalmologists to assist in post- operative management. With respect to corneal pathology, restoring vision can now be achieved, in some cases, by applying corneal transplants using less risky, more predictable procedures. As transplant procedures become safer and more precise, more are performed both in the United States and worldwide.1 According to the Eye Bank Association of America, 79,304 keratoplasties were performed in 2015, an increase of 3.75% from 2014.1 As optometrists managing corneal dis- ease, our job is to be well-versed in cornea transplant options, educate the patient, make the appropriate referrals and actively DSEK with gas/air bubble posterior to the iris causing pupillary block. participate in patients’ postoperative care. The term corneal transplant is no longer synonymous Penetrating Keratoplasty with full-thickness penetrating keratoplasty (PKP). It is A traditional PKP involves the removal of all cornea now divided into subcategories with different tissue lay- layers, which essentially leaves the globe open for a ers. This family of procedures includes traditional PKP, period of time (called an “open sky” procedure) until deep anterior lamellar keratoplasty (DALK), Descemet’s the donor tissue can be secured. Next, the donor graft stripping endothelial keratoplasty (DSEK/DSAEK), Des- is attached using four interrupted cardinal sutures, cemet’s membrane endothelial keratoplasty (DMEK) and secured sequentially 180 degrees from one another, pre-Descemet’s endothelial keratoplasty (PDEK). ensuring proper tension on the graft to minimize This article reviews these options, what patients need induced astigmatism. Next, either more interrupted to know and the optometrist’s role in comanagement. sutures are placed in the primary clock hours or, in

44 REVIEW OF OPTOMETRY JANUARY 15, 2018

044_ro0118_f3_Ibach v2.indd 44 1/8/18 6:33 PM This postoperative patient demonstrates full-thickness penetrating keratoplasty graft with a running suture in place.

some cases, a long, single running suture is placed in a circumferential fashion to assist in securing the donor tissue to the host. Some surgeons prefer place- ment of a combination of interrupted and running sutures. The advent of femtosecond laser technology has made a significant impact on the world of anterior segment surgery—from the creation of LASIK flaps to employment in cataract surgery for precutting the capsulorhexis and “prechopping” the lens prior to phacoemulsification. During corneal transplants, a femtosecond laser may also be used in place of the corneal trephine to create the initial incisions into The most advanced the host cornea, as well as cutting of the donor but- ton. The graft-host junction may be manipulated and ® customized to a specific architecture, theoretically Phoroptor ever built. providing a more secure interface with greater sur- face area. Phoroptor® VRx Digital Refraction System In a procedure as invasive as a full-thickness PKP, suprachoroidal hemorrhage is an intraoperative Incredibly fast. Ultra-quiet. Endless connectivity. risk. The incidence of this complication ranges from Made in the USA with premium components. 0.1% to 1.08%.2 If the eye is not closed quickly, total prolapse of the contents of the eye may occur, resulting in complete vision loss.2 Postoperative PKP Watch the video at reichert.com/vrx risks include retinal detachment, endophthalmitis, glaucoma, cataract, ocular surface disease, infectious keratitis, graft dehiscence, graft failure and graft rejection.3

© 2017 AMETEK, Inc. & Reichert, Inc. (12-2017) · Made in USA

Phoroptor is a registered trademark of Reichert, Inc. · www.reichert.com ·

044_ro0118_f3_Ibach v2.indd 45 1/8/18 6:34 PM Graft Management

tophobia, pain and blurred vision.5 The clinical signs of a graft rejec- tion include decreased acuity, conjunctival hyperemia, corneal edema, subepithelial infiltrates and keratic precipitates, often in a pathognomonic pattern called a Khodadoust line.5 Risk of graft rejection is increased with corneal neovascularization, and researchers have tested drugs to help minimize the vascular ingrowth. One study shows com- plete regression of deep stromal vessels in 16 patients using Avastin (bevacizumab, Genentech), partial regression in six and improved As opposed to the pristine DMEK patient (at right), you can see this detached DMEK is visual acuity in five.6 Researchers rolled up in the patient’s anterior chamber. have looked into in various delivery methods for Avastin, including topi- PKP Postoperative Care cal, subconjunctival and intrastromal injections.6 Following the procedure, medications include topical immunosuppression, antibiotic coverage and lubrica- Lamellar Keratoplasties tion in support of the ocular surface. Common corti- The goal of all posterior lamellar keratoplasties is to costeroids following PKP include prednisolone acetate remove the diseased endothelial pump cells while leav- 1% and Durezol (difluprednate, Novartis). Typically, ing unaffected layers intact. Healthy endothelial cells these medications are maintained for several months are critical for stromal deturgescence and corneal clar- to years following surgery to modulate the recipient’s ity. These transplants offer improved quality of vision immune response to graft tissue. These topical drugs and ocular health to patients with endothelial diseases may be supplemented by systemic immunomodula- such as Fuchs’ dystrophy and pseudophakic bullous tory agents such as CellCept (mycophenolate mofetil, keratopathy.7 These transplants also offer the advan- Genentech) in patients at high risk for graft rejection.4 tage of keeping more native anatomy in place, decreas- A typical graft appearance on day one will show ing the antigenic burden of foreign donor tissue. moderate graft edema throughout the donor tissue In DSEK, the surgeon removes the host Descemet’s and the margins of the host rim. In the first few weeks membrane and endothelium before inserting a donor following the procedure, control, tissue integrity main- graft of posterior stroma, Descemet’s and endothelium. tenance and ocular surface recovery are the focus. The incision—through which the graft is inserted—is Patients may also have a wide variety of pain from per- larger and is closed by the surgeon with one dissolvable sistent foreign body sensation to more intense aching, suture. Finally, soreness and photophobia. Generally, these symptoms an air or sulfur improve over the first few days. Persistent or increasing hexafluoride

inflammation over the first few days, especially in asso- (SF6) gas bubble ciation with anterior chamber reaction or presence of is inserted into hypopyon, may indicate infection. the anterior As the new cornea stabilizes over the first two to four chamber and weeks, vision will gradually improve. You may encoun- the patient ter issues such as high or irregular astigmatism. In eyes is positioned that do not show improvement of edema and vision, with their nose monitor for signs of primary graft failure.5 pointed to the Endothelial rejection is a leading cause of graft ceiling, capital- This is how a pristine post-DMEK patient failure.5 Symptoms of this will include redness, pho- izing on gravity should appear.

46 REVIEW OF OPTOMETRY JANUARY 15, 2018

044_ro0118_f3_Ibach v2.indd 46 1/8/18 6:36 PM All-new!

This photo shows a one-day postoperative DSEK patient with bubble in place.

to tamponade the graft into place. Topical steroids are used to maintain graft clarity and prevent rejection episodes. Steroids dosed four times per day in the early postoperative period is common, then tapering down over one year. Postoperative complications can be segmented into two stages: early (one to 28 days postoperatively) and late (28 days and later). In the early stage, adverse events include problems with graft adhesion and iatrogenic pupillary block secondary to the anterior chamber. We typically instruct patients to maintain a supine position as often as possible after the pro- cedure to maximize the tamponade effect of the air bubble on the graft position. An inferior peripheral iridotomy (PI) is placed in Pixel-perfect endothelial keratoplasties (EK), but if the bubble is blocking the PI, the iridotomy is non-patent or the acuity testing. bubble moves posterior to the iris causing chamber shallowing, iatrogenic pupillary block with a sky-high ClearChart® 4 · 4X · 4P Digital Acuity Systems intraocular pressure (IOP), headache and nausea/ vomiting can ensue. Simple-to-use interface. 24-inch, LED backlit display. Symptoms of pupillary block are similar to acute Custom developed for acuity testing. Made in USA. angle-closure glaucoma and include headache, nau- sea, blurred vision and halos.8 You can initiate a simple intervention when these patients first call the See the full line at reichert.com/clearchart office by having the patient sit up, a position that will cause the air bubble to rise. If in 20 minutes to 30 minutes the patient experiences no relief, they must be seen. During an office visit, a corneal surgeon will

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ClearChart is a registered trademark of Reichert, Inc. · www.reichert.com ·

044_ro0118_f3_Ibach v2.indd 47 1/8/18 6:37 PM Graft Management

induced astigmatism coupled with a thin- ner graft offers faster recovery and better potential visual acuity in DSEK patients when compared with PKP.9-11 If a rejection episode does occur, treat aggressively with strong topical steroids such as Durezol (difluprednate, Novartis) or Pred Forte (prednisolone acetate, Aller- gan) dosed up to every hour as first-line treatment. Comparing Techniques Research suggests DSAEK does better than PKP when it comes to risk for rejection.12 A five-year survival study of DSAEK vs. PKP in a large cohort of Asian eyes with Khodadoust line and corneal graft rejection as seen in a PKP patient. Fuchs’ dystrophy and bullous keratopathy shows statistically significant differences in manipulate the bubble with a partial removal through graft survival, endothelial cell loss, graft rejection and the corneal wound or paracentesis (similar to “burp- wound dehiscence.12 Another study shows that out- ing” a wound). Once the bubble diffuses out of the comes were stronger for patients who had a failed PKP anterior chamber (approximately four to seven days and underwent a second full-thickness keratoplasty after the procedure) EK grafts should attach to the than for patients whose doctors replaced only the dis- host tissue. In instances when they don’t, the surgeon eased posterior layers of the failed transplant.13 may opt to place a second air bubble at the slit lamp DMEK is an even thinner transplant for patients with subsequent patient positioning. In rare cases, the with endothelial disease. In DMEK, the surgeon surgeon may need to refloat the graft in the operating removes the patients Descemet’s membrane and endo- room or consider a graft exchange if graft attachment thelium and inserts a donor button of Descemet’s is unlikely through in-office manipulations. Once the membrane and endothelium. Similar to DSEK, one problem has been resolved, the patient needs to be dissolvable suture is placed and an air or sulfur hexa- monitored carefully until the gas bubble has dissolved fluoride gas bubble is used for graft tamponade. Again, and they are no longer at risk. in DMEK a postoperative steroid is used to maintain In all these procedures, it is critical to monitor IOP transplant health, tapering over one year without stop- at each visit because the patient will be on steroid ping. In our clinic, the steroid is tapered over one year therapy for an extended period. If IOP increases in the before stopping with the same guidelines for graft rejec- short term, use a topical IOP agent such as Combigan tion episodes occurs. (brimonidine/timolol, Allergan) or Simbrinza (brinzol- The visual acuity achieved with DMEK is generally amide/brimonidine, Novartis) to decrease ciliary body superior to DSAEK.7,11,14 This may be due in part to production while the steroid is tapered. Cosopt (dorzol- DMEK’s use of a thinner graft with more native cor- amide/timolol, Akorn) is also an option. neal anatomy, less induced hyperopia and less induced higher-order aberrations.7,11,14 Dealing With Rejection A disadvantage of DMEK, however, is graft disloca- Late-stage complications and management involve tions. The literature documents higher graft re-bubble restoring visual acuity and preventing graft rejection rates compared with DSEK.7 Researchers suspect better or failure. In comparison with PKP, DSEK offers fewer graft adhesion in DSEK is due to additional stromal tis- corneal sutures and more native anterior corneal tissue, sue from the graft.7 resulting in less total astigmatism.9 Generally, the thin- Lastly, PDEK involves Dua’s layer. This graft is similar ner the transplant tissue and the more host anatomy to DMEK with an additional 10µm to 15µm anterior to left in place results in better acuity and less risk of graft Descemet’s membrane. This new approach is not widely rejection.9,10 A review of DSEK found astigmatic shift performed or studied thus far. but the hope is this varia- post-DSEK to be near neutral at 0.11D.9 Clinically, less tion provides the benefits of both DMEK and DSEK.15

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Corneal transplant surgery has undergone several changes throughout the years and continues to evolve alongside innovations in technology. The movement towards lamellar grafts and replacing only the dis- eased tissue instead of the entire cornea has been ben- eficial for graft survival, as well as recovery times and improved visual outcomes for patients. As primary eye care providers with increasing patient demands, it is imperative that we comanage corneal transplanta- tion when necessary and can make appropriate refer- rals for our patients to achieve optimal outcomes. ■ Dr. Ibach specializes in advanced anterior seg- ment surgery care and pathology at Vance Thompson Vision in Sioux Falls, SD. He is a fellow of the Ameri- can Academy of Optometry and a member of the American Optometric Association. He has a consulting agreement with Alcon. Dr. Hauswirth is a practicing optometrist at Min- nesota Eye Consultants and an adjunct clinical faculty at Southern California College of Optometry. He is an active industry consultant and speaker. Relevant disclosures: Alcon, Allergan, Bausch+Lomb, BioTissue, Shire, Sun and TearScience.

1. Eye Bank Association of America. 2015 Eye Banking Statistical Report. Washington, DC; Eye Bank Association of America;2015. 2. Price F, Whitson W, Ahad K, Tavakkoli H. Suprachoroidal hemorrhage in penetrating keratoplasty. Ophthalmic Surg. 1994 Aug;25(8):521-5. 3. Greenlee EC, Kwon YH. Graft failure: III. Glaucoma escalation after penetrating kerato- plasty. Int Ophthalmol. 2008 Jun;28(3):191-207. 4. Szaflik JP, Major J, Izdebska J, et al. Systemic immunosuppression with mycophenolate mofetil to prevent corneal graft rejection after high-risk penetrating keratoplasty: a 2-year follow-up study. Graefes Arch Clin Exp Ophthalmol. 2016 Feb;254(2):307-14. 5. Szczotka-Flynn L. Examining corneal transplant patients. Contact Lens Spectrum. www. clspectrum.com/issues/2007/december-2007/the-contact-lens-exam. December 1, 2007. Accessed October 20, 2017. 6. Sarah B, Ibtissam H, Mohammed B, et al. Intrastromal injection of bevacizumab in the management of corneal neovascularization: about 25 eyes. J Ophthalmol. 2016;2016:6084270. Epub 2016 Aug 17. 7. Tourtas T, Laaser K, Bachmann B, et al. Descemet membrane endothelial keratoplasty versus descemet stripping automated endothelial keratoplasty. American Journal of Oph- thalmology. 2012;153(6):1082-90. 8. Allingham R, Damji K, Freedman S, et al. Shields Textbook of Glaucoma 6th ed. Phila- Elements of pre-test. delphia: Lippincott, 2011. 9. Lee B, Jacobs D, Musch D, et al. Descemet’s stripping endothelial keratoplasty: safety and outcomes. Ophthalmology. 2009;116(9):1818-30. 10. Anshu A, Price M, Price F. Risk of corneal transplant rejection significantly reduced OptoChek™ Plus with Descemet’s membrane endothelial keratoplasty. Ophthalmology. 2012;119:536-40. Auto Refractor + Keratometer 11. Deng S, Lee B, Hammersmith K, et al. Descemet membrane endothelial keratoplasty: Safety and Outcomes. Ophthalmology. 2017;S0161-6420(17)32521-6. LensChek™ Plus & Pro Digital Lensometers 12. Ang M, Soh Y, Htoon HM, Mehta JA, et al. Five-year graft survival comparing Descemet stripping automated keratoplasty and penetrating keratoplasty. Ophthalmology. 2016 Aug;123(8):1646-52. Reichert® combines technology, simplicity, 13. Keane MC, Galettis RA, Mills RA, Coster DJ, et al. A comparison of endothelial and and value at the core of your exam. penetrating keratoplasty outcomes following failed penetrating keratoplasty: a registry study. Br J Ophthalmol. 2016 Nov;100(11):1569-75. 14. Hamzaoglu E, Straiko M, Mayko Z, et al. The first 100 eyes of standardized Descemet stripping automated endothelial keratoplasty versus standardized Descemet membrane Learn more at reichert.com/exam endothelial keratoplasty. Ophthalmology. 2015;122:2193-9. 15. Agarwal A, Jacob S. Pre-Descemet’s endothelial keratoplasty combines advan- tages of DSAEK, DMEK. Ocular Surgery News. www.healio.com/ophthalmology/ cornea-external-disease/news/print/ocular-surgery-news/%7Bba1c7a80-94ae-4fe3- b043-b634ecc755ac%7D/pre-descemets-endothelial-keratoplasty-combines-advan- tages-of-dsaek-dmek. July 10, 2014. Accessed October 20, 2017.

© 2017 AMETEK, Inc. & Reichert, Inc. (12-2017)

www.reichert.com ·

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Intruder Alert: Diagnosing Corneal Infiltrative Disease The age-old question, “is this sterile or infectious?” may be an oversimplification. This review will help you find the underlying cause of your patient’s issue. By Suzanne Sherman, OD, and Fiza Shuja, OD

onquering corneal infiltrates is something clinicians have attempted to do for decades. CDespite continued research and elevated clinical acumen, if you were to put 20 clinicians in front of 20 slit lamps and ask them to properly distinguish between sterile and infectious corneal infiltrates (whether bacterial, viral, fungal or protozoan), you would hear many differing opinions. Fig. 1. These subepithelial infiltrates are a hallmark sign of EKC. Perhaps that is because the ques- tion itself is inherently flawed—an fies infection and infiltrates do not. contact lens wear or even corneal infiltrative process accompanies Instead, optometrists must rely surgery. A firm grasp of corneal every infection. Likewise, a loss on patient history, symptoms and mechanics is a first important step of stromal substance in corneal clinical presentation when deter- toward understanding how an infil- ulceration is often (but not always) mining the type of corneal infiltrate. trate occurs. accompanied by an infectious pro- Once we know what we are dealing The cornea, devoid of blood cess. Some infections (e.g., fungal or with, only then can we choose the or lymph vessels, relies on cel- protozoan keratitis) have an intact proper treatment and management lular and molecular properties epithelium even though an infec- regimen. Here is a look at the pro- within it and the surrounding tis- tious process is at play. Therefore, cesses that lead to infiltrates and sue.1 Corneal epithelial cells are both infiltrates and ulcers can be how to distinguish the various types an important asset in activating either sterile or infectious. While it you will encounter in your practice. the immune response. As the first is true that diffuse infiltrates with line of defense, corneal epithelial little to no epithelial involvement How it All Begins cells identify an invading patho- are commonly sterile, clinicians Corneal infiltrates represent an gen or other corneal insult and need to avoid over-reliance on the immune response to corneal insult, release cytokines and chemokines rule of thumb that ulceration signi- whether from a microbial antigen, to begin the immune defense. In

50 REVIEW OF OPTOMETRY JANUARY 15, 2018

050_ro0118_f4.indd 50 1/5/18 3:59 PM addition to epithelial cells, a vari- Table 1. Sterile Infiltrates vs. Infectious Infiltrates4 ety of other players are also key in the corneal defense mechanism, Sterile Infectious (MK) including keratocytes, interferons, • Smaller lesion (<1mm) • Larger lesion (>1mm) neutrophils, natural killer cells and • More peripheral • More central • Minimal epithelial damage (defect size • Significant epithelial defect (size of macrophages.2 The active immune compared with underlying infiltrate) staining defect closely mirrors size of response involves immune cells • No mucous discharge underlying stromal lesion) arriving to repair the corneal dam- • Less pain and photophobia • Mucopurulent discharge age, eventually leading to the aggre- • Little or no anterior chamber reaction • Pain and photophobia gation of white blood cells in the • No lid involvement • Anterior chamber reaction cornea—known as an infiltrate.3 • Lid edema, tear film debris, hypopyon Although every infection has an infiltrative process, not every history questions that can help nar- between EKC and a herpes simplex infiltrate is infectious. One of the row the diagnosis include whether virus (HSV) infection. important distinguishing factors they feel fatigued and if they had an • HSV and HZO keratitis. These between sterile and infectious infil- upper respiratory infection recently. are the most commonly known trates is the status of the epithelium. • EKC. This often presents viral keratitis infections other than With an intact epithelium, more bilaterally, and patients sometimes EKC. Patient history questions per- often the infiltrates are sterile; with have a history of respiratory tract taining to previous infections such an infectious etiology, a defect is infections. Around one week to 10 as chicken pox, inordinate stress or usually present (Table 1).4 The most days after inoculation, patients may recent sun exposure are helpful to important information needed to develop follicular conjunctivitis, identify this etiology. diagnose infiltrative events arises petechial hemorrhages, prominent HSV comes in various forms that through patient history and presen- preauricular adenopathy, occasion- can affect different layers of the

tation (Table 2). ally pseudo- or true membranes Photos: Aaron Bronner, OD and, often, associated punctate Infections: keratitis. These patients commonly The Usual Suspects complain of tearing, light sensitiv- Although patient history and ity, pain and foreign body sensa- presentation will provide a better tion. Seven to 14 days after their understanding of the initial antigen initial eye symptoms, patients may causing the infiltrate, it is best to develop multifocal subepithelial proceed with caution in diagnosis (anterior stromal) corneal infiltrates and treatment. (Figure 1). These become quite Because it is difficult to clearly apparent on slit lamp examination Fig. 2. Above, this infiltrate, known as a differentiate between a benign, self- and can range from a few to many.6 Wessely ring, was caused by a bacterial limiting corneal insult and an infec- The punctate erosions (keratitis) source. Below, the migrating stromal tious event, clinicians should first arise due to adenovirus replica- white blood cells, seen as an area of treat all infiltrative events as infec- tion within the corneal epithelium, granularity on the edge of retro beam, tious in nature.5 Any number of dif- whereas the infiltrates are due to an are a response to the infiltrate above. ferent infectious etiologies may be immunopathologic response to a at play, and knowing what you are viral infection of keratocytes in the looking at is crucial. Let’s review superficial corneal stroma. Patients the most common infectious causes who complain of photophobia and of corneal infiltrates. decreased vision as a result of the • Viral subepithelial infiltrates. SEIs often have symptoms that Adenoviruses—including epidemic persist for months after the initial keratoconjunctivitis (EKC), herpes presentation.6 simplex virus (HSV) and herpes In the case of EKC, laboratory zoster (HZO)—can have significant testing is rarely indicated. However, corneal involvement. Some patient a viral culture may differentiate

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cornea, ranging from epithe- HZO may present with epithelial lial, neurotrophic, necrotiz- keratitis comprised of small, non- ing stromal and endotheliitis. ulcerated pseudodendrites without Epithelial keratitis can pres- terminal bulbs.7 ent with blepharoconjunctivi- • Bacterial keratitis. This can tis—macropunctate epithelial involve a suppurative corneal infil- lesions that progress to trate with an overlying epithelial dendritic ulceration with defect after a bacterial corneal terminal end bulbs.7 Anterior insult (Figure 2). The ocular flora is stromal haze can develop home to both Staphylococcus and “ghost dendrites” below the Streptococcus, the most common epithelial lesions. HSV can agents found in opportunistic infec- also have a non-necrotizing tions due to ocular surface trauma and necrotizing stromal (e.g., corneal abrasion, surgery, keratitis. This appears differ- severe ocular surface disease). In ently than a small infiltrate, contact lens wearers, however, bac- as there is a central disc of terial keratitis is most often due to stromal or epithelial edema, Pseudomonas.9,10 Although contact keratic precipitates and endo- lens infiltrates are usually thought thelial folds. Associated signs to be “sterile,” on culture they can also include anterior uveitis, be either sterile or infectious; thus, decreased corneal sensation infiltrates in a patient who wears Fig. 3. Severe meibomian gland dysfunction with and elevated intraocular contact lenses should be treated as telangiectatic vessels. pressure.8 infectious until proven otherwise.9

Table 2. Clinical Characterization of Corneal Infiltrative Events with Soft Contact Lens Wear11 Classification Categories Signs and Symptoms Serious and Microbial keratitis • Infection of the cornea with excavation of corneal epithelium, Bowman’s layer symptomatic and stroma with infiltration and necrosis of tissue. • Focal infiltrates usually larger (>1mm) and irregular with small satellite lesions and significant diffuse infiltration. • Severe limbal and bulbar redness. • Rapid onset of moderate to severe pain, decreased visual acuity, mucopurulent or purulent discharge, tearing, photophobia and puffiness of lids. Clinically significant Contact lens-induced acute • Small multiple focal infiltrates and diffuse infiltration in the mid-periphery to and symptomatic red eye (CLARE) periphery of the cornea. • Moderate to severe circumferential redness. • Moderate pain, tearing and photophobia soon after waking. Contact lens peripheral ulcer • In active stage: focal excavation of the epithelium, infiltration and necrosis of (CLPU) the anterior stroma. • Small (up to 2mm), single, circular focal infiltrates. • Limbal and bulbar redness. • Severe to moderate pain, foreign body sensation. • Could be asymptomatic. Infiltrative keratitis • Anterior stromal infiltration, with or without epithelial involvement, in the mid- periphery to periphery of the cornea. • Small infiltrates, possibly multiple. • Mild to moderate irritation, redness and occasional discharge. Clinically non- Asymptomatic infiltrative • Infiltration of the cornea without patient symptoms. significant and keratitis • Small focal infiltrates (up to .4mm). asymptomatic • Could be associated with punctate staining. • Could have mild to moderate limbal and bulbar redness. Asymptomatic infiltrates • Infiltrates in the cornea without other patient signs or symptoms.

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050_ro0118_f4.indd 52 1/5/18 3:58 PM Bacteria often reside in contact virulence of the fungal lens cases, patient’s hands, eye- organism, which results lids and in tap water; basically in a decrease in resis- any entity that comes in contact tance to the infection.13 with the lenses can cause a bacte- • Protozoan infec- rial infection.11 The antigens are tions. The parasitic infec- trapped between the contact lens tion we hear most about and cornea, remaining on the cor- in eye care is Acantham- nea longer due to slow epithelial oeba. Diagnostic delay is cell renewal.12 The benefit with common because of the rigid gas permeable (GP) lenses is nonspecific presentation. the increase in tear exchange vs. Presenting symptoms are soft lenses, which have 10 to 20 often severe ocular pain times higher incidence of infiltrative and photophobia. In the events.10,12 GPs are also consider- early stages, a localized ably more deposit resistant, reduc- infection may appear in ing a key predisposing factor for a mildly symptomatic infection. patient with diffuse Asking contact lens patients punctate epitheliopathy about wear time and lens hygiene or dendritic epithelial are important points in the his- lesion. A gray-white tory, as these two are commonly superficial infiltrate may associated with bacterial infections occur in the central cor- from contact lens wear.12 Extended nea. This infection can contact lens wear carries a 43% progress into a partial or risk of bacterial keratitis.12 Hypoxia Figs. 4 and 5. Central corneal infiltrates from contact complete ring infiltrate. because of overnight wear, extended lens wear. It is important to ques- wear or hypersensitivity to lens tion these patients if they material triggers the inflammatory It represents around 5% to 10% have worn their contact lenses in a response, leading to the formation of corneal infections in the United pool, hot tub or fresh water source. of an infiltrate. The infiltrate is States. The leading cause of fungal A diagnosis can be made by using irregular with surrounding corneal keratitis is trauma to the cornea a stained smear or by culturing edema, and is usually described with plant or vegetable material; organisms from the corneal scrap- as greater than 1mm, with the however, contact lenses are another ing. Most cases are diagnosed by possibility of adjacent satellite risk factor. Clinicians should ask clinical presentation or confocal lesions.11,12 A deep corneal defect patients about their recent activities microscopy.13 extending from the epithelial layer outdoors in addition to their con- into the stroma with necrotic tissue tact lens habits.13 Non-infectious Infiltrates is also present. The infiltrate is usu- These infections usually present If you have ruled out an infectious ally located in the central or para- with fewer symptoms than bacte- etiology, be on the lookout for central cornea. rial keratitis, but a deep stromal several sterile infiltrative events: With a Pseudomonas infection gray-white dry infiltrate with a You should begin by examining the in particular, a large central defect feathery margin may be present. If company the infiltrate keeps—lid can be present.9 Symptoms often the infiltrate is extremely deep, it is margin disease and blepharitis are include severe pain, severe redness, possible to have multifocal or satel- often found in conjunction with photophobia, hypopyon, marked lite infiltrates, endothelial hypopyon non-infectious infiltrates. anterior chamber reaction, muco- or both. It is very important to dis- • Marginal corneal infiltrates. purulent discharge and decreased tinguish this type of infiltrate from These are caused by non-infectious visual acuity. other forms, as topical corticoste- conditions. Although the complete • Fungal keratitis. This is less roids are a significant risk factor. pathological process of these infil- common than bacterial keratitis. They can activate and increase the trates is still not fully understood,

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RO0917_House VEW.indd 1 8/17/17 1:51 PM Infiltrates

cally. Research has yet to determine if the lymphocytic cells arise from Do you wear contact lenses? donor keratocytes or the donor epi- thelial cells. These infiltrates can be accompanied by an anterior cham- ber reaction. If infiltrates are seen in Ye s No a post-corneal transplant patient, it is important to rule out subepithe- lial rejection.10 • Contact lens-induced infiltra- tive events. Infiltrative events can also be specifically associated with Sterile Bacterial Marginal Viral contact lens use (Figures 4 and 5). A lens wearer’s habits will help clini- cians better understand the possible Fig. 6. While this grid is a simplification for categorization of an infiltrative event, it cause of an infiltrative event. Proper functions as a good starting point in identifying the infiltrative cause. follow-up questions include: Which type of lens? How often? For how researchers do know that Staphy- minal capillary loops, causing a many hours? Are you practicing lococcus grows on the eyelids and variety of immune responses in the appropriate lens hygiene? Do you spills bacterial byproducts onto the corneal periphery.15 If the infiltrates sleep in them? Do you change them corneal surface, beginning a hyper- are due to chronic Staphylococcal regularly? What solution do you sensitivity reaction thought to lead lid disease, superficial blood vessels use? Do you swim in them? With to infiltrates.14 may occur across the clear interval the appropriate questions during The introduction of an antigen between the limbus and the infil- patient history, a diagnosis, such onto the cornea surface will cause a trates (Figure 3).15 They more com- as Acanthamoeba, should begin to release of inflammatory mediators monly appear individually, but can form (Figure 6). to the peripheral cornea, leading to appear in groups or bilaterally.16 • Contact lens-induced periph- vasodilation. The corneal limbus is Infiltrates may be non-staining or eral ulcer (CLPU) is a sudden cor- very important in immune-mediated have early overlying staining, and neal inflammatory response after corneal disorders because it has are usually present where the eyelid contact lens wear that presents with antigen-presenting cells (APCs), margin intersects the corneal sur- moderate-severe limbal and bulbar such as Langerhan cells, that face (i.e., at the 2 to 10 o’clock and redness (Figures 7 and 8).5 A small express major histocompatibility 4 to 8 o’clock areas).15 circular subepithelial infiltrate is complex class II antigens, which Slit lamp exam may also reveal often present in the periphery or are capable of efficient mobiliza- mild quadrant-specific conjunctival mid-periphery as well (0.1mm to tion and induction of B- and T-cell hyperemia, little or no chemosis, 1.2mm in diameter).5 There is an responses. This is why immune- trace or mild ocular irritation and associated epithelial defect with mediated corneal changes occur at normal vision. These infiltrates are surrounding infiltrates. Presenting peripheral locations adjacent to the self-limiting and usually disappear symptoms can include moderate- limbus.15 within one to two weeks.15 to-severe pain, foreign body sensa- These sterile corneal infiltrates Clinicians should always be tion and irritation, or patients may are often small, gray-white circum- on the lookout for masquerad- present asymptomatically.11 CLPU limbal lesions separated from the ers as well. Krachmer’s spots, is self-limiting and will resolve after limbus by a 1mm clear space. The for example, are a type of sterile discontinuing contact lens wear. location of these infiltrates is due infiltrate that can be mistaken for There can be recurrences with con- to the APCs that are capable of either marginal or viral subepithe- tact lens wear; however, proper lens mobilization of the T-cell response. lial infiltrates.17 These are a sign of hygiene is stressed to prevent fur- In addition, the posterior limbus is subepithelial corneal graft rejection ther inflammation. vascularized, circulating immune after penetrating keratoplasty, and • Contact lens-induced acute red cells and complexes near the ter- patients may present asymptomati- eye (CLARE) also an inflammatory

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reaction of the cornea, often occurs • Infiltrative keratitis. This occur with asymptomatic patients, after sleeping with lenses overnight. condition is an inflammatory reac- where smaller infiltrates, 0.4mm in Patients will present with pain tion with infiltrates occurring in diameter, are present in the corneal upon awakening, photophobia and the anterior stroma. An epithelial periphery.11 Punctate staining may tearing.11 Multiple focal infiltrates defect can be present, but is not be present with mild redness, which of 1mm in diameter or less can be a certainty. Infiltrates are located differentiates this from asymptom- present in the mid-periphery or in the corneal mid-periphery or atic infiltrates. As opposed to CLPU periphery of the cornea.13 There is periphery and are smaller in size, and CLARE, this occurs during minimal staining and no epithelial usually less than 1mm in diam- the day and the focal infiltrates are defect present on examination.18 eter.18 Patients may present with irregular. Resolution typically occurs quickly symptoms of irritation and red- after lens removal. ness.11 Infiltrative keratitis can also Differentiation is Key Classifying infiltrates as sterile or infectious is a challenging task, and differentiating their underlying eti- ologies can be complicated due to the multiple potential causes and their often-overlapping signs and symptoms. Patient presentation and a thorough case history will provide crucial information needed to narrowing down the diagnosis. Figs. 7 and 8. Contact lens-induced peripheral corneal infiltrates. Once the most likely etiology of

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2018_seco_HalfPage.indd050_ro0118_f4.indd 56 1 1/5/18 3:553:57 PM the infiltrate has been determined, She received her undergraduate 7. Krachmer JH, Mannis MJ, Holland EJ. Cornea. St, Louis, MO: Mosby/Elsevier; 2011. appropriate treatment can be degree from SUNY at Stony Brook 8. Rapuano C. Corneal infections, inflammations, and surface disorders. In: Color Atlas and Synopsis of Clinical Ophthal- undertaken. With infectious etiolo- and her optometry degree from mology. Wills Eye Institute. Philadelphia: Wolters Kluwer; gies in particular, the case should Pennsylvania College of Optometry 2012:188. 9. Cohen EJ. Management of small corneal infiltrates in con- be approached with the most up- at Salus University. She completed tact lens wearers. Arch Opthalmol. 2000;118:276-277. to-date protocols for treatment or her residency at the Northport Vet- 10. Bourcier T, Thomas F, Borderie V, et al. Bacterial keratitis: predisposing factors, clinical and microbiological review of the appropriate consultation or eran Affairs Medical Center. 300 cases. British J Ophthalmol. 2003;87:834-8. referral. ■ 11. Sweeney DF, Jalbert I, Covey M, et al. Clinical character- 1. Kumar A, Yu F-SX. Toll-like receptors and corneal innate ization of corneal infiltrative events observed with soft contact Dr. Sherman is an instructor in immunity. Current Molecular Medicine. 2006;6(3):327-37. lens wear. Cornea. 2003;22(5):435-42. Optometric Science (in Ophthal- 2. Akpek EK, Gottsch JD. Immune defense at the ocular sur- 12. Carnt N, Samarawickrama C, White A, Stapleton F. The diagnosis and management of contact lens-related microbial mology) at Columbia University face. Eye. 2003;17:949-56. 3. Bazan NG, Bazan HP. Ocular responses to inflammation keratitis. Clin Exp Optom. 2017;100:482-93. Medical Center. She received her and the triggering of wound healing: lipid mediators, proto- 13. The American Academy of Ophthalmology. Infectious oncogenes, gene expression, and neuromodulation. In: Bazan diseases of the external eye: microbial and parasitic infec- undergraduate degree from the Uni- tions. In: External Disease and Cornea (Basic and Clinical NG, ed. Lipid Mediators in Eye Inflammation. Braquet P, ed. Science Course). American Academy of Ophthalmology; versity of Michigan and graduated New Trends in Lipid Mediators Research, 5th ed. Basel: 2016-2017:152-7. Karger; 1990:168-80. from SUNY College of Optometry. 14. Mondino BJ. Inflammatory disease of the peripheral cor- 4. Stein RM, Clinch TE, Cohen EJ, et al. Infected vs. sterile nea. Ophthalmology. 1988;95(4):463-72. She completed her optometric resi- corneal infiltrates in contact lens wearers. AM J Ophthalmol. 15. The American Academy of Ophthalmology. Immune- dency in ocular disease and primary 1988;105(6):632-6. related disorders of the external eye. In: External Disease and 5. Holden BA, Reddy MK, Sankaridurg PR, et al. Contact lens- Cornea (Basic and Clinical Science Course). American Acad- care at Bronx Lebanon Hospital induced peripheral ulcers with extended wear of disposable emy of Ophthalmology; 2016-2017:195. Center. She specializes in complex hydrogel lenses: Histopathologic observations on the nature 16. Donshik PC. Editorial: Peripheral corneal infiltrates and and type of corneal infiltrate. Cornea. 1999;18(5):538-43. contact lens wear. CLAO J. 1998;24:3:134-6. and medically necessary contact 6. The American Academy of Ophthalmology. Infectious 17. Panda A, Vanathi M, Kumar A, Priya S. Corneal graft rejec- lens fittings and ocular disease. diseases of the external eye: basic concepts and viral infec- tion. Surv Ophthalmol. 2007;52(4):375-95. tions. In: External Disease and Cornea (Basic and Clinical 18. Efron N, Morgan PB. Can subtypes of contact lens-asso- Dr. Shuja is an optometrist at Science Course). American Academy of Ophthalmology; ciated corneal infiltrative events be clinically differentiated? New York-Presbyterian Hospital. 2016-2017:113-7. Cornea. 2006;25:540-4.

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POSITIVE VISUAL PHENOMENA: ETIOLOGIES BEYOND THE EYE Prepare to investigate the many non-ocular events that cause patients to see flashes or bright lights. By Sara Weidmayer, OD

e are all familiar Photo: George T. Banyas, OD MAWH or even other benign causes. with positive visual It is critical that we carefully differ- phenomena and entiate the source of these symptoms, photopsias. They are as positive visual phenomena may Wgenerally an entopic concern: visual indicate serious—even life-threaten- perceptions produced from inside ing—systemic health concerns. the eye, from vitreous traction on A key feature to differentiate the the retina, for example.1,2 However, source of a flash is laterality; a uni- other positive visual phenomena rep- lateral flash generally corresponds resent false visual images—the brain Migraine aura often includes a to an ocular etiology, whereas bilat- perceives them without correspond- scintillating, or fortification, scotoma. eral flashes are more likely at, or ing visual stimuli. Often, the central scotoma is bordered by posterior to, the chiasm.2 Because When a patient reports any sort of a crescent of shimmering zigzags. clinicians are already well-versed in bright light or flash in their vision, ocular sources of flashes, this article our first thought is often vitreous such symptoms to a migraine aura discusses them only briefly, focusing detachment, retinal break or retinal without headache (MAWH). How- instead on less common—but higher detachment. During a normal dilated ever, the etiology of positive visual risk—etiologies of positive visual eye exam, it is easy to attribute phenomena is often not intraocular, phenomena.

Release Date: January 2018 Faculty/Editorial Board: Sara Weidmayer, OD Expiration Date: January 15, 2021 Credit Statement: This course is COPE approved for 2 hours of CE Goal Statement: Often, clinicians assume a patient’s complaint of credit. Course ID is 55956-SD. Check with your local state licensing bright lights or flashes in vision are associated with vitreous detach- board to see if this counts toward your CE requirement for relicen- ment, retinal break or retinal detachment. However, it is critical that sure. ODs carefully differentiate the source of these symptoms, as positive Disclosure Statements: visual phenomena may indicate serious—even life-threatening— Authors: The author has no relationships to disclose. systemic health concerns. This article discusses how to identify less Editorial staff: Jack Persico, Rebecca Hepp, William Kekevian and common—but higher risk—etiologies of positive visual phenomena. Michael Iannucci all have no relationships to disclose.

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058_ro0118_f5_OSC.indd 58 1/5/18 2:30 PM OPTOMETRIC STUDY CENTER Photos: Ellen Marie Petrilla and Gina G. Wong, OD

This 36-year-old patient was complaining of constant periorbital headaches on the right side, accompanied by ptosis and miotic pupil. Four weeks earlier, she developed a temporal scintillating scotoma in her right eye that lasted 15 to 30 minutes, followed by an acute, painful headache on the right side. Sagittal MRI (left) shows an internal carotid artery dissection in the wall of the petrous and cavernous sinus segments. Coronal MRI (right) shows significant narrowing of the carotid lumen in the cavernous sinus and supraclinoid segments of the right internal carotid artery. The patient was diagnosed with a post-ganglionic right Horner’s syndrome with concurrent headache and scintillating scotomas.

Ocular Sources such as progressive outer retinal conditions such as transient ischemic Many flashes can be attributed to necrosis, acute zonal occult outer attack (TIA) or cerebrovascular acci- retinal pathology, such as posterior retinopathy, retinitis pigmentosa, dent (CVA, stroke) and should be vitreous detachment, any vitreoreti- degenerative retinopathies or other evaluated for such immediately. nal traction or a retinal break. Any issues that lead to photoreceptor Flashes or streaks of light can mechanical stimulation—such as tug- death or dysfunction may produce a occur due to the positioning of an ging or compression—of the photo- photopsia.1 Unlike many other ocu- intraocular lens—known as pseudo- receptors can trigger an entopic flash lar sources of flashes, these diseases phakic dysphotopsia.5 These often in vision.1 In these cases, the flashes most frequently affect both eyes, present as arcs of light in the supe- are often accompanied by floaters, though they can be unilateral or rior temporal periphery and can be such a Weiss ring, red blood cells or asymmetric. quite bothersome to patients, but are pigmented cells within the vitreous Retinal vasospasm causes a focal otherwise benign. (“Shafer’s sign”) and associated fun- narrowing of the retinal arteriolar dus evaluation findings. Compres- lumen, effectively limiting blood Non-ocular Etiologies sion from mass effect within or onto flow and possibly producing a visual Generally, non-ocular causes of posi- the globe may occur from a variety phenomenon in the area of relative tive visual phenomena are binocular of intraocular or orbital sources, ischemia. Although this generally and originate from vascular- or non- ranging from choroidal lesions to would produce a negative visual vascular changes involving the cere- orbital abnormalities such as tumors. phenomenon, in some cases it may bral cortex. A thorough dilated examination be accompanied by flashing lights. Migraine aura. This represents should easily differentiate many Retinal vasospasms are temporary focal neurological symptoms that of these sources of photopsia, and and usually recover within a few are reversible and may be seen in any signs indicating a retro-ocular minutes.3,4 In cases of unrecovered up to about 30% of patients with compressive lesion such as proptosis, vasospasm, an associated visual migraine.6,7 It also accounts for most extraocular muscle motility restric- field defect would be expected, as cases of bilateral positive visual phe- tion or diplopia would warrant fur- would an area of hypoperfusion on nomena.6,8 In migraine sufferers with ther neuroimaging. fluorescein angiography (FA) similar aura symptoms, 90% have visual Photoreceptor dysfunction from to a branch retinal artery occlusion. symptoms.6,8 Visual migraine aura inflammation or infections can also This diagnosis is rare and should be often follows a predictable pattern: it produce flashes in vision. Diseases one of exclusion from more serious precedes or accompanies a headache

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Table 1. Features Typically Associated with MAWH, TIA, CVA and Seizure

History Visual Symptoms Onset Duration Neuroimaging/Ancillary Studies

MAWH History of migraine Predominantly positive, Gradual Five to 60 minutes Normal dynamic TIA Vasculopathic risks Predominantly Acute Less than five minutes, Likely ischemic cerebrovascular negative, static typically; up to 24 hours disease, no infarct CVA Vasculopathic risks Predominantly Acute Less than five minutes Area of cerebral infarct negative, static Seizure History of seizure or epilepsy, Predominantly positive, Acute Transient EEG most useful head trauma, vasculopathic risks dynamic

and may also present with symptoms but can be ipsilateral.8 While many a TIA/stroke workup.7 Addition- typical of migraine, such as nausea, variations exist, a key component is ally, any aura that is less than five photophobia and phonophobia, the scintillating scotoma’s dynamic, minutes or longer than an hour sometimes with focal weakness, traveling presentation. should be further evaluated for other numbness or paresthesia, dizziness Typically, after visual aura comes causes.7,16 or dysphasia.6,7,9 While migraine a speech aura in about one-fourth Of note, migraine is an indepen- with typical aura is a straightforward of patients, followed by a sensory dent risk factor for ischemic stroke, clinical diagnosis, aura symptoms in aura in about one-third of patients. or migrainous infarction.7,10,12 How- the absence of headache is more dif- While this order of aura is typical, it ever, transient visual symptoms, ficult to discriminate from more seri- may vary in about 30% of patients. similar to those of MAWH, are not ous etiologies such as TIA. Migraine Motor involvement describes hemi- uncommon—even later in life—and aura is rarely a stand-alone migraine plegic migraine. Progressing through do not appear to be associated with variant; this entity is known, among sequential aura is consistent with the an absolute higher stroke risk.10 other names, as acephalgic migraine, cortical spreading depression from Transient ischemic attack. TIA optical migraine, migraine accom- brief cortical hyperexcitability, which symptoms result from local ischemia, paniments, migraine equivalents or is thought to cause MAWH and may usually due to thrombotic or embolic typical MAWH.6,10 be helpful in diagnosing MAWH.13-15 vascular disease, but the TIA itself Migraine aura normally starts In cases where patients present does not result in acute or permanent gradually with a generally binocular, with visual symptoms similar to a infarction.11,17 TIA affects about five typical scintillating scotoma that migraine aura, especially with any million people per year in the United subsequently intensifies over the associated neurological deficits and States.17 Ischemic stroke, on the course of five minutes to one hour, particularly in older patients or other hand, indicates cerebral or cen- though 15% to 30% may extend those with cardiovascular risk fac- tral nervous system infarction and beyond one hour.6,7,11 Many patients tors but no history of migraine or may either share similar symptoms describe its onset as a small central similar previous episodes of migraine with TIA or may happen without flashing light expanding radially to or aura, clinicians must conduct a symptoms.17 include an enlarging area of visual careful case history to rule out TIA, The clinical symptoms of TIA are field; it is often arcuate, or in many CVA, seizure, inflammatory cerebro- generally brief (a few seconds to a cases forms a shimmering or flicker- vascular disease and vertebrobasilar few minutes), and by definition there ing jagged circular pattern, often insufficiency—all of which can cause must be no infarct of the central ner- called teichopsia, or described as positive visual phenomena.6,10 vous system.7 Common symptoms a fortification spectrum.6,12 It usu- The current criteria for diagnosing include numbness, weakness, tingling ally also includes areas of negative MAWH require at least two episodes or paralysis of one side of the face visual features such as scotomas or of aura. Therefore, any inaugural or body; transient monocular vision hemianopia, a heat wave sensation episode should first be treated as a loss (amaurosis fugax); aphasia and visual blur.6,7,10 When the aura is TIA, as stroke risk is highest within or dysphasia; and dizziness.18 The associated with migraine, it is most two days of TIA—not to mention visual symptoms are predominantly often contralateral to the headache, other causes are often uncovered in negative, present in corresponding

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0058_ro0118_f5_OSC.indd58_ro0118_f5_OSC.indd 6600 11/5/18/5/18 2:302:30 PMPM hemianopic fields if the affected area There is no standard for cardiac for seizure to present with visual is chiasmal or post-chiasmal, tend to evaluation in TIA patients, but the symptoms alone.13,22 Subtle seizures be abrupt and at maximum within heart can be the underlying cause of in epilepsy may present with ocu- a couple minutes of onset and are TIA and accounts for 14% to 30% lomotor signs such as nystagmus, stationary, as opposed to the gradual of ischemic CVA; for example, atrial abnormal repetitive blinking or eye- and dynamic visual symptoms with fibrillation and recent myocardial lid flutter and tonic alignment devia- migraine aura.1,12,13 Though positive infarction can lead to thromboem- tions.13 visual phenomena are less common, boli, and valve stenosis can lead to Visual symptoms associated with they can occur within an area of sco- calcific emboli.21 Electrocardiograpy seizure are quite diverse; they may toma.12,13,19 As with non-visual symp- (ECG/EKG), cardiac event monitor- appear as flashes, patterns or colors toms, visual manifestations usually ing and echocardiography may be in the vision. Patterns can change last less than five minutes, but may assessed if the initial evaluation did and may look similar to a fortifica- last up to 24 hours. not uncover a source of the TIA tion pattern. Complex visual hal- Patients who have experienced symptoms; however, few patients lucinations, including perception of TIA symptoms should immediately with either no history of heart dis- animals or people, may occur, as can undergo neuroimaging to evaluate ease or with normal ECG will have a image enlargement (macropsia) or for CVA, preferably MRI with diffu- cardioembolic source for TIA.17 reduction (micropsia), to name a few. sion-weighted imaging (DWI), within Seizures. These have a number of The visual phenomena may be 24 hours of when the symptoms causes, including developmental mal- stationary, traveling, localized or began, if possible; however, acute formations, ischemia or infarction, encompassing the entire visual field. infarcts may initially appear normal compressive lesions or trauma; they Negative visual symptoms such as on MRI because tissue injury has may also be idiopathic.13 scotomas, ranging from focal to not yet become radiologically signifi- While epilepsy, or recurrent sei- hemifield to complete visual loss, cant, and some deep brain infarcts zures, usually presents with obvi- may also occur, though negative cannot be well visualized with MRI ous seizure manifestations, seizure symptoms are less frequent than imaging. Regardless, MRI is more without convulsions are possible.13 positive visual symptoms.13,22 sensitive than CT for identifying isch- In addition to motor, sensory and Focal occipital seizure most emic areas, and DWI-MRI studies cognitive symptoms, seizure may be frequently causes these visual phe- are even more precise than standard associated with nausea, headache nomena, particularly the positive MRI or CT.17 Positive DWI signals and both positive and negative visual symptoms. Visual symptoms with imply higher risk of subsequent isch- symptoms; however, it is uncommon seizure tend to be brief, lasting only a

emic events. If MRI is unavailable Photos: Michael Trottini, OD, and Michael DelGiodice, OD or contraindicated, clinicians should order a CT.17 An assessment of the intracranial arteries is often done concomitantly (with MR or CT angi- ography).20 Neuroimaging is impor- tant to identify or rule out a vascular (hypoperfusion, acute infarction, or large-vessel stenosis) or non-vascular (e.g., mass, abscess) origin of the TIA symptom.17 Clinicians should also evaluate the carotid arteries via noninvasive testing, such as Doppler ultrasound, as carotid stenosis is common in This patient presented emergently with a complaint of three isolated instances of patients with atherothrombotic TIA “blue-colored shadows” that transiently and incompletely blocked the vision of the or CVA. Basic TIA/CVA lab tests right eye for five minutes at a time. At left, her MRA revealed severe stenosis of the include complete blood count (CBC), right internal carotid artery (ICA), and she was diagnosed with amaurosis fugax and blood chemistry panel and a basic right hemispheric subacute CVA secondary to severe right ICA stenosis. At right, coagulation assessment (prothrombin imaging also showed two restricted diffusion foci located within the right posterior time, partial thromboplastin time).17 parietal-occipital junction, consistent with a subacute infarct.

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few seconds, and may recur through- LSD, marijuana, mescaline, digoxin have acquired vision loss for any out the day.13 If seizure is suspected, or other drug use.12,23 In these cases, number of reasons, whereby the electroencephalogram (EEG) may the hallucination may be quite com- visual cortex produces the perception help detect an epileptic wave of plex and may have accompanying of these hallucinations, thought to be activity, though it may be difficult auditory or other sensory hallucina- due to chronic lack of sensory input to detect in cases where only a small tions.12 (deafferentation).24 Visual hallucina- area of cortex is involved.6,22 Charles Bonnet syndrome, also tions in Charles Bonnet syndrome Other visual hallucinations. known as visual release phenom- are not accompanied by any other Visual hallucinations may occur as a enon, may also produce simple or sensory hallucinations.23 result of psychiatric disorders; alco- complex visual hallucinations. This Positive visual phenomena, often a hol intoxication or withdrawal; and condition is seen in patients who flickering sensation, may also occur

Case Report A 70-year-old white male presented to the clinic with complaints of Given that the patient was experiencing a visual phenomenon rainbows and lights in his vision. It had started about one week prior, with both positive and negative features and visual hallucinations, and he described rainbows and shadows moving across the walls along with subacute confusion, he was escorted to our hospital’s intermittently; he reported that he could see the rainbows and lights emergency department and was worked up for stroke. with either eye covered; he also reported that he saw some formed He was diagnosed with a left occipital lobe (left posterior cerebral images, which he perceived as animals, but he recognized that other artery territory) subacute infarct with restricted diffusion extending people could not see what he was seeing. He hadn’t noticed any into the left temporo-occipital region, and ultimately was admitted peripheral vision deficits. (Figure 1). Days after admission, the patient began to notice visual When questioned, he said he had a headache a couple days prior loss in the bottom right portion of his vision, and the neurologist to the onset of the visual symptoms, and his ex-wife had recently noted that the patient had developed a right homonymous inferior asked if he had developed some speech problems, but he himself quadrantanopia. Neurology initially thought his positive visual phe- hadn’t noticed any changes. He denied tingling, weakness or numb- nomena represented either simple focal seizures or were a result of ness on either side of his face or body. the infarct itself. During the exam, it became quite apparent that the patient was An EEG indicated left hemispeheric slowing and moderate confused and forgetful, and he exhibited some labile emotional encephalopathy but no epileptiform discharges or seizures. His visual responses (such as spontaneously starting to cry when asked ques- hallucinations and positive visual phenomena persisted even beyond tions). The patient’s ocular health exam was largely unremarkable. discharge; they varied from seconds to 30 minutes and presented from every hour to five to six Fig. 1. These axial T2/FLAIR, left, times per day and predomi- and DWI, below, MRI images show nantly presented in the inferior hyperintensity in the left occipital right quadrant of his vision, lobe extending to the left temporo- where he’d developed the visual occipital region, consistent with field defect; at subsequent the patient’s left posterior cerebral follow up, neurology felt his artery territory acute/subacute visual hallucinations were most infarct. consistent with visual release phenomenon. As evidenced by this patient, some cases of posi- tive visual phenomenon can be quite complex. This patient’s positive visual phenomenon was the first stroke symptom, and, as his eye care provider, I was well- positioned to take a thorough history and ensure he was appropriately referred.

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058_ro0118_f5_OSC.indd 62 1/5/18 2:30 PM due to systemic hypo- or hypergly- The Evolution of Migraine Headache/Aura and CBS Hallucination cemia, or orthostatic hypotension.25 Image: Michael N. Block, OD Researchers have reported formed Migraine CBS and unformed visual hallucinations, particularly in hyperglycemia, which Deafferentation Glial Depolarization may precede or accompany other and Denervation systemic symptoms of hypeglycemia such as change in mentation.26 These visual phenomena should subside with the normalization of systemic glucose or blood pressure. Neuronal Aura Hyperexcitability Differentiating TIA, MAWH and Seizure Visual symptoms are quite similar for seizure, MAWH, TIA and CVA. Altered Receptive Field and Migraines are frequently associated Cortical Depression with epilepsy, as they share similar Spontaneous Discharge clinical features and pathophysi- Migrane Headache ologic components; migraine and CBS and Scotoma epilepsy may be concomitant, and Hallucination the incidence of migraine in patients with epilepsy is about twice that of vasculopathic risk factors for cere- eye exam. Clinicians often need to the general population.13,27 Because brovascular disease such as diabetes order ancillary studies and consult positive visual phenomena from sei- and hypertension. with other disciplines to arrive at zure are brief and rarely stand-alone, In addition, MAWH presents with the appropriate diagnosis, or to rule any additional seizure-like symptoms bright, glistening, dynamic visual out pertinent differentials before would warrant an evaluation by aura that gradually progresses, while attributing a more benign diagnosis neurology. TIA generally shows a largely nega- of exclusion to a patient’s symptoms. No specific features uniformly tive visual phenomenon with a flat, Understanding the many potential differentiate TIA from migrainous static, non-progressive presenta- underlying etiologies and other typi- visual phenomena, and neurologi- tion that is maximum at onset. On cal features of these conditions can cal work up is generally normal for neuroimaging, MAWH often has help guide clinicians to the appropri- both.7 Differentiating the two, normal results; TIA must not show ate diagnosis and subsequent man- however, is crucial, since TIA carries infarction, but often shows evidence agement. ■ a 10% to 15% risk of subsequent of cerebrovascular ischemia, such Dr. Weidmayer is staff at the VA stroke within three months, with as chronic small-vessel changes, and Ann Arbor Healthcare System in half of those occurring within two additional vascular testing would Ann Arbor, Mich., and a clinical days.7,17 The long-term risk of stroke likely show atherosclerosis.6 assistant professor at the Kellogg Eye and major cardiac events such as In cases of positive visual phe- Center, Department of Ophthalmol- myocardial infarction also increases; nomenon or aura that are inaugural ogy and Visual Sciences at the Uni- thus, misdiagnosing a TIA as a in patients older than 40, if visual versity of Michigan. migrainous aura could have seri- symptoms are purely negative or if 1. Brown GC, Brown MM, Fischer DH. Photopsias: a key to diagnosis. ous—potentially life threatening— the duration of aura is atypical for Ophthalmol. 2015;122:2084-94. implications.7,17 MAWH, the episode must be treated 2. Murtha T, Stasheff SF. Visual dysfunction in retinal and optic nerve disease. Neurol Clin N Am. 2003;21:445-81. While no universal differentia- as TIA until proven otherwise, and 3. Bernard GA, Bennett JL. Vasospastic amaurosis fugax. Arch Ophthal- tors exist, some frequent differences clinicians must promptly initiate a mol. 1999;117(11):1568-9. 4. Ota I, Kuroshima K, Nagaoka T. Fundus video of retinal migraine. between MAWH and TIA can help full TIA evaluation.16 JAMA Ophthalmol. 2013;131(11):1481-2. 5. Schwiegerling J. Recent developments in pseudophakic dysphotopsia. (Table 1). First, history is important; Curr Opin Ophthalmol. 2006;17(1):27-30. often, patients with MAWH have Positive visual phenomena may 6. He Y, Li Y, Nie Z. Typical aura without headache: a case report and review of the literature. J Medical Case Reports. 2015;9:40. had a history of migraine earlier in occur for a number of reasons not 7. Fogang Y, Naeije G, Ligot N. Transient neurologic deficits: can life. Patients with TIA usually have easily detectable on a comprehensive transient ischemic attacks be discriminated from migraine aura without

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headache? J Stroke and Cerebrovascular Diseases. 2015;25(5);1047-51. In: Fernández-de-las-Peñas C, Chaitow L, Schoenen J, eds. Multidis- 20. Lavallée PC, Babrejo L, Labreuche J, et al. Spectrum of transient 8. Goadsby PJ. Migraine, aura and cortical spreading depression: why ciplinary Management of Migraine. Burlington, MA: Jones and Bartlett visual symptoms in a transient ischemic attack cohort. Stroke. are we still talking about it? Ann Neurol. 2001;49(1):4-6. Learning; 2013:11-4. 2013;44:3312-7. 9. Schankin CJ, Goadsby PJ. Visual snow—persistent positive visual 15. Ghadiri MK, Kozian M, Ghaffarian N, et al. Sequential changes in 21. Arboix A, Alió J. Cardioembolic stroke: clinical features, specific phenomenon distinct from migraine aura. Curr Pain Headache Rep. neuronal activity in single neocortical neurons after spreading depres- cardiac disorders and prognosis. Curr Cardiol Rev. 2010;6:150-61. 2015;19:23. sion. Cephalagia. 2011;32(2):116-24. 22. Siatouni A, Gatzonis S, Alexopoulos A, et al. Simple partial status 10. Wijman CAC, Wolf PA, Kase CS, et al. Migrainous visual accom- 16. Headache Classification Committee of the International Headache epilepticus manifested as homonymous hemianopsia: a rare intracranial paniments are not rare in late life: the Framingham Study. Stroke. Society (IHS). The International Classification of Headache Disorders, recording. Clinics and Practice. 2016;6:840. 1998;29:1539-43. 3rd edition. Cephalagia. 2013;33:629-808. 23. Pang L. Hallucinations experienced by visually impaired: Charles Bonnet Syndrome. Optom Vis Sci. 2016;93(12):1466-78. 11. Dennis M, Warlow C. Migraine aura without headache: transient 17. AHA/ASA Scientific Statement. Definition and evaluation of transient 24. Ffytche DH. Visual hallucinations in eye disease. Curr Opin Neurol. ischaemic attack or not? J Neurol, Neurosurgery and Psychiatry. ischemic attack. Stroke. 2009;40:2276-93. 2009;22(1):28-35. 1992;55:437-40. 18. American Stroke Association. Warning Signs. www.strokeassocia- 25. Fletcher P, Pereira A. Visual hallucination of coloured numbers sec- 12. Liu GT, Schatz NJ, Galetta SL, et al. Persistent positive visual phe- tion.org/strokeorg/warningsigns/stroke-warning-signs-and-symptoms_ ondary to hyperglycaemia. BMJ Case Rep. February 10, 2011. [Epub]. nomena in migraine. Neurology. 1995;45:664-8. UCM_308528_SubHomePage.jsp. Accessed September 1, 2017. 26. Maccari M. Neurological dysfunction associated with nonketotic 13. Bajwa R, Jay WM, Asconapé J. Neuro-ophthalmologic manifesta- 19. Vaphiades MS, Celesia GG, Brigell MG. Positive spontaneous visual hyperglycemia. Arch Neurolol. 1968;19:525-34. tions of epilepsy. Seminars in Ophthalmol. 2015;21(4):255-61. phenomena limited to the hemianopic field in lesions of central visual 27. Kim DW, Lee SK. Headache and epilepsy. J Epilepsy Res. 14. Russell MB. The differential diagnosis and boundaries of migraine. pathways. Neurol. 1996;47:408-17. 2017;7(1):7-15.

OSC QUIZ

ou can obtain transcript-qual- of exclusion. d. Carotid Doppler ultrasound. ity continuing education credit d. They produce positive more often than Ythrough the Optometric Study negative visual symptoms. 10. Which of the following is not typically Center. Com plete the test form and return associated with seizures? it with the $35 fee to: Jobson Medical 4. Most cases of bilateral positive visual a. Head trauma. Information, Dept.: Optometric CE, 440 9th phenomena are due to: b. Intracranial lesions. Avenue, 14th Floor, New York, NY 10001. a. Migraine aura. c. Intracranial ischemia or infarction. To be eligible, please return the card b. Bilateral retinal detachments. d. Intraocular ischemia or infarction. within one year of publication. c. Seizures. You can also access the test form and d. Strokes. 11. What oculomotor signs may be submit your answers and payment via associated with seizure? credit card at Review of Optometry online, 5. Migraine aura generally lasts how long? a. Nystagmus. www.reviewofoptometry.com/ce. a. Less than five minutes. b. Abnormal repetitive blinking. You must achieve a score of 70 or b. Five to 60 minutes. c. Eyelid flutter. higher to receive credit. Allow eight to 10 c. 60 to 90 minutes. d. All of the above. weeks for processing. For each Optomet ric d. More than 90 minutes. Study Center course you pass, you earn 12. What focal seizures most frequently 2 hours of transcript-quality credit from 6. Most migraine aura symptoms are: cause visual phenomena? Pennsyl vania College of Optometry and a. Auditory. a. Parietal seizures. double credit toward the AOA Optom et ric b. Visual. b. Occipital seizures. Recog nition Award—Cate gory 1. c. Speech related. c. Temporal seizures. Please check with your state licensing d. Motor (hemiplegic migraine). d. Frontal seizures. board to see if this approval counts toward your CE requirement for relicensure. 7. Which of the following episodes similar 13. Which is true of visual hallucinations to migraine aura without headache (MAWH) associated with Charles Bonnet syndrome? 1. Where is the source of entopic should be evaluated as if it were a transient a. They are accompanied by other sensory phenomena? ischemic attack (TIA)? hallucinations. a. Inside the eye. a. The first episode of MAWH. b. They are due to sensory overstimulation b. The orbit. b. Aura lasting less than five minutes. of the visual cortex. c. The chiasm. c. Aura lasting longer than 60 minutes. c. They may be simple or complex d. The occipital cortex. d. All of the above. hallucinations. d. They happen in people with normal vision. 2. Which of the following is the most likely 8. Which symptom is not typically consistent source of bilateral flashes in the vision? with TIA? 14. Which of these systemic issues is not a. Inside the eye. a. Sudden confusion. typically associated with positive visual b. The optic nerves. b. Sudden numbness, tingling or weakness phenomena? c. The orbits. on either side of the face or body. a. Hyperglycemia. d. The chiasm. c. Left arm or chest pain or tightness. b. Orthostatic hypertension. d. Slurring of speech. c. Hypoglycemia. 3. Which of the following is true of retinal d. Orthostatic hypotension. arterial vasospasms? 9. What neuroimaging, when immediately a. They are a common cause of positive available and not contraindicated, is usually 15. After a TIA, what is the approximate risk visual phenomena. preferred in acute TIA or CVA? of subsequent stroke within three months? b. They usually cause permanent focal a. Brain x-ray. a. Less than 5%. retinal arterial flow obstruction. b. Brain MRI. b. 10% to 15%. c. They are uncommon and are a diagnosis c. Brain CT. c. 30% to 40%.

64 REVIEW OF OPTOMETRY JANUARY 15, 2018

0058_ro0118_f5_OSC.indd58_ro0118_f5_OSC.indd 6644 11/5/18/5/18 2:312:31 PMPM OSC QUIZ Examination Answer Sheet Positive Visual Phenomena: Etiologies Beyond the Eye d. More than 50%. Valid for credit through January 15, 2021

16. Of those who have a stroke within Online: This exam can be taken online at www.reviewofoptometry.com/ce. Upon passing the exam, you can three months after a TIA, nearly half of view your results immediately and download a real-time CE certificate. You can also view your test history at those occur within what time frame? any time from the website. a. Two days. Directions: Select one answer for each question in the exam and completely darken the appropriate circle. A minimum score of 70% is required to earn credit. b. One week. c. Two weeks. Mail to: Jobson Medical Information, Dept.: Optometric CE, 440 9th Avenue, 14th Floor, New York, NY 10001. d. Four weeks. Payment: Remit $35 with this exam. Make check payable to Jobson Medical Information LLC. Credit: This course is COPE approved for 2 hours of CE credit. Course ID is 55956-SD. 17. Which presentation of visual Sponsorship: This course is joint-sponsored by the Pennsylvania College of Optometry. phenomena is most common with TIA? Processing: There is an eight- to 10-week processing time for this exam. a. Predominantly positive aura that is dynamic and progresses. Answers to CE exam: Post-activity evaluation questions: b. Predominantly positive aura that is flat 1. A B C D Rate how well the activity supported your achievement of these learning objectives: and static. 2. A B C D 1=Poor, 2=Fair, 3=Neutral, 4=Good, 5=Excellent c. Predominantly negative aura that is 3. A B C D dynamic and progresses. 21. Improve my clinical understanding of positive visual phenomena. 1 2 3 4 5 d. Predominantly negative aura that is flat 4. A B C D 22. Become familiar with the ocular sources of positive 5. A B C D and static. visual phenomena. 1 2 3 4 5 6. A B C D 23. Increase my understanding of non-ocular causes of 7. A B C D 18. Which presentation of visual positive visual phenomena. 1 2 3 4 5 phenomena is most common with MAWH? 8. A B C D 24. Better identify the clinical features of migraine aura, 1 2 3 4 5 a. Predominantly positive aura that is 9. A B C D transient ischemic attack and seizures.

dynamic and progresses. 10. A B C D 25. Increase my clinical ability to differentiate the various source of positive visual phenomena. 1 2 3 4 5 b. Predominantly positive aura that is flat 11. A B C D and static. 26. Improve my ability to order the proper testing to 12. A B C D c. Predominantly negative aura that is confirm the cause of positive visual phenomena. 1 2 3 4 5 13. A B C D dynamic and progresses. Rate the quality of the material provided: 14. A B C D d. Predominantly negative aura that is flat 1=Strongly disagree, 2=Somewhat disagree, 3=Neutral, 4=Somewhat agree, 5=Strongly agree 15. A B C D and static. 27. The content was evidence-based. 1 2 3 4 5 16. A B C D 28. The content was balanced and free of bias. 1 2 3 4 5 19. What neuroimaging results are 17. A B C D 29. The presentation was clear and effective. 1 2 3 4 5 expected with MAWH? 18. A B C D 30. Additional comments on this course: a. Area of hemorrhagic stroke. 19. A B C D b. Area of ischemic stroke. 20. A B C D c. Occipital mass lesion. d. Normal neuroimaging with no acute Please retain a copy for your records. Please print clearly. infarct. First Name 20. What neuroimaging results are Last Name expected with TIA? E-Mail a. Area of hemorrhagic stroke b. Area of ischemic stroke The following is your: Home Address Business Address c. Occipital mass lesion d. Normal neuroimaging with no acute Business Name infarct. Address

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Lesson 115870 RO-OSC-0118

REVIEW OF OPTOMETRY JANUARY 15, 2018 65

0058_ro0118_f5_OSC.indd58_ro0118_f5_OSC.indd 6655 11/5/18/5/18 2:312:31 PMPM Earn up to 20 CE Credits* ANNUAL

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RO0118_House SECO.indd 1 1/3/18 11:13 AM Cornea+Contact Lens Q+A

Heroes and Shields Because VKC occurs mostly in children, swift, aggressive treatment is crucial. Edited by Joseph P. Shovlin, OD Photo: M.S. McMeekin, OD I have an 11-year-old patient direct threat to vision, and that threat Q with refractory severe vernal needs to be eliminated.” keratoconjunctivitis (VKC) and significant corneal staining, mostly in What Next? the left eye. I tried the typical topical Since a weaker steroid has already agents such as low-dose steroids failed in this case, Dr. Bronner rec- and mast-cell stabilizer/antihistamine ommends a high-dose, high-potency drops. There is no shield ulcer yet, but corticosteroid such as Durezol (dif- I’m concerned it might happen. Are luprednate, Novartis). Aggressive VKC requires careful long-term therapy. there any heroic options for this case? dosing is imperative to eliminate the A “VKC is a chronic issue, inflammation. “Though there is a If the patient experiences a flare-up typically lasting several years greater risk of steroid-related side each time the steroid is reduced or with seasonal exacerbation,” says effects with difluprednate compared eliminated, consider steroid-sparing Aaron Bronner, OD, of Pacific with weaker steroids (especially in therapies. “Compounded topical Cataract and Laser Institute. “That the juvenile population), its dosing cyclcosporin A or tacrolimus have means even the most effective duration should be short,” says Dr. been shown to be effective at dimin- treatment regimen possible won’t Bronner, “just long enough to control ishing both signs and symptoms of truly eradicate it, though it will inflammation acutely before transi- VKC. However, keep in mind that burn out eventually.” Also, it most tioning to the longer-term therapy stringent regulations have made it typically occurs in children and with weaker steroids and antihista- more difficult to find pharmacies adolescents, “which raises the stakes mine/mast-cell stabilizers. If a shield to compound ophthalmic agents,” for both permanent sequelae of the ulcer has already formed, the acute says Dr. Bronner, “and there are disease, such a corneal scarring, and steroid therapy should be paired with also expected burdens with cost and treatment, such as steroid-induced an antibiotic.” insurance coverage.” cataract development or increased Next up is what Dr. Bronner calls Additionally, Dr. Bronner notes intraocular pressure.” the long-term goal: keeping exac- that “Restasis (cyclosporine 0.05%, At its root, the condition is an erbations as infrequent and as mild Allergan) is generally too weak to be inflammatory and allergic process, so as possible. To do this, ODs should effective for cases of VKC.” reducing the inflammatory response rapidly taper the steroid and move Xiidra (lifitegrast, Shire) could be is important. However, concerns to a combination of the lowest dose considered as an off-label, adjunc- about inconveniencing the patient or and weakest steroid that maintains tive treatment because “intercellular risk of treatment sequelae can get in control. Mast-cell stabilizers/anti- adhesion molecule-1 has also been the way of this step. histamines should also be added to shown to be upregulated in VKC,” “In this case, the clinician treating this treatment. “While short dos- Dr. Bronner says. the patient has raised concerns with ing of steroids is safe and effective, “Though there are no clinical potential for a shield ulcer, a problem we know that the risk of cataracts reports of Xiidra for maintenance that can cause permanent reduction and ocular hypertension rises with therapy of VKC, it would likely be in vision, should it develop,” says Dr. increased duration and frequency of a safe approach and one with some Bronner. “This risk should trump any steroid use,” says Dr. Bronner. “Ide- scientific rationale; barring success concerns over patient inconvenience ally, these patients will be tapered off with other, more standard therapy, I or treatment sequelae risk. There is of steroids for all periods other than wouldn’t hesitate to try it after coun- potential for the VKC to present a acute flare-ups.” seling the patient appropriately.” ■

REVIEW OF OPTOMETRY JANUARY 15, 2018 69

069_ro0118_CLQA.indd 69 1/5/18 2:33 PM Review of Systems

Streaks of Concern Although uncommon, angioid streaks often have a systemic cause and warrant prompt attention. By Carlo J. Pelino, OD, and Joseph J. Pizzimenti, OD

67-year-old Hispanic female presented with complaints of Along-standing bilateral cen- tral visual field loss. She reported being diagnosed with age-related macular degeneration (AMD) nine years prior and receiving laser retinal treatment in each eye. Her health history was positive for Pag- et’s disease and Type 2 diabetes. Best-corrected visual acuities were 20/200 OD and 20/400 OS, Fig. 1. This patient has angioid streaks that radiate from the optic disc, in addition to both using eccentric viewing. Given macular laser scarring and blot hemes. her health history, we were unsur- prised that dilated funduscopy as bilateral deep red or grayish lines scars, optic nerve head drusen and revealed bilateral angioid streaks, with irregularly serrated edges.1 reticular pigment dystrophy of the moderate nonproliferative diabetic When you see angioid streaks macula may also be found in asso- retinopathy and laser treatment as a clinical sign, it’s time to take a ciation with angioid streaks. In the scars in each eye. No drusen or closer look at the patient’s detailed event of blunt trauma, eyes with other signs of AMD were evident history and review of systems, angioid streaks may be more likely (Figure 1). and conduct a thorough ophthal- to suffer vision loss due to the exist- This clinical picture led us to mic and, in most cases, systemic ing break in Bruch’s membrane.1,2 believe our patient did not have workup to determine the underly- Patients with angioid streaks are AMD; instead, she most likely ing cause. strongly advised to wear polycar- developed choroidal neovascular- bonate eyeglasses to protect against ization (CNV) associated with the Clinical Picture traumatic retinal damage. Because contamination of Bruch’s mem- Angioid streaks intercommunicate eyes with angioid streaks will brane that occurs with angioid in a ring-like pattern around the streaks. She was referred to a low optic disc in approximately 30% of Table 1. Common Systemic vision rehabilitation clinic, where cases and radiate outward from the Conditions Associated with she achieved success using various disc in 70% of cases.1,2 The streaks Angioid Streaks optical and non-optical devices. come to an abrupt end and seldom • Hemochromatosis extend past the equator. Additional • Acromegaly A Streaky Past posterior segment findings in eyes • Diabetes This patient provides a classic with angioid streaks may include • Sickle-cell hemoglobinopathies example of angioid streaks—struc- a peau d’orange or leopard-skin • Pseudoxanthoma elasticum tural defects linked to several spotting that consists of speckled, • Acquired hemolytic anemia systemic conditions, the frequency yellowish mottling of the posterior • Myopia of which increases with age. They pole, most apparent in the temporal • Neurofibromatosis occur at the level of Bruch’s mem- aspect of the macula. • Paget’s disease brane, lying beneath normal retinal Peripapillary chorioretinal atro- • Ehlers–Danlos syndrome blood vessels, and typically present phy, focal peripheral chorioretinal

70 REVIEW OF OPTOMETRY JANUARY 15, 2018

070_ro0118_RoS.indd 70 1/5/18 2:37 PM always be at risk for CNV due to the damage to Bruch’s membrane, they should have eye exams at regu- lar intervals. CNV in the peripapillary and macular regions can occur in a small percentage of patients with angioid streaks, leading to severe vision loss.3 The visual prognosis, if untreated, is poor, and most traditional treatment modalities have failed to limit the devastating Fig. 2. Advanced atrophic AMD may masquerade as angioid streaks. impact on central vision. However, research shows novel treatment syndrome.6 In addition to angioid zygous B-thalassemia major, inter- with anti-VEGF agents may yield streaks, the literature reports other media and minor, and hereditary favorable results.1,4,5 The research- fundus lesions, including optic disc spherocytosis. The frequency of ers also found early treatment and drusen, macular pattern dystrophy, angioid streaks in the hemoglobin- extended follow up were critical to crystalline bodies and midperiph- opathies increases with age, with a therapeutic success.5 To help detect eral “comet-tail” atrophic spots.6 rate of occurrence of approximately CNV early, clinicians should per- Ehlers-Danlos syndrome is a 1.5% in younger patients and 22% form optical coherence tomography disease of collagen resulting from in patients 55 and older.1,8,9 in addition to dilated funduscopy at a deficiency of hydroxylysine. Other systemic conditions that each follow up visit.1 Patients may develop dermatologic, may be associated with angioid musculoskeletal, cardiovascular, streaks include acromegaly, dwarf- Systemic Involvement gastrointestinal and respiratory ism, diabetes mellitus, idiopathic While angioid streaks should raise signs and symptoms. Ocular com- thrombocytopenia purpura and suspicion of a serious underlying sys- plications include epicanthal folds, acquired homolytic anemia. temic condition, the patient’s whole keratoconus, high myopia, retinal Researchers have also reported clinical picture will help you uncover breaks and detachment, ectopia len- cases of angioid streaks in patients the exact etiology (Table 1). tis, blue sclera and angioid streaks.1 with lead poisoning.1,9 Pseudoxanthoma elasticum Paget’s disease, our patient’s After an extensive workup (PXE) is an inherited connective diagnosis, is a chronic, progressive with negative findings for com- tissue disorder. It affects elastin condition whose key clinical feature mon systemic associations, some fibrils in the skin’s dermis layer, and is bone deformity. It appears as yellow papules known may become evident as “chicken skin.” PXE may cause as an enlargement of changes in arterial walls, the heart, the skull, deafness and gastrointestinal tract and Bruch’s malformation of long membrane, causing mineralization bones. Angioid streaks and deposition of phosphorus. Car- and optic atrophy are diovascular findings in PXE may the main ocular mani- include hypertension due to athero- festations.7 sclerosis, coronary artery disease, Hemoglobin- peripheral vascular disease and opathies occasionally mitral incompetence. Neurological associated with angi- findings may include cerebrovascu- oid streaks include lar accident, intracranial aneurysms homozygous sickle cell and cerebral ischemia.5 disease, sickle cell trait, Of patients with PXE, 85% sickle cell thalassemia, develop ocular involvement, sickle cell hemoglobin, Fig. 3. CNV and subretinal hemorrhage in an eye with referred to as Grönblad–Strandberg hemoglobin H, homo- past trauma.

REVIEW OF OPTOMETRY JANUARY 15, 2018 71

070_ro0118_RoS.indd 71 1/5/18 2:37 PM Earn up to EW TECHNOLOGIES N2018 19 CE & TREATMENTS IN Credits* Eye Care

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Fig. 4. Traumatic choroidal rupture may also injure Bruch’s membrane, leading to CNV.

patients may be diagnosed with idiopathic angioid streaks. Masqueraders Clinicians should always be on the lookout for condi- tions that can mimic angioid streaks. Among the most common are exudative and advanced atrophic AMD, choroidal rupture, toxoplasmosis, choroidal sclerosis, myopic lacquer cracks, histoplasmosis, retinal vascu- t
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1. Abusamak M, Abdelal OM, Kharouf I, Hamdan SM. Improving differential diagnosis of angi- t
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MFOTFT oid streaks: diagnostic considerations and a case study. Retinal Physician. November 1, 2011. www.retinalphysician.com/issues/2011/nov-dec/improving-differential-diagnosis-of-angioid- streak. Accessed December 5, 2017. 2. Gass JDM. Stereoscopic Atlas of Macular Diseases: Diagnosis and Treatment. Vol. l, 4th ed. St. Louis, MO; Mosby; 1997:120. 3. Schiano-Lomoriello D, Parravano MC, Chiaravalloti A, Varano M. Choroidal neovasculariza- tion in angioid streaks and pseudoxanthoma elasticum: 1 year follow-up. Eur J Ophthalmol. 877-220-9710 2009;19(1):151-3. 4. Wiegand TW, Rogers AH, McCabe F, et al. Intravitreal bevacizumab (Avastin) treatment of choroidal neovascularization in patients with angioid streaks. Br J Ophthalmol. 2009 Jan;93(1):47-51. 5. Bahloul M, Chraïbi F, Aounzou S, et al. Treatment of choroidal noevascularization secondary to angioid streaks with bevacizumab and response: Experience of the ophthalmology depart- ment of Hassan II university hospital. J Fr Ophtalmol. 2017;40(9):731-7. 6. Connor PJ, Jr, Juergens JL, Perry HO, et al. Pseudoxanthoma elasticum and angioid streaks. A review of 106 cases. Am J Med. 1961;30:537-43. 7. Dabbs TR, Skjodt K. Prevalence of angioid streaks and other ocular complications of Paget’s disease of bone. Br J Ophthalmol. 1990;74(10):579-82. 8. Condon PI, Serjeant GR. Ocular findings of elderly cases of homozygous sickle-cell disease in Jamaica. Br J Ophthalmol. 1976;60(5):361-4. 9. Paton D. Angioid streaks and sickle cell anemia. Arch Ophthalmol. 1959;62(5):852-8.

070_ro0118_RoS.indd 73 1/5/18 2:37 PM Retina Quiz

Leak Investigation A recent cataract surgery patient showed some unusual findings in a postoperative exam, but is it related to the procedure? By Mark T. Dunbar, OD

72-year-old Hispanic Take the Retina Quiz female presented to 1. What do the yellow Aour office for her changes in the macula rep- postoperative eye exam. She resent? had undergone an uncom- a. Drusen. plicated cataract surgery b. Lipofuscin. along with intraocular lens c. Hard exudate. (IOL) implantation four d. Calcium. weeks earlier in her left eye. The right eye had prior 2. How would you charac- cataract extraction approxi- terize the spectral-domain mately eight weeks earlier. OCT? She was extremely happy a. Localized ischemia. with her visual outcome and b. Intraretinal neovascular- had stopped using her drops. ization. c. Macular thickening with Evaluation Posterior pole image of the left eye of our patient. How do intraretinal fluid. On exam, her best-corrected you explain these finding in a patient who recently had d. Macular thickening with visual acuity was 20/20 OD, cataract surgery? subretinal fluid. 20/30 OS. Confrontation fields were full-to-careful finger moderate-sized cups with good rim 3. Based on the clinical appear- counting in both eyes. The pupils coloration and perfusion in both ance, what is the overall diagnosis? were equally round and reactive to eyes. The right eye was completely a. Coats’ disease. light. There was no afferent pupil- normal. Upon exam, the left eye b. Macular telangiectasis. lary defect. showed changes. c. Branch retinal vein occlusion. Anterior segment examination Optical coherence tomography d. Irvine-Gass Cystoid macular was significant for posterior cham- (OCT) and optical coherence edema. ber IOL implants that were well tomography angiography (OCT-A) centered and clear visual axes. images were also obtained and are 4. How should this patient be Dilated fundus exam showed available for review. managed?

SD-OCT images through the macula of the 72-year-old patient’s left eye.

74 REVIEW OF OPTOMETRY JANUARY 15, 2018

074_ro0118_RQ.indd 74 1/5/18 2:38 PM a. Focal laser treatment to the macula. b. Intravitreal kenalog. c. Intravitreal anti-VEGF injection. d. Observation.

For answers, see page 82. Discussion The yellow precipitates in the macula represent hard exudate. On clinical exam, it was evident that the macula was thickened and there was edema. The spectral domain optical coherence tomog- raphy (SD-OCT) confirmed retinal thickening as well as intraretinal fluid and mild cystoid macular edema. The 3D thickness map highlights this nicely, where the red area represents a localized area of retinal thickening. These OCT-A scans show our patient’s macula in great detail. Diagnosis Decisions So, what is going on with our usual presentation of BRVO is a It is impossible to know the true patient? Are these changes related triangular or wedge-shaped area of effect of the patient’s hyperten- to her cataract surgery? The hemorrhage that extends beyond sive status on her vision because OCT-A provides some valuable the site of where the artery crosses approximately half of all patients insight as to the cause. Microvas- the vein. Our patient doesn’t have with RVOs have hypertension. cular changes are clearly visible on that. This could be because it is Regardless, it is important that the the OCT-A scan as well as some almost resolved and we are see- hypertension be controlled. collateral vessel formation around ing her in the resolution phase, or the superior portion of the foveal because it was a very mild retinal Management avascular zone. vein occlusion to begin with. Anti-VEGF therapy has emerged Based on these findings, we As the hemorrhage from the as the standard of care in treating can surmise that our patient has occlusion resolves, there are still macular edema associated with a small branch retinal vein occlu- some leaking and incompetent reti- retinal vein occlusions. Lucentis sion (BRVO). Another clue to nal vessels that are releasing exu- (ranibizumab, Genentech), Avastin this etiology is the presence of the date that extends into the macula, (bevacizumab, Genentech) and anomalous vessel superior to the resulting in macular edema. One Eylea (aflibercept, Regeneron) are disc that can be seen in the color thing is for certain: it’s not related all potential treatment options for fundus photo. It looks like it may to her cataract surgery. our patient. be a dilated collateral vessel. Per- There is a strong association Even though our patient has haps this is the location where the between hypertension and the mild macular edema and this con- occlusion occurred. development of retinal vein occlu- dition could resolve on its own, we It’s difficult to know for how sion. Our patient does, in fact, referred her to the retinal specialist long she has had the occlusion or have hypertension, but it is well for consideration of treatment. ■

where she is in the course of the controlled with Norvasc (amlo- 1. Interim Guidelines for Management of Retinal Vein Occlu- disease. It was not present two dipine, Pfizer) and hydrochloro- sion; Royal College of Ophthalmologists (December 2010). www.rcophth.ac.uk/wp-content/uploads/2015/07/Retinal- months prior when she was being thyiazide. So, is the small BRVO a Vein-Occlusion-RVO-Guidelines-July-2015.pdf. Accessed: examined for her cataracts. The result of her high blood pressure? December 15, 2017.

REVIEW OF OPTOMETRY JANUARY 15, 2018 75

074_ro0118_RQ.indd 75 1/5/18 2:38 PM Therapeutic Review

Spot the Dot When an OD notes this unusual presentation, it’s time to spring into action. By Alan G. Kabat, OD, and Joseph W. Sowka, OD

51-year-old black woman presented for ocular examination complaining of blurry vision in both eyes.A Her ocular history was unre- markable, but her systemic history was complex. In addition to hyper- tension, she had cardiovascular dis- ease, thyroid disease, asthma, herpes zoster and multiple strokes, the most recent of which was one year ago. Currently under the care of an internist and a cardiologist, her medications included metoprolol, furosemide, spironolactone, digoxin, levothyroxine, baby aspirin, Xarelto Our patient’s right fundus demonstrates scattered midperipheral, white-centered (rivaroxaban, Janssen) and Protonix retinal hemorrhages. Similar findings also appeared in the left fundus. (pantozaprole, Pfizer). cotton-wool spots or neovascular including hypertensive and diabetic Evaluation changes in either eye. retinopathy, as well as connective Upon examination, best-corrected White-centered retinal hemor- tissue disorders such as systemic visual acuity was 20/20 OD and rhages— commonly known as lupus, ankylosing spondylitis and 20/25+ OS. Motilities and visual “Roth spots”—can be an alarming Behçet’s disease.1,2,4,7,8 Additionally, fields by confrontation were normal finding for any eye care practitio- other infectious diseases may present in both eyes, and pupils were reac- ner. These lesions are believed to with this retinal finding, including tive without afferent defect. Intraoc- represent a rupture of retinal capil- toxoplasmosis, leishmaniasis and ular pressures (IOP) were 20mm Hg laries, with extrusion of blood and human immunodeficiency virus OD, 23mm Hg OS. Examination of subsequent platelet adhesion to the (HIV).9-11 Numerous blood dyscra- the anterior segment revealed mild damaged endothelium.1,2 The release sias have also been associated with lenticular changes, but was other- of platelets initiates a coagulation Roth spots, and this finding can wise unremarkable. Fundus evalua- cascade, which leads to the forma- portend such insidious conditions tion disclosed a pink, healthy optic tion of a platelet-fibrin thrombus; as anemia, thrombocytopenia and disc and an intact fovea in each eye. this accounts for the white center of even several types of leukemia.2,5,12-16 The retinal vasculature was mildly each hemorrhagic lesion.1,2 Rarely, Roth spots have been noted dilated and tortuous in both eyes, For years, Roth spots were in association with anoxia and car- with minimal crossing changes. Of believed to be pathognomonic for bon monoxide poisoning, severe note, there were multiple, deep, subacute bacterial endocarditis, a head trauma (especially in children round retinal hemorrhages, many potentially life-threatening infec- and infants) and intracranial hemor- with distinctively white centers, pri- tion of the cardiac endothelium.1-6 rhage.1,12,16-18 The central stimulating marily located in the midperiphery Today, however, we recognize that factor seems to be increased capil- of both eyes. There was no evidence these lesions can be encountered lary fragility, intravascular coagu- of macular edema, retinal exudate, in numerous other conditions, lopathy or both.4

76 REVIEW OF OPTOMETRY JANUARY 15, 2018

076_ro0118_TR.indd 76 1/5/18 4:37 PM Advertisers Index

Testing Protocol 19 Akorn Consumer Health ...... 37 effect. Neither we nor the PCP Phone ...... (800) 579-8327 When funduscopic exam reveals were aware of any reports of Roth ...... www.akornconsumerhealth.com Roth spots, particularly in cases spots associated with the use of where the medical history is rivaroxaban or any other anticoagu- Alcon Laboratories ...... 84 Phone ...... (800) 451-3937 unknown or reportedly unremark- lants. Moreover, the only potential Fax ...... (817) 551-4352 able, a systemic evaluation for dis- drug interaction in this case was ease is crucial. Initial testing should between rivaroxaban and aspirin. Bausch + Lomb ...... 7, 8, 19 include an assessment for hyper- While numerous drugs can potenti- Phone ...... (800) 323-0000 Fax ...... 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[email protected] blood cultures, cardiac evaluation laboratory evaluation. ■ ...... www.eyecheck.com and specific serology for infectious 1. Ling R, James B. White-centred retinal haemorrhages (Roth Katena ...... 2 disorders or autoimmune disease. spots). Postgrad Med J. 1998 Oct;74(876):581-2. Phone ...... (800) 225-1195 2. Zhang J, Chen Y, Yu Z, Liu L. Bilateral Hemorrhagic Retinopathy ...... www.katena.com If the patient is not in acute dis- with Roth Spots in Pediatric-Onset Systemic Lupus Erythematosus tress, and if they have an established and Associated Thrombocytopenia: A Case Report and Review of Literature. Ocul Immunol Inflamm. 2017 Oct;11:1-4. Keeler Instruments ...... 5, 25 primary care provider (PCP), we 3. Chong Y, Han SJ, Rhee YJ, et al. Classic Peripheral Signs of Phone ...... (800) 523-5620 coordinate care with that physician Subacute Bacterial Endocarditis. Korean J Thorac Cardiovasc Surg. Fax ...... (610) 353-7814 2016 Oct;49(5):408-12. rather than ordering testing directly. 4. Ceglowska K, Nowomiejska K, Kiszka A, et al. Bilateral Macular In most cases, the PCP has detailed Roth Spots as a Manifestation of Subacute Endocarditis. Case Rep Lombart Instruments ...... 15 Ophthalmol Med. 2015;2015:493947. Phone ...... (800) 446-8092 knowledge of the patient’s condition 5. Macauley M, Nag S. Roth spots in pernicious anaemia. BMJ Case Fax ...... (757) 855-1232 and medications that may provide Rep. 2011 Apr 19;2011. pii: bcr0120113734. 6. Hess RL. Roth spots in native valve endocarditis. J Am Osteopath Menicon ...... 27 additional insight, thereby reduc- Assoc. 2013 Nov;113(11):863. ing the number of diagnostic tests 7. Yülek F, Erten S, Orhan N, Simsek S. Anterior optic neuropathy, Phone ...... (800) MENICON Roth spots, and ankylosing spondylitis. J Clin Rheumatol. 2009 ...... [email protected] required. Also, the PCP will ulti- Sep;15(6):309-10...... www.meniconamerica.com mately be the one to initiate treat- 8. Blumenthal EZ, Zamir E. Images in cardiovascular medicine. Roth’s spots. Circulation. 1999 Mar 9;99(9):1271. ment for any underlying disease, and 9. Furtado JM, Toscano M, Castro V, Rodrigues MW. Roth Spots in Mentholatum Company ...... 21 having the laboratory results sent Ocular Toxoplasmosis. Ocul Immunol Inflamm. 2016 Oct;24(5):568-70. Phone ...... (877) 636-2677 10. Meena J, Juneja M, Mishra D, et al. Visceral leishmaniasis with ...... [email protected] directly to that individual facilitates Roth spots. Oxf Med Case Reports. 2014 Sep 16;2014(6):110-1...... www.mentholatum.com more efficient care of the patient. 11. Rodríguez-Adrián LJ, King RT, Tamayo-Derat LG, et al. Retinal lesions as clues to disseminated bacterial and candidal infections: frequency, natural history, and etiology. Medicine (Baltimore). 2003 Natural Ophthalmics, Inc...... 73 Comanagement May;82(3):187-202. Phone ...... (877) 220-9710 12. Zehetner C, Bechrakis NE. White centered retinal hemorrhages ...... [email protected] In our case, we elected to communi- in vitamin b(12) deficiency anemia. Case Rep Ophthalmol. 2011 ...... www.natoph.com May;2(2):140-4. cate with the PCP and inform him 13. Zaidi FH. Roth spots obscure the picture. Lancet. 2003 Jun of the noted changes. We reviewed 14;361(9374):2086; author reply 2086. Reichert Technologies ...... 45, 47, 49 14. Kapadia RK, Steeves JH. Roth spots in chronic myelogenous Phone ...... (888) 849-8955 the potential etiologies associated leukemia. CMAJ. 2011 Dec 13;183(18):E1352. Fax ...... (716) 686-4545 with white-centered hemorrhages 15. Sharma T, Grewal J, Gupta S, Murray PI. Ophthalmic manifesta- ...... www.reichert.com tions of acute leukaemias: the ophthalmologist’s role. Eye (Lond). and suggested the diagnostic evalu- 2004 Jul;18(7):663-72. ation. We also asked about rivar- 16. Lorenzi U, Buschini E, Fea A, et al. Terson syndrome and leuke- S4OPTIK ...... 31, 33, 35 mia: a case report. Clin Ophthalmol. 2014 Apr 3;8:681-3. Phone ...... (888) 224-6012 oxaban—which has been associated 17. Levin M, Hall JP, Guerami A. Vitreous hemorrhage from with retinal hemorrhages in several carbon monoxide retinopathy. Retin Cases Brief Rep. 2016 Spring;10(2):157-9. case reports—and whether that or 18. Morad Y, Wygnansky-Jaffe T, Levin AV. Retinal haemorrhage in This advertiser index is published as a convenience and not as part of any of her other medications might abusive head trauma. Clin Exp Ophthalmol. 2010 Jul;38(5):514-20. the advertising contract. Every care will be taken to index correctly. 19. Talany G, Guo M, Etminan M. Risk of intraocular hemorrhage No allowance will be made for errors due to spelling, incorrect page be potentiating the anticoagulation with new oral anticoagulants. Eye (Lond). 2017 Apr;31(4):628-631. number, or failure to insert.

REVIEW OF OPTOMETRY JANUARY 15, 2018 77

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ROPT0118.indd 79 1/2/18 9:59 PM Review Classifi eds

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ROPT0118.indd 80 1/2/18 10:00 PM Meetings + Conferences

February 2018 at [email protected], call (419) 475-6226 or go to ■ 9-11. 57th Annual Heart of America Eye Care Congress. www.eyeskiutah.com. Sheraton Kansas City Hotel at Crown Center, Kansas City, ■ 7-11. Ocular Therapeutics in Cancun. Fiesta Americana MO. Hosted by: Heart of America Eye Care Congress. Key Condesa All Inclusive Resort, Cancun, Mexico. Hosted by: Ocular faculty: Marc Bloomenstein, Alan Glazier, Blair Lonsberry, Justin Therapeutics CE. Key faculty: Anthony Litwak, Diana Shechtman, Schweitzer. CE hours: 63 total, 17 per OD. For more information, James Thimons. CE hours: 20. For more information, email email Ron Fiegel at [email protected] or go to hoaecc.org. Anthony Litwak at [email protected], call (443) 895-1682 or go to ■ 9-11. 34th Annual Palm Beach Winter Seminar. Hilton West www.otce.net. Palm Beach, West Palm Beach, FL. Hosted by: Palm Beach ■ 15-18. International Vision Expo & Conference East. Jacob County Optometric Association. Key faculty: Bruce Onofrey, Greg Javits Center, New York City. Hosted by: Reed Exhibitions and The Caldwell. CE hours: 20. For more information, email Tamara Maule Vision Council. Key faculty: Ben Gaddie, Mark Dunbar, Kirk Smick, at [email protected], call (561) 477-3524 or go to Jack Schaeffer, Dave Ziegler, Douglas Devries. CE hours: 275 www.pbcoa.org. total, 30 per OD. For more information, go to east.visionexpo.com. ■ 10-17. Tropical CE— Cap Cana 2018. Secrets Cap Cana Resort & Spa, Punta Cana, Dominican Republic. Hosted by: April 2018 Tropical CE. Key faculty: Ben Gaddie, Walter Whitley. CE hours: 20. ■ 6-8. New Technologies & Treatments in Eye Care. Nashville For more information, email Stuart Autry at [email protected], Marriott at Vanderbilt, Nashville. Hosted by: Review of call (281) 808-5763 or go to www.tropicalce.com. Optometry. Key faculty: Paul Karpecki. CE hours: Up to 19. ■ 16-18. Optometric Education Consultants Mid-Winter For more information, email Kristina Furner at kfurner@jobson. Educational Getaway. JW Marriott Scottsdale Camelback Inn com, call (610) 492-1009 or go to www.reviewofoptometry.com/ Resort & Spa, Scottsdale, AZ. Hosted by: Optometric Education nashville2018. Consultants. Key faculty: Greg Caldwell, Joseph Sowka, Joseph ■ 19-21. MWCO Annual Congress. Aria Resort & Casino, Las Pizzimenti, Andrew Gurwood, Marc Meyers. CE hours: 15. For Vegas. Hosted by: Mountain West Council of Optometrists. more information, email Vanessa McDonald at [email protected], Key faculty: Alison Bozung, John McGreal, Julie Rodman, call (954) 262-4224 or go to www.optometricedu.com. Jessica Steen, Jim Thimons, Rob Wooldridge. CE hours: 56 ■ 16-18. Final Eyes CE 2018. DuPont Auditorium, Baptist Medical total, 24 per OD. For more information, email Tracy Abel at Center, Jacksonville, FL. Hosted by: Florida Eye Specialists. [email protected], call (888) 376-6926 or go to Key faculty: Edward Bennett, Rajesh Shetty, Richard Van De www.mwco.org. Velde, Harry S. Campbell, Carlo Pelino. CE hours: 18. For more ■ 25-28. Innovations in Optometry. Harbour Town Clubhouse information, email Susan Frick at [email protected], call Sea Pines Resort, Hilton Head Island, SC. Hosted by: Brittany (904) 200-1852 or go to finaleyesce.com. Stiegemeier. Key faculty: John Schachet, Bill Potter, Jeff Genos, ■ 16-20. Winter Ophthalmic Conference. Westin Snowmass Leo Semes, Howard Purcell, Ryan McKinnis, Peter Shaw, Jason Conference Center, Aspen, CO. Hosted by: Review of Optometry. Jedlicka, Nathan Lighthizer. CE hours: 19. For more information, Key faculty: Murray Fingeret, Leo Semes. CE hours: Up to 20. For email Brittany Stiegemeier at [email protected] more information, email Lois DiDomenico at reviewmeetings@ or call (937) 623-1690. jobson.com, call (866)730-9257 or go to www.skivision.com. ■ 26-29. New Technologies & Treatments in Eye Care San Diego/ ■ 28-March 4. SECO 2018. Georgia World Congress Center, OCCRS Joint Symposium. San Diego Marriott Del Mar, San Diego. Atlanta. Hosted by: SECO International. Key faculty: Brad R. Hosted by: Review of Optometry & OCCRS. Key faculty: Paul Grimsley, William J. Harbour, Donald R. Korb, Jay Haynie, Justin Karpecki, David Friess. CE hours: Up to 28. For more information, Bazan, Jenn Lim. CE hours: 178 total, 209 staff, 46 per OD. For email Lois DiDomenico at [email protected], call (866) more information, email Elizabeth Taylor DeMayo at 658-1772 or go to www.reviewofoptometry.com/sandiego2018. [email protected], call (770) 451-8206 or go to attendseco.com. To list your meeting, please send the details to: March 2018 Michael Iannucci ■ 4-9. 32nd Annual EyeSki Conference. Shadow Ridge Associate Editor Conference Center, Park City, UT. Hosted by: EyeSki. Key faculty: Email: [email protected] Joseph Pizzimenti, Leonard Messner, Tom Arnold, Mile Brujic, Phone: (610) 492-1043 James Fanelli. CE hours: 22. For more information, email Tim Kime

REVIEW OF OPTOMETRY JANUARY 15, 2018 81

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Ram On By Andrew S. Gurwood, OD

History At left, OCT imaging A 76-year-old female presented emer- of our 76-year- gently with a chief complaint of “a dark old patient who spot” in the visual field of her right eye complained of a of one day’s duration. Her ocular his- “dark spot” in her tory was remarkable for uncomplicated vision. bilateral cataract extraction in 2010. She did not report any recent ocular or head Below, the top two injury. Her systemic history was signifi- fundus images cant for hypertension, hypercholester- show the patient’s olemia and Type 2 diabetes, for which right eye and the she was medicated with losartan/HCTZ, bottom fundus atorvastatin and glipizide. She reported image shows the no allergies. left eye. Can you identify the cause Diagnostic Data of the patient’s Her entering corrected visual acuities visual disruption? measured 20/120 OD with no improve- ment on pinhole and 20/30- OS. Her extraocular muscle movements were full and without pain, there was no affer- ent pupillary defect and the vision could not be improved with refraction, but she was able to position the black spot using the facial Amsler grid. Color vision was unaffected. Biomicroscopy of the anterior segment found normal structures and open angles with Goldmann intraocular pressures measuring 13mm Hg OU. The dilated fundus findings are demonstrated in the photographs. Your Diagnosis How would you approach this case? Does this patient require any additional tests? How would you manage this patient? Retina Quiz Answers What is the patient’s likely prognosis? (from page 74): To find out, please visit us online at 1) a; 2) c; 3) d; 4) d. www.reviewofoptometry.com. ■

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