CRO Volume 28 Number 4

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Clinical & Refractive Optometry VOLUME 28, NUMBER 4, 2017

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Ocular Manifestations of Valsalva Maneuver Glaucomatocyclitic Crisis: A Case Report and Review Adult Onset Coats’ Disease Blind Spot Mapping: A Case Report Case Consultations: Dry Eye Treatment Regimens

Clinical&Refractive Optometry

Editorial Board • Volume 28, Number 4, 2017 Associate Editors Henry Reis, MD Burnaby, British Columbia

François Piuze, OD Quebec City, Quebec

Leonid Skorin, Jr., OD, DO Albert Lea, Minnesota

Editors Emeriti Brad Almond, OD Calgary, Alberta

Barbara Caffery, OD Toronto, Ontario

John Jantzi, OD Vancouver, British Columbia

Yvon Rhéaume, OD Montreal, Quebec

Contributing Editors Scott D. Brisbin, OD Edmonton, Alberta

Gerald Komarnicky, OD Vancouver, British Columbia

Langis Michaud, OD Montreal, Quebec

Barbara Robinson, OD Waterloo, Ontario

Lorance Bumgarner, OD Pinehurst, North Carolina

Bart McRoberts, OD Vancouver, British Columbia

Rodger Pace, OD Waterloo, Ontario

Jacob Sivak, OD, PhD Waterloo, Ontario

Louis Catania, OD Philadelphia, Pennsylvania

Ron Melton, OD Charlotte, North Carolina

Maynard Pohl, OD Bellevue, Washington

Randall Thomas, OD Concord, North Carolina

Publication Staff Publisher Lawrence Goldstein

Managing Editor Mary Di Lemme

Senior Medical Editor Evra Taylor

Layout Editor Colin MacPherson

Graphics & Design Mediconcept Inc.

Mission Statement Clinical & Refractive Optometry is a peer-reviewed professional journal dedicated to the publishing and disseminating of COPE approved CE credit scientific articles. The contents of each issue are composed of a mixture of original: state-of-the-art/technical, therapeutic/clinical, or practice management articles which are of particular interest to and use by practicing optometrists. Participants achieving 70% or more on the questionnaires that accompany each of the articles in the journal, will receive a course credit certificate.

WE’VE IMPROVED THE CE TEST SUBMISSION PROCESS In addition to completing the CE-Credit test questionnaires in this issue by hand and then submitting them by regular mail, you now have the option of completing and submitting the test questionnaires completely online and receiving your COPE CE Certificate literally seconds later by return email. For more detailed instructions, please refer to the Instruction Page of each test questionnaire in this issue.

Clinical&Refractive Optometry Contents • Volume 28, Number 4, 2017

CE CREDIT ARTICLES 132 Ocular Manifestations of Valsalva Maneuver Cindy Tampoya, OD; Mark H. Sawamura, OD; Judy Tong, OD; Pauline F. Ilsen, OD ABSTRACT: The Valsalva maneuver is classically described as an increase in intrathoracic pressure against the closed glottis, which causes a subsequent increase in venous pressure above the neck. Veins anterior to the heart use gravity to maintain proper circulation and thus lack valves that are normally required to prevent backflow. This unique mechanism potentially allows blood to surge backwards into the ocular circulation and damage the capillary vessels. Clinical ocular manifestations include hemorrhages within the periorbital skin, conjunctiva, retina, or in the vitreous. Patients experiencing Valsalva retinopathy may complain of sudden and painless vision loss.

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Glaucomatocyclitic Crisis: A Case Report and Review Rex B. Villegas, OD ABSTRACT: Glaucomatocyclitic crisis is an ocular disease that is characterized by a minimal non-granulomatous anterior uveitis that coincides with a dramatic elevation in intraocular pressure. The disease is usually unilateral and typically affects young adults, with males affected more than females. It is treated with and responds well to topical steroidal and ocular hypotensive agents.

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Adult Onset Coats’ Disease Melissa Contreras, OD; Steven Ferrucci, OD ABSRACT: Coats’ disease is a condition involving retinal telangiectasias and retinal vessel aneurysms causing sub-retinal and intraretinal exudation and lipid accumulation in healthy individuals. It is found to occur most frequently unilaterally in young males. In the case of two Latino male patients diagnosed with adult onset Coats’ disease, non-macular peripheral exudation and telangectasias were evident.

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Blind Spot Mapping: A Case Report Stacey Chong, OD, MSc, BSc; Patricia K. Hrynchak, OD; Michelle J. Steenbakkers, OD; Derek Y. Ho, MD; Natalie Hutchings, MCOptom, PhD; Nadine M. Furtado, OD ABSTRACT: The blind spot is an essential element in static perimetry as the absolute scotoma produced is used to ensure that the patient is fixating steadily throughout the test. If the optic nerve is anomalous, the scotoma might not be in the predicted location. This case outlines a few potential pitfalls in perimetry in a patient with an anomalous optic nerve head.

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CASE CONSULTATIONS 166 Treatment Regimens for a Challenging Dry Eye Case Presented by: Henry Reis, MD Responses from: Ben Barrus, OD; Edward Chow, OD; Krista Flynn, OD; Francis Gaudreault, OD; Jules Plante, OD; Susana Sebestyen, OD 170

NEWS & NOTES

ISSN: 2371-7017; Date of Issue: October 2017

Courtesy of: Dr. Cindy Tampoya Petechial hemorrhages on inferior palpebral conjunctiva OS.

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Clinical & Refractive Optometry is pleased to present this continuing education (CE) article

by Dr. Cindy Tampoya et al entitled Ocular Manifestations of Valsalva Maneuver. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit, please refer to page 139 for complete instructions.

Ocular Manifestations of Valsalva Maneuver Cindy Tampoya, OD; Mark H. Sawamura, OD, FAAO; Judy Tong, OD, FAAO; Pauline F. Ilsen, OD

ABSTRACT Background: The Valsalva maneuver is classically described as an increase in intrathoracic pressure against the closed glottis, which causes a subsequent increase in venous pressure above the neck. Veins anterior to the heart use gravity to maintain proper circulation and thus lack valves that are normally required to prevent backflow. This unique mechanism potentially allows blood to surge backwards into the ocular circulation and damage the capillary vessels.

Clinical ocular manifestations include hemorrhages within the periorbital skin, conjunctiva, retina, or in the vitreous. Patients experiencing Valsalva retinopathy may complain of sudden and painless vision loss.

We present three cases that demonstrate the myriad ways in which Valsalva maneuver can present clinically within or around the eye. Case Reports: The first case is a 57-year-old male patient with a history of self-induced emesis who presented with petechial hemorrhages located on his periorbital skin and conjunctiva. The second case is a 38-year-old female patient with a history of recent laproscopic surgery that resulted in deep intraretinal hemorrhages in the posterior pole of both eyes. The third case is a 34-year-old male who engaged in power exercising including strenuous weightlifting noticed within hours a leaf shaped floater in front of his central vision which paralleled a similarly shaped intraretinal C. Tampoya — Tri-Cities Eyecare Center, Kennewick, WA; M.H. Sawamura — Associate Professor, Southern California College of Optometry, Ketchum Health, Anaheim, CA; J. Tong — Assistant Dean of Residencies, Associate Professor, Southern California College of Optometry, Ketchum Health, Anaheim, CA; P.F. Ilsen — Professor, Southern California College of Optometry, Marshall B. Ketchum University; West Los Angeles Veterans Affairs Healthcare Center, Los Angeles, CA Correspondence to: Dr. Pauline F. Ilsen, West Los Angeles Veterans Affairs Healthcare Center, Optometry Clinic (123) Bldg. 304, Room 2-123, 11301 Wilshire Blvd., Los Angeles, CA USA 90073; E-mail: Pauline.Ilsen@va.gov The authors have no financial or proprietary interests in the products mentioned in this article.

This article has been peer-reviewed.

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hemorrhage juxtaposition to the macula. Conclusion: The optometrist should be aware of Valsalva maneuver as a possible cause for periorbital, conjunctival or retinal hemorrhages. One must keep in mind that Valsalva retinopathy is a diagnosis of exclusion and should be considered only after confirming a history of induced Valsalva and ruling out any underlying retinal or systemic diseases. Spontaneous resolution is the treatment of choice, but other options, such as Nd:YAG laser hyaloidotomy and vitrectomy are also utilized if warranted.

INTRODUCTION Valsalva maneuver is named after Antonio Maria Valsalva, an Italian anatomist of the 17th century.1 The Valsalva maneuver occurs when a person forcibly exhales against a closed glottis, which in turn causes an increase in intrathoracic and intra-abdominal pressure.2,3 Increased pressure in these cavities compresses the vena cava, which decreases venous return to the right side of the heart. Subsequently, there is a decrease in cardiac output.

Intrathoracic and intra-abdominal pressure returns to baseline when the glottis is released causing a rapid rise in venous return and a subsequent rise in cardiac output.

This, in turn, leads to a sudden rise in peripheral arterial and venous pressure.4 Elevated venous pressure transmits to the head and neck, where the blood vessels lack valves.2,3,5,6,7 Consequently, circulation unobtrusively gets channeled to the fine parafoveal capillary nets above the heart, resulting in hemorrhages located in or around the eye.1,2,8,9 A Valsalva event involves a centripetal force that moves superior to inferior; that is, the force moves in the head-to-toe or toe-to-head direction.2 Activities that generate pressure gradients in this way are coughing; strenuous exercise; weight-lifting; vomiting; sexual activity; end-stage labor; colonoscopy procedures; fiber optic gastroenteroscopy; blowing high-resistance musical instruments; inflating balloons; compressive surgeries; and endotracheal intubation.2,10 Playing wind instruments, more specifically trumpet playing, involves repeated and prolonged Valsalva maneuvers.11 Additionally, laserassisted in situ keratomileusis (LASIK) with a microkeratome suction ring replicates a Valsalva maneuver by

causing a rapid increase in IOP as high as 65 mmHg.12 Weightlifters who hold their breath or athletes who are unaware of exerting intense physical exertion are also at a higher risk for Valsalva retinopathy.13 Valsalva retinopathy is a term used to characterize retinal hemorrhages caused by a Valsalva maneuver.1 It was first described by Thomas Duane in 1972 and is noted to present infrequently. As a result, there is no reported epidemiological data in ophthalmic literature.2,3,6 We present three patients with varied ocular manifestations of the Valsalva maneuver, the first induced by vomiting, second by intra-abdominal laproscopic surgery, and last by strenuous repetitive weightlifting.

A

CASE REPORTS

B

C

Fig. 1 (A) Petechial hemorrhages on upper and lower lid OS resulting from self-induced vomiting (B) petechial hemorrhages on inferior palpebral conjunctiva OS (C) petechial hemorrhages on inferior palpebral conjunctiva OD

Case 1 A 57-year-old male new to the eye clinic reported a black spot in his vision for the past few months in both eyes.

There was no decrease in his vision and he denied any associated flashes. There were no complaints of eye pain, itching and no history of trauma. His medical history was remarkable for asthma and post-traumatic stress syndrome. Additionally, he smoked half a pack of cigarettes per day for the past thirty years and had a history of alcoholism. The patient was taking trazodone (DesyrelÂŽ, Bristol-Myers Squibb, Montreal, QC) for sleep and using an albuterol inhaler for his asthma. He denied taking any herbal supplements.

Best-corrected visual acuity was 6/6 (20/20) OD and 6/6 (20/20) OS. Extraocular muscle testing revealed full versions and cover testing demonstrated 2 exophoria at distance and near. The pupils were round, 4+ reactive to light, and there was no afferent pupillary defect. Amsler grid was unremarkable for metamorphopsia OD and OS. Slit lamp biomicroscopy revealed multiple pinpoint hemorrhages on the periorbital skin as well as on the palpebral and bulbar subconjunctiva OS>OD (Fig. 1A-C).

In addition, slit lamp biomicroscopy was remarkable for cortical cataracts and nuclear sclerosis in both eyes.

The intraocular pressure was 16 mmHg OD and OS

by Goldmann applanation tonometry. Fundoscopic examination revealed cup-to-disc ratios of 0.30 OD and OS with pink neuroretinal rims and distinct disc margins.

There was vitreous syneresis, but no Weiss ring, mild vessel tortuosity and nicking, and trace retinal pigment epithelium mottling with pinpoint soft drusen in both eyes. The periphery was unremarkable for holes, tears, or breaks in both eyes. A review of recent laboratory testing indicated the following: hemoglobin was 14.5 gm/dL (normal range: 13.3-17.7 gm/dL); hematocrit 42.5% (normal range: 39-52%); platelet count 244 k/uL (normal range 150-440 k/uL); serum glucose of 108 mg/dL (normal range: 70-110 mg/dL); hemoglobin A1c 5.6%

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A

B

Fig. 2 (A) Pinpoint to 1 disc diameter sized intraretinal hemorrhages resulting from complicated exploratory laproscopic surgery OD (B) intraretinal hemorrhages resulting from complicated exploratory laproscopic surgery OS

(normal range: 4.2-5.8%); cholesterol 196 mg/dL, high density lipoprotein 57 mg/dL; and low density lipoprotein of 127 mg/dL. The urine microalbumin level was 0.2 mg/dL (normal range: 0.0-1.8 mg/dL); and urine creatinine was 56 mg/dL. Urinalysis was negative for protein, glucose, ketones, and bilirubin. His most recent blood pressure measurement at our facility was 122/83 mmHg; the patient reported monitoring his blood pressure at home.

Upon further questioning, the patient denied taking any non-steroidal anti-inflammatory drugs, aspirin or other blood thinners. He suffered from a chronic cough and reported that he self-induced vomiting 2 to 3 times each month to help relieve indigestion and heartburn after his evening meals. As a precaution, a prothrombin time and international normalized ratio (PT/INR) was ordered to rule out other blood disorders as the cause for the periorbital and subjconjunctival hemorrhages; a complete blood count (CBC) was not ordered since it had been done recently and was normal. The patient was also referred to gastroenterology for evaluation and management of his heartburn. He was asked to return in 6 weeks.

At his 6-week follow-up, all hemorrhages had resolved and the patient reported he had not vomited since his prior visit. Given his history of self-induced vomiting and the normal PT/INR and CBC, Valsalva maneuver was determined to be the primary cause for the hemorrhages.

Case 2 A 38-year-old Caucasian female presented with complaints of bilateral, diffuse, non-moving “rings and feathers” in her vision immediately following exploratory laproscopic surgery in her abdomen the previous afternoon. As a complication of the procedure, excessive

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gas was placed into her abdominal cavity resulting in pneumothorax or the collapsing of her lungs. Emergency treatment protocol required immediate endotracheal intubation of the patient, during which she struggled to breathe for several minutes. When she awoke, she noted the presence of the floaters. The patient’s medical history was otherwise significant for depression, gastrointestinal distress, and post-surgical pain. She was taking fluoxetine (Prozac®, Eli Lilly, Montreal, QC), esomeprazole (Nexium®, AstraZeneca), and acetaminophen/hydrocodone (Norco). There was no significant family medical or ocular history.

Best corrected visual acuities were 6/6- (20/20-), 6/6- (20/20-) in the right and left eyes, respectively. Pupils were equal, round and 4+ reactive to light and there was no afferent pupillary defect. There were no misses OD or OS with Dvorine color plates. Extraocular muscles were full and unrestricted in both eyes. Biomicroscopy revealed an unremarkable anterior segment OU and deep anterior chamber angles. No signs of anterior segment hemorrhaging were noted in the periorbital skin or conjunctiva.

Goldmann applanation tonometry readings were 13 mmHg OD and OS. She reported multiple scotomas scattered across the Amsler grid OD and OS. The blood pressure measured 138/82 mmHg (right arm sitting).

Dilated fundus examination revealed multiple bilateral well-circumscribed deep intraretinal hemorrhages in the posterior pole of both eyes. The hemorrhages were pinwheel in shape, some white-centered, and ranged in size from 1/8 to 1 disc diameter (Fig. 2A,B). Previously documented macular drusen changes were also present.

The optic nerve and choroid appeared undisturbed OD and OS. The cup to disc ratios were 0.15 round OU. The

Fig. 3 OCT of the macula OD. The white arrow designates where the hemorrhage is located.

vitreous was clear and there was no sign of intravitreal hemorrhage in either eye. The patient was instructed to avoid strenuous activities and use of nonsteroidal anti-inflammatory drugs or aspirin. She was scheduled for follow-up evaluations but failed to keep multiple appointments due to her current medical condition and diagnostic testing. However, she reported via a telephone conversation 1 month later that her visual symptoms had resolved.

Case 3 A 34-year-old Latino male presented with a complaint of a “leaf” shaped floater in the central vision of his right eye that developed 2 days prior. It had remained unchanged and appeared to move with his eye. The patient reported that the previous evening, he had performed strenuous exercise involving hundreds of repetition of pushups and jumping jacks, and weightlifting. He reported good health and was not on any current medications. He had a history of renal lithiasis 1 year prior, which had completely resolved. There was a maternal history of diabetes and paternal history of heart disease. Entering acuities were 6/7.5 (20/25) and 6/4- (20/15-) in the right and left eyes, respectively, through his habitual spectacles. Pupil responses were 4+ reactive to light without an afferent pupillary defect. Extraocular muscles were unrestricted in all fields of gaze. Biomicroscopy of the anterior segment showed no signs of petechial or subconjunctival hemorrhages, the anterior chambers were deep and quiet and the corneas were clear. Intraocular pressure measured by Goldmann applanation was 13 mmHg and 14 mmHg in the right and left eyes, respectively. Blood pressure was

measured at 128/88 on the right arm, sitting. Funduscopic examination revealed a 1/3 disc diameter intraretinal hemorrhage, inferior temporal to the fovea of the right eye in the shape of a leaf. The cup to disc ratios were 0.5 round in the right eye and 0.45 round in the left. The vasculature showed a slight arteriovenous compression in the superior arcade in each eye. OCT of the macula revealed an area of intraretinal thickening adjacent to the fovea in the right eye (Fig. 3). En Face (anterior to posterior) analysis of the hemorrhage lies at the level of approximately the outer plexiform layer (Fig. 3). The dense nature of the hemorrhage creates a shadow below this area in the scan, appearing as if there is an absence of tissue. The patient was instructed to refrain from weightlifting or strenuous activities and avoid anticoagulants and non-steroidal anti-inflammatory agents until the follow-up visit. The patient was instructed to return in 2 weeks for re-evaluation. Since his symptoms had markedly improved, the patient failed to show up for his follow up visit since his symptoms markedly improved and because of financial hardship.

DISCUSSION Ocular Pathology Precipitated by Valsalva Maneuver The various ocular manifestations of Valsalva maneuver are summarized in Table I. Of greatest visual consequence is Valsalva retinopathy, which is a rare condition that is usually found in healthy individuals.36 The sudden increase in venous pressure experienced during a Valsalva event disrupts the retinal vessels creating intraretinal or preretinal hemorrhages located in the posterior pole and macula.3,6,10,14 In general, they are located below the inner limiting membrane (ILM), subhyaloid area, or both and range in size from a punctate spot to more than 1 disc diameter.2,3,16,17,18 As time passes, the blood will slowly settle due to gravity and create the classic boat-keel or dome appearance.8,10 Increased venous pressure not only affects the fine capillaries within the eye, but also travels to the periorbital vessels as well.1 Thus, ocular manifestations may include subconjunctival hemorrhages and superficial petechiae of the skin of the head and neck.1,2,19 Ocular Signs and Symptoms Classic symptomatology of Valsalva retinopathy have been previously described as sudden, painless vision loss, a central scotoma ocular pain , and nausea resulting from increased IOP.8,20,22 There are three ways vision loss can occur: by detachment of the ILM, vitreous hemorrhage, or preretinal hemorrhage at the macula.2,8,14 Increased IOP can result from a suprachoroidal hemorrhage, which occurs when blood gathers in the space between the sclera and choroid and evolves into massive areas of

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Table I Ocular manifestations of Valsalva maneuver2, 5, 15, 22, 32 • • • • • • • •

Superficial petechial hemorrhages on the head and neck Subconjunctival hemorrhage Preretinal macular hemorrhages Superchoroidal hemorrhage Vitreous hemorrhage Increased IOP Detachment of the inner limiting membrane (ILM) Globe protrusion

choroidal effusion and secondary flattening of the anterior chamber.21,22 In cases involving repeated Valsalva maneuvers, as seen with trumpet or other high resistance wind instrument musicians, the patient is at a higher risk for Valsalva retinopathy and transient increases in IOP.23 Although rare, transient increases in IOP may cause long-term damage to the eye such as glaucomatous visual field loss with significant optic nerve head cupping.23 Schuman states this scenario could be misdiagnosed as normal-tension glaucoma and should instead be named “intermittent high pressure glaucoma.” Additionally, the increased cumulative lifetime hours of playing high wind instruments also factors into the degree of presentation.

Protrusion of the globe during Valsalva maneuver is rare; however, Elfar et al suggested inquiring about past Valsalva events with patients who present with significant exophthalmos.24 In particular, individuals who perform yoga headstands and forward bending moves may experience globe propulsion due to increased orbital venous pressure associated with these positions.5 Differential Diagnosis One must determine the underlying cause for retinal hemorrhages in order to appropriately manage the patient.3,8 There are three possible types of etiologies to consider: retinal disease, systemic disease and physical stress.3,6,18 Valsalva retinopathy is a diagnosis of exclusion and requires a positive history of “Valsalva stress;” therefore, a thorough case history is key.1,10,20 The optometrist must also keep in mind that patients may elect not to report embarrassing yet crucial behaviors or activities in their case history.25 In the absence of a past Valsalva event, underlying retinal and systemic diseases that might cause retinopathy must be ruled out.13,25,28 Fluorescein angiography is an essential test used to detect neovascularization and reveal retinal diseases such as macroaneurysm; branch or central retinal vein occlusion; sickle cell retinopathy; radiation retinopathy; Terson syndrome; hypertensive retinopathy; anemic retinopathy; or proliferative diabetic retinopathy.3,6,8,20,26,27 Optical coherence tomography (OCT) is another important tool used to confirm the location of bleeding and offers additional clues to help confirm Valsalva retinopathy.3,7,20

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Hemorrhages associated with Valsalva have historically been observed in the subhyaloid or ILM spaces, but the exact location cannot be determined unless both the ILM and subhyaloid face are visible on the OCT.16,18 In our patient, the ability of the RTVue OCT (Optovue, Inc., Fremont, CA) software to identify the level of the hemorrhage within the retina places the blood posterior to where previous reports have described.

Systemic diseases in question are diabetes, hypertension, sickle cell disease, anemia, coagulopathy, and blood dyscrasias.28,29 Blood tests should be ordered in order to further investigate the presence of these diseases, which include: CBC; prothrombin time; partial thromboplastin time and platelet count; glycosylated hemoglobin (HbA1C); hemoglobin solubility; hemoglobin fractionation (electrophoresis); and peripheral blood smear.13,20,25 As far as physical stress is concerned, Purtscher’s retinopathy is an important differential to consider and is caused by a major trauma, pancreatitis, childbirth, and renal failure.30,31 It is different from Valsalva maneuver in that it involves a centrifugal force that moves in the ventral-dorsal direction (e.g., a chest compression injury) instead of the centripetal force associated with a Valsalva event.2 It always results in reduction of vision and one may observe multiple bilateral hemorrhages greater than 1 disc diameter in size, which are confined to the posterior pole.18 Unlike Valsalva retinopathy, Purtscher’s retinopathy has no predilection for the macula and is accompanied by soft exudates and capillary infarction.18 Purtscher’s retinopathy usually resolves within weeks, and it is rare to have Valsalva and Purtscher’s occur together after trauma.30,31 Another differential are hemorrhages that result from exposure to high altitudes. They present in the peripapillary region throughout the fundus and spare the macula.32 The hemorrhages are described as diffuse, punctate or flame-shaped, and confluent.32 Interestingly, underlying retinal or systemic diseases are not only considered differentials, but are also important risk factors to take into account. Weak retinal vessels leave a patient at a higher risk for developing Valsalva retinopathy than a patient who is without preexisting retinal or systemic diseases.2,20,29 One suggestion by Carlson et al described performing hypertension screening for those who are avid weight lifters or wind-instrument musicians to better detect those at a higher risk.

A very important consideration includes infants with a history of vomiting who present with retinal hemorrhages.33 The intrathoracic and intra-abdominal pressure in infants cannot be elevated high enough to rupture the retinal capillaries, so Valsalva retinopathy does not occur in infants.33 For this reason, the optometrist should suspect child abuse (i.e., shaken baby syndrome) as the primary cause of retinal hemorrhages rather than attribute them to Valsalva maneuver from vomiting.33

Management Management options for preretinal hemorrhages include observation, neodymium: yttrium-aluminum-garnet (Nd:YAG) vitreous hyaloidotomy, or vitrectomy.3,8,15,20 Very few cases require invasive treatment at all.8 Observation is the preferred treatment of choice, but surgical intervention may be favored depending on the size of the lesion, the age of the patient, and the health of the eye.8,20 Patients are instructed to refrain from vigorous activity, sleep in an upright or sitting position, use stool softeners if indicated, and to avoid using unprescribed anti-coagulating agents.3,8 Weight lifters are urged to inhale before lifting and exhale during lifting to prevent occurrence or recurrence.34,35 Hemorrhages will typically spontaneously resolve within weeks to a few months.3,18,20,36 Hyaloidotomy with Nd:YAG laser drains blood into the vitreous cavity by puncturing a hole in the vitreous face.8,14,38 There are four indications for Nd:YAG hyaloidotomy: first, rapid restoration of binocular vision is needed; second , visual acuity is poorer in the other eye; third, the patient is unwilling to have a vitrectomy; and, fourth, vitrectomy is contraindicated.1,14,37 Nd: YAG laser hyaloidotomy is recommended for macular hemorrhages that are greater than 3 disc diameters in size and are less than 3 weeks old.3,15,37 It is not, however, recommended for a hemorrhage that is resolving.20 It is thought that macular hemorrhages older than 3 weeks have already formed clots and will drain less readily even with a visible vitreous puncture.3,15,38 Therefore, it is important to adhere to these recommendations in order to obtain the best visual prognosis if treating with Nd:YAG laser.38 Vitrectomy is a third treatment option that is considered if Nd:YAG hyaloidotomy is initially unsuccessful due to clotted blood; second, epiretinal membrane, macular hole, or retinal detachment develops after Nd:YAG; third, sub-ILM hemorrhages are not spontaneously resolving or are extensive; and fourth, for cases where blood disperses into the vitreous following Nd:YAG treatment, the latter occurring 30% of the time.15 De Maeyer described cases in which there was excellent visual recovery after vitrectomy plus ILM peeling.39 This is a safer alternative for quick visual recovery and has a low risk of complications.39 When adverse events do occur, they present as are retinal tear, retinal detachment, epiretinal membrane and cataract.15,39 Prognosis Overall, the visual prognosis for Valsalva retinopathy is very promising, but there are factors that guard complete visual recovery.1,15,20,36 Macular hemorrhages approximately 1 disc diameter in size and treated conservatively

generally resolve within 6 months without further complications.3,18,20,36 On the other hand, an eye with a preexisting retinal disease has limited visual potential and prognosis is guarded.15 Such conditions include diabetic retinopathy, retinal macroaneurysm, or branch retinal vein occlusion.15 Whether conservative treatment is implemented or a laser procedure is carried out, a diseased retina with Valsalva retinopathy will have a poorer visual outcome than if Valsalva retinopathy presented alone.14,15,40 In cases where a vitreous hemorrhage is present, Nd:YAG hyaloidotomy typically restores vision in 1 month.15,38 In the absence of a vitreous hemorrhage recovery to 6/6 (20/20) visual acuity is usually achieved within 24 hours to 1 week.15,37,40 There have been no reported complications 6 months after Nd:YAG laser hyaloidotomy treatment.15,38 Visual prognosis for vitrectomy is very good, where 80% of patients recover to a visual acuity of 6/15 (20/50) or better.41 As with any surgical procedure, complications may arise following Nd:YAG hyaloidotomy or vitrectomy.7,14,15,17,37,40 Although conservative treatment such as monitoring is noninvasive, there are complications associated with it as well.37,40 Because it takes several months before blood is completely absorbed, the macula has prolonged exposure to hemoglobin, which may prevent complete healing.37,40 Blood that settles over a long period of time will turn yellow, due to hemoglobin degeneration, and become toxic.38 This in turn reduces the final visual outcome from its original baseline.15,37 Nd:YAG laser hyaloidotomy is also associated with the development of a macular hole, retinal detachment, and epiretinal formation.7,15,17,20 The risk of ERM formation or metamorphopsia 2 years after treatment, however, is fortunately low.20,37 Complications associated with vitrectomy are retinal tear, retinal detachment, cataract and ERM.20 Ulbig reports that a vitrectomy was needed in only one-third of patients who developed an ERM or macular hole from Nd:YAG hyaloidotomy.15

CONCLUSION Valsalva retinopathy is an important differential to consider in adult patients who present with acute onset of painless vision loss and retinal hemorrhages. This diagnosis, however, should be reserved until a thorough case history is taken and an associated Valsalva event is confirmed. It is important to keep in mind that preexisting retinal diseases will prolong the time for visual recovery and may hinder vision from returning to baseline. The optometrist should remember to rule out retinal and systemic diseases by obtaining the appropriate tests such as fluorescein angiography, OCT and blood studies. â??

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Duane TD. Valsalva hemorrhagic retinopathy. Tr Am Ophthalmol Soc 1972; 70: 298-313.

Skorin L. Jr and Keith JF. Valsalva retinopathy: examples of classic and secondary occurrences. Clin Surg Ophthal 2010; 28(7): 150-154.

Jones WL. Valsalva maneuver induced vitreous hemorrhage.

J Am Optom Assoc 1995; 66(5): 301-304.

Cohen JA., Char DH, Norman D. Bilateral orbital varices associated with habitual bending. Arch Ophthalmol 1995; 113: 1360-1362.

Androudi S, Ahmed M, Brazitikos P, Foster CS. Valsalva retinopathy: diagnostic challenges in a patient with parsplanitis. Acta Ophthalmol Scandinavica 2005; 83: 256-257.

Gibran SK, Kenaway N, Wong, D, et al. Changes in the retinal inner limiting membrane associated with Valsalva retinopathy.

Br J Ophthalmol 2007; 91: 701-702.

Bar-Sela SM., Moisseiev J. Valsalva retinopathy associated with vigorous dancing in a discotheque. Ophthalmic Surg Lasers Imaging 2007; 38(1): 69-71.

Connor,AJ. Valsalva-related retinal venous dilation caused by defaecation. Acta Ophthalmologica 2010: e149.

Tildsley J, Srinivasan S. Valsalva retinopathy. Postgrad Med J 2009; 85(1000): 110.

Carlson AP, Pappu S Keep MF, Turner P. Large cerebellar hemorrhage during trumpet playing: importance of blood pressure elevation during the Valsalva maneuver: case report.

Neurosurgery 2008; 62(2): E1377.

Moshfeghi AA., Harrison SA., Reinstein DZ, Ferrone PJ. Valsalva-like retinopathy following hyperopic laser in situ keratomileusis. Ophthalmic Surg Lasers Imaging 2006; 37(6): 486-488.

Labriola LT, Friberg TR, Hein A. Marathon runner’s retinopathy. Sem Ophthalmol 2009; 26(6): 247-250.

Khan MT, Saeed MU, Shehzad MS, Qazi ZA. Nd:YAG laser treatment for Valsalva premacular hemorrhages: 6 month follow up. Int Ophthalmol 2008; 28: 325-327.

Ulbig MW, Mangouritsas, G, Rothbacher H. Long-term results after drainage of premacular subhyaloid hemorrhage into the vitreous with a pulsed Nd:YAG laser. Arch Ophthalmol 1998; 116: 1465-1469.

Schukla D, Naresh K, Kim R. Optical coherence tomography findings in Valsalva retinopathy. Am J Ophthalmol 2005; 140(1): 134-136.

Kwok AK, Lai TY, Chan NR. Epiretinal membrane formation with internal limiting membrane wrinkling after Nd:YAG laser membranotomy in Valsalva retinopathy. Am J Ophthalmol 2003; 136(4): 763-766.

Pitta CG, Steinert RF, Gragoudas ES, Regan CDJ. Small unilateral foveal hemorrhages in young adults. Am J Ophthalmol 1980; 89: 96-102.

Geyer O, Wasserman D, Rothkoff L, Lazar M. Orbital hemorrhage induced by labour. Br J Ophthalmol 1990; 74: 242.

Ball WL. OCT is key to confirming Valsalva retinopathy.

Review of Optometry. Continuing Education Lesson (August 2010).

Hammam, T, Madhavan C. Spontaneous suprachoroidal haemorrhage following a Valsalva manoeuvre. Eye 2003; 17: 261-262.

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22. Elfar A, Barnes SD. A real eye-opener. Anesth Analg 2009; 90: 1000-1008.

23. Schuman JS, Massicotte EC, Connolly S, Hertzmark E, et al.

Increased intraocular pressure and visual field defects in high resistance wind instrument players. Ophthalmology 2000; 107(1): 127-133.

24. Walsh TJ, Gilman M. Voluntary propulsion of the eyes.

Am J Ophthalmol 1969; 67(4): 583-585.

25. Friberg TR., Braunstein RA., Bressler NM. Sudden visual loss associated with sexual activity. Arch Ophthalmol 1995; 113: 738-742.

26. Callender D, Beirouty ZA., Saba SN. Valsalva haemorrhagic retinopathy in a pregnant woman. Eye (Lond) 1995; 9(6): 808-809.

27. Georgiou T, Pearce IA, Taylor RH. Valsalva retinopathy associated with blowing balloons. Eye (Lond) 1999; 13(5): 686-687.

28. Al-Mujaini AS, Montana CC. Valsalva retinopathy in pregnancy: a case report. J Med Case Reports 2008; 2(101): 1-3.

29. Wickremasinghe SS., Tranos PG., Davey C. Valsalva haemorrhagic retinopathy in a pregnant woman: implications for delivery. Acta Ophthalmologica Scandinavica 2003: 420-422.

30. Chandra P, Azad R., Pal N, Sharma, Y. Valsalva and Purtscher’s retinopathy with optic neuropathy in compressive thoracic injury. Eye 2005; 19: 914-933.

31. Buckley SA, James B. Purtscher’s retinopathy. Postgrad Med J 1996; 72: 409-412.

32. Shults WT, Swan, KC. High altitude retinopathy in mountain climbers. Arch Ophthalmol 1975; 93: 404-408.

33. Herr S, Pierce MC, Berger RP, Ford, H. “Does Valsalva retinopathy occur in infants? An initial investigation in infants With vomiting caused by pyloric stenosis. Pediatrics 2004; 113: 1658-1661.

34. Romano PE. Exhale while lifting or straining to avoid Valsalva retinopathy or bleeding from stressed retinal vessels. Eur J Ophthalmol 2003; 13: 113.

35. Ikeda ER., Borg A, Brown, D, Malouf J, et al. The Valsalva maneuver revisited: the influence of voluntary breathing on isometric muscle strength. J Strength Cond Res 2009; 23(1): 127-132.

36. Oboh AM, Weilke F, Sheindlin J. Valsalva retinopathy as a complication of colonoscopy. J Clin Gastroenterol 2004; 38(9): 793-794.

37. Durukan AH., Kerimoglu H., Erdurman C, Demirel A. Long-term results of Nd:YAG laser treatment for pre-macular subhyaloid haemorrhage owing to Valsalva retinopathy. Eye 2008; 22: 214-218.

38. Mumcuoglu T, Durukan AH., Erdurman C, Hurmeric V. Outcomes of Nd:YAG laser treament for Valsalva retino-pathy due to intense military exercise. Ophthalmic Surg Lasers Imaging 2009; 40(1): 19-24.

39. DeMaeyer K., Van Ginderdeuren R., Postelmans L, Stalmans P. Sub-inner limiting membrane haemorrhage: causes and treatment with vitrectomy. Br J Ophthalmol 2007; 91(7): 869-872.

40. Rennie CA, Newman DK, Snead MP, Flanagan DW. Nd:YAG laser treatment for premacular subhyaloid haemorrhage. Eye 2000; 519-524.

41. Sedwick LA. Long-term visual outcome in Terson syndrome. J Clin Neuro-Ophthalmol 1992; 12(2): 134.

28:4, 17

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QUESTIONNAIRE Ocular Manifestations of Valsalva Maneuver Cindy Tampoya, OD; Mark H. Sawamura, OD, FAAO; Judy Tong, OD, FAAO; Pauline F. Ilsen, OD 1.

(A) (B) (C) (D)

Which of the following clinical signs or symptoms is associated with Valsalva maneuver?

Sudden and painless vision loss Dizziness Nausea Both A & C are correct

2.

(A) (B) (C) (D)

Which type of etiology is a common precursor to Valsalva maneuver?

Diabetes Immune deficiency Heredity Traumatic injury

Ocular Manifestations of Valsalva Maneuver â&#x20AC;&#x201D; Tampoya et al

139

COPE-APPROVED CE CREDIT APPLICATION FORM

All of the following statements about Valsalva maneuver are false, EXCEPT: It presents infrequently It is most common in individuals over age 50 It is typically a reaction to emotional stress It frequently causes sudden loss of visual acuity

4.

(A) (B) (C) (D)

In Case 1, which clinical finding was not present at the patient’s initial presentation?

Absence of afferent pupillary defect Unaffected visual acuity Nuclear sclerosis in both eyes Elevated intraocular pressure in both eyes

5.

(A) (B) (C) (D)

Which of the following is an ocular manifestation of Valsalva maneuver?

Valsalva retinopathy Subconjunctival hemorrhages Superficial petechiae of the skin of the head and neck All of the above

6.

(A) (B) (C) (D)

Which of the following conditions is not a cause of Valsalva maneuver?

Amyotrophic lateral sclerosis (ALS) Hypertension Sickle cell disease Anemia

7.

(A) (B) (C) (D)

Which of the following is the preferred treatment for Valsalva maneuver?

Observation Nd:YAG hyaloidotomy Vitrectomy Vitrectomy plus ILM peeling

8.

(A) (B) (C) (D)

Which of the following statements is true about Valsalva retinopathy?

It can occur in infants It presents infrequently It’s a high risk for weightlifters who hold their breath Both B & C are correct

9.

(A) (B) (C) (D)

Which of the following statements is true for the patient in Case 3?

Floaters not visible in right eye Diminished reactive pupil responses to light Clear corneas Subconjunctival hemorrhage in his right eye

10.

(A) (B) (C) (D)

In Case 2, what was the patient’s chief initial complaint?

Glare Nausea “Rings and feathers” in her vision Ocular pain in both eyes

28.4:17

3.

(A) (B) (C) (D)

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Clinical and Refractive Optometry 28:4, 2017

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Clinical & Refractive Optometry is pleased to present this continuing education (CE) article

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Glaucomatocyclitic Crisis: A Case Report and Review Rex B. Villegas, OD, FAAO

ABSTRACT Background: Glaucomatocyclitic crisis is an ocular disease that is characterized by a minimal nongranulomatous anterior uveitis that coincides with a dramatic elevation in intraocular pressure. The disease is usually unilateral and typically affects young adults, with males affected more than females. It is treated with and responds well to topical steroidal and ocular hypotensive agents. Case Report: A healthy 26-year-old Asian male presented with minimal, intermittent pain in the left eye for three days. Ocular health examination revealed a minimal, non-granulomatous anterior uveitis and elevated intraocular pressure in the left eye. The patient was treated with topical steroidal, ocular hypotensive, and cycloplegic agents for the subsequent days following the initial visit with complete resolution of the iritis. No glaucomatous damage to the optic nerve was detected, and the patient is currently being managed as a glaucoma suspect. The case report includes a discussion on the diagnosis and management of glaucomatocyclitic crisis, the possible etiologies, and the various differential diagnoses. Conclusion: The exact cause of the disease is unknown, although it is widely speculated that it is associated with a herpes-related trabeculitis. Regardless of the etiology, treatment is aimed at controlling the inflammation and uveitis. Management includes careful monitoring of the patient as the disease is recurrent and patients have an increased risk of developing primary open-angle glaucoma.

INTRODUCTION Glaucomatocyclitic crisis, also known as PosnerSchlossman Syndrome, is an acute, minimal nongranulomatous anterior uveitis associated with a dramatic R.B. Villegas — Private Practice, Burbank, CA Correspondence to: Dr. Rex B. Villegas, 201 E. Angeleno Avenue, Unit 408, Burbank, California 91502; E-mail: rex.villegas@gmail.com The author has no financial interest in any material mentioned in this article.

This article has been peer-reviewed.

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elevation in intraocular pressure.1 The disease is typically unilateral although bilateral cases have been reported.

The disease typically affects young adult males, and its propensity for recurrence puts the patient at risk for developing optic nerve changes and, thus, open-angle glaucoma.2 No etiology has been clearly defined, although there is support for an infective trigger from the herpes virus.2-4 An autoimmune etiology has also been proposed as it has been associated with HLA-Bw54.5 A case report is presented that details the diagnosis and appropriate management of the condition.

CASE REPORT A 26-year-old Asian male presented to our office on a Monday morning (Day #1) for a walk-in emergency visit.

His chief complaint was having minimal and intermittent pain in his left eye for three days. He described the pain as feeling mildly “bruising,” although he reported that it was tolerable and not extremely painful. He reported having no other ocular complaints, including having no conjunctival discharge, redness, itchiness, or foreign body sensation. He reported having no visual complaints as well and that his vision seemed to be unaffected by the pain. Additionally, he said that he experienced no photophobia, photopsia, or floaters. This was the patient’s first visit to our office, although he reported having a comprehensive eye exam one year prior. His ocular history was remarkable for prescription computer-only spectacles, which were prescribed the previous year. He reported to be in good medical health and was not taking any medications. At the time of the exam, he had no headaches, muscle weakness, or other physical symptoms.

He had no recent ocular or head trauma. His last physical examination was eight months ago and he reported it to be unremarkable. He had no known drug allergies. His occupation was a computer programmer. He was alert to person, place, and time.

His entering uncorrected distance and near visual acuities were 6/6 (20/20) OD, OS, and OU. Uncorrected cover test at distance and near showed no movement.

Pupillary responses were tested with a transilluminator.

Pupils were equal, round, and reactive to light without an afferent defect. The patient reported minimal pain in the

left eye when the transilluminator was placed in front of either eye. Extraocular motilities were smooth, accurate, full, extensive, and painless while pursuing a transilluminator. Confrontational fields were full to finger counting OD and OS. Blood pressure was 125/75 mmHg and resting pulse was 75 beats/minute. Objective refraction by retinoscopy was OD +0.50 DS and OS +0.50 DS. Subjective manifest refraction was OD +0.75 DS and OS +0.75 DS with visual acuities of 6/6 (20/20) OD, OS, and OU. Distance phoria through the subjective refraction showed no lateral or vertical phoria. Near visual acuities through the distance subjective refraction was 6/6 (20/20) OD, OS, and OU. Near phoria through the distance subjective refraction was 3D exophoria with no vertical phoria. Negative and positive relative accommodations at 40 cm were +2.50 and >-3.00, respectively.

Anterior segment slit lamp examination of both eyes showed clear eyelids and lashes, clear conjunctiva and sclera, flat and intact irises, and clear crystalline lenses.

Nasal and temporal anterior chamber angles in both eyes were grade 4 open as measured by the Van Herrick technique. Examination of the cornea in the right eye was clear. Corneal examination in the left eye showed two discreet, fine, and white keratic precipitates on the infero-central mid-peripheral endothelium. There was no corneal edema in the left eye. The anterior chamber of the right eye was deep and quiet without signs of inflammation. The anterior chamber of the left eye was deep and had trace cells and no flare with the observation of a single cell when examined with a 2-mm conical slit lamp beam. Intraocular pressures (IOP) were measured

by Goldmann applanation tonometry (GAT) and were 16 mmHg OD and 42 mmHg OS at 9:30 am. Gonioscopy showed anterior chamber angles that were open to the ciliary body band 360 degrees with 1+ pigment in the trabecular meshwork in both eyes. There was no evidence of angle closure or peripheral anterior synechiae in either eye.

The right eye was dilated in office with phenylepherine hydrochloride 2.5% and tropicamide 1.0%. In the left eye, one drop of prednisone acetate 1.0% (Pred Forte™, Allergan), one drop of timolol maleate 0.5%, and one drop of scopolamine 0.25% were instilled in office.

Post-dilated IOPs were measured at 10:30 am and were 16 mmHg OD and 41 mmHg OS. There was no closure of the anterior chamber angles upon dilation of either eye.

Dilated fundus examination showed cup:disc (C/D) of 0.4/0.4 (vertical/horizontal) OD and OS with deep cups and no damage to the neural rims. The optic nerves of both eyes were pink with distinct rims. Nerve fiber layers of both eyes were healthy with no apparent defects. There were no signs of retinal vascular hemorrhaging or inflammation in either eye. The retinal peripheries in both eyes were flat and intact. The vitreal chambers were clear with no signs of inflammation OU.

The patient was diagnosed with a minimal, nongranulomatous anterior uveitis with a concurrent marked elevation in IOP in the left eye. There was no evidence of acute, intermittent, chronic, partial, or complete angle closure. There was also no evidence of posterior uveitis or retinal vasculitis. These signs and the patient’s minimal symptoms were consistent with glaucomatocyclitic crisis.

The patient was prescribed Pred Forte q3h OS. He was instructed to return to the office later in the day at 5:00 pm for an IOP check and instillation of additional topical ocular hypotensive agents if necessary.

The patient returned in the afternoon and reported improvement in his symptoms. He said he was compliant with Pred Forte and that he instilled two drops since the morning office visit. He reported no pain in the left eye although he was mildly photophobic in the left eye. Anterior segment slit lamp examination of the right eye showed no changes from the earlier visit.

Examination of the left eye showed a dilated left pupil and the presence of trace cells in the anterior chamber, which was unchanged from the previous examination in the morning. IOP measured by GAT was 16 mmHg OD and 25 mmHg OS at 5:30 pm. Dilated posterior segment examination of the left eye was unchanged from the morning examination.

At the conclusion of the exam, one drop of timolol maleate 0.5% and one drop of scopolamine 0.25% were instilled in the left eye. Based on the patient’s improving symptoms and decreasing IOP, he was diagnosed with resolving glaucomatocyclitic crisis OS. The patient was educated about his condition, including the risk for the development of glaucoma and the potential for the condition to cause damage to his vision. Compliance with Pred Forte was stressed to control the inflammation. It was also stressed for him to return the next morning for an IOP check and instillation of additional ocular hypotensive and/or cycloplegic agents if necessary.

The patient returned the next morning (Day #2) and reported compliance with Pred Forte q3h OS throughout the previous evening. He said his left eye felt well with no pain or discomfort. Entering uncorrected visual acuities were 6/6 (20/20) OD, OS, and OU. Anterior segment slit lamp examination was unchanged in the right eye. The left eye showed a dilated pupil (secondary to the previous day instillation of scopolamine) with no cells or flare in the anterior chamber. There was a single KP on the corneal endothelium of the left eye. IOP measured by GAT were 16 mmHg OD and 16 mmHg OS at 9:30 am.

Dilated fundus examination was unchanged from the previous visits OU. Because of the marked improvement in IOP and the resolved iritis in the left eye, the patient was instructed to decrease Pred Forte instillation to q.i.d.

The patient returned to the office later that same day for an IOP check, which was 16 mmHg OD and 16 mmHg

Glaucomatocyclitic Crisis: A Case Report and Review — Villegas

143

Fig. 1 Mean deviation for the right visual field measured -0.91 db

OS at 5:30 pm. At the conclusion of the exam (Day #2) he was instructed to continue Pred Forte q.i.d. OS for 2 days and then discontinue, and he was scheduled for daily IOP checks over the next several days, with alternating morning and afternoon appointments to rule out diurnal variation.

Ocular health examinations were unchanged over the next several visits. The IOPs over the subsequent visits were: • Day #3: 15 mmHg OD and 16 mmHg OS at 10:00 am • Day #4: 16 mmHg OD and 15 mmHg OS at 4:30 pm • Day #5: 16 mmHg OD and 16 mmHg OS at 9:30 am • Day #6: not checked • Day #7: 16 mmHg OD and 16 mmHg OS at 3:30 pm • On Day #7, a Humphrey visual field 24-2 SITA-Fast test was performed. The results for the right eye were reliable (1/11 fixation losses, no false positives, no false negatives) and showed no specific defects and patterns of depressions. The mean deviation for the right visual field measured -0.91 db (Fig. 1). The results for the left eye were reliable (1/10 fixation losses, no false positives, 9% false negative) and showed a minimal depression in the infero-nasal quadrant just below the horizontal midline. The mean deviation for the left visual field measured -2.78 db (Fig. 2). IOP measured 16 mmHg OD and OS at 3:30 pm. The anterior chamber angles were reevaluated by

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Fig. 2 Mean deviation for the left visual field measured -2.78 db

gonioscopy and showed angles open to the ciliary body band and 1+ trabecular meshwork pigment 360 degrees in both eyes with no evidence of angle closure or peripheral anterior synechiae. Dilated fundus exams were unchanged from previous examinations and showed no apparent damage or cupping to the optic nerves in both eyes.

The patient was diagnosed with resolved glaucomatocyclitic crisis OS. However, the visual field findings in the left eye were anomalous. They were consistent with an early, inferior nasal step that could have resulted from elevated IOP. He was diagnosed as a glaucoma suspect secondary to the hypertensive episode and visual field changes. The patient was educated on the signs and symptoms of angle closure and uveitis and was told to return to the office should he experience any symptoms.

He was also educated on glaucoma and the relationship between elevated IOP and visual field changes. The importance of periodic IOP checks and visual field tests were stressed. The patient opted to seek medical care with a provider within his HMO network. A letter was written for the patient to bring to the specialist in his network. In the letter, the patient’s condition was explained in detail, and a copy of the visual fields was included that noted the inferior nasal area of the left eye field. It was recommended that threshold visual fields be repeated and

baseline retinal tomography, nerve fiber layer analysis, and optic nerve photos be taken. It was also recommended that if the visual fields were reliable and repeatable that the patient begin medical treatment with aqueous suppressants (beta-blockers or -adrenergic agonists) to prevent fluctuations in IOP. To rule out an underlying cause for the iridocyclitic attack, a baseline medical workup was recommended, including complete blood count, erythrocyte sedimentation rate, Venereal Disease Research Laboratory test, and fluorescent treponemal antibody absorption test.

A phone call from the patient’s ophthalmologist was received two weeks after the patient’s last visit. He received the letter that was sent and agreed with the diagnosis of glaucomatocyclitic crisis, noting the presence of a single keratic precipitate in the left eye.

The ophthalmologist reported that Humphrey visual field 30-2 SITA-Std tests were performed and were reliable, full, and repeatable OD and OS. The area of depression OS in the initial 24-2 SITA-Fast test was not repeatable and was likely due to patient error (the patient’s first time taking the test). The ophthalmologist reported consistent IOPs of 15 mmHg OD and OS and no signs of angle closure or uveitis. The patient was scheduled for follow-up every 6 months for IOP checks and visual field tests. The patient has been co-managed over the past 3 years and has not had any recurrent attacks.

DISCUSSION Glaucomatocyclitic crisis is a syndrome that was first described by Adolph Posner and Abraham Schlossman in 1948. They described seven general characteristics of the syndrome: • The disease is unilateral.

• The presenting symptom is usually slight discomfort or visual blur, although the patient may also be asymptomatic.

• The eye appears generally white and quiet, although mild corneal edema may develop as a result of ocular hypertension.

• Ocular hypertension coincides with a mild anterior uveitis, indicated by trace cells, flare, and keratic precipitates.

• The anterior chamber angle is open with no angle closure or peripheral anterior synechiae.

• The ocular hypertension can last from a few hours to one month, but rarely over two weeks.

• Episodes of attacks may occur without apparent cause and vary in frequency from many attacks in a short period of time to few attacks over a long period of time.1 Glaucomatocyclitic crisis, also called PosnerSchlossman syndrome (PSS), typically affects young adults, with males affected more frequently than females.

Attacks are initially unilateral, although 50% of patients develop bilateral attacks at different times.2 The hallmark of the condition is a dramatic elevation in intraocular pressure (IOP) (usually between 40-60 mmHg) associated with a disproportionately minimal non-granulomatous anterior uveitis.1,6-9 The high IOP can cause a mild corneal edema. During the active phase of the condition, very few cells are seen in the anterior chamber and very few keratic precipitates are seen on the inferior corneal endothelium. The disease responds well to medical therapy10,11 with complete resolution of attacks, although patients should be followed closely over time as the condition can recur and these patients have an increased risk of developing primary open-angle glaucoma (POAG).2,12 The exact pathogenesis of the disease is not known, although several etiologies have been postulated in the past. In 1935, Kraupa described patients with uniocular inflammation and glaucoma, and emphasized that his patients were “neurasthenic, angiopathic, heavy cigarette smokers, and one had [spastic intestinal disturbance].”13 Posner and Schlossman suggested an abnormality of the hypothalamus and autonomic nervous system due to their observation of PSS in patients with hypertensive vascular disease, migraine, anisocoria, and iris heterochromia.1 In 1949, Givner described a patient with episodes of cyclitic uniocular glaucoma that were inexplicably associated with afternoon fever, fatigue, and diarrhea.13 Israel, Rouher, and Levatin described cases that were coincident with dental anomalies in 1952, 1955, and 1956, respectively. In 1957, Burton described a patient whose 15 episodes of the disease were preceded by exposure to cold temperatures.13 More recently, Hirose et al found a relationship between PSS and HLA-Bw54, suggesting that PSS is an autoimmune condition.5 While no etiology has been confirmed, it is widely speculated that PSS is caused by an acute inflammation of the trabecular meshwork that impedes aqueous humor outflow.2-4,7 Furthermore, the exact cause of this trabeculitis has not been determined, although there is support for an infective trigger. In a study of three patients with active attacks of PSS, Yamamoto et al found that all three patients had evidence of the herpes simplex virus (HSV) in the aqueous humor when the humor was examined by polymerase chain reaction (PCR) amplification. Because HSV commonly infects cranial nerve V (and can remain latent in the trigeminal ganglion), and considering that the trabecular meshwork is innervated by the ophthalmic division of the trigeminal nerve, it is suggestive that HSV is the cause of the trabeculitis in PSS.3 Support for an HSV-related cause for PSS is strengthened by the fact that HSV is known to cause herpetic kerato-uveitis.3 In 2005, Teoh et al described a case of a recurring, and eventually recalcitrant, case of bilateral PSS. When the aqueous

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humor of this patient was examined by PCR amplification, the results were strongly positive for the presence of cytomegalovirus.4 This was consistent with a study by Bloch-Michel et al, who found the presence of antibodies to cytomegalovirus in patients with active PSS.4 The findings of both HSV and cytomegalovirus in the aqueous humor of active PSS may indicate that PSS is an inflammatory response to infections from the Herpesviridae family.4 The most prominent clinical characteristic of PSS is its dramatic elevation in IOP, which usually ranges between 40-60mm Hg during attacks. IOP in this range puts the eye at risk for developing optic nerve damage due to acute glaucoma. Park et al studied optic nerve topography using confocal scanning laser tomography in a group of six patients with recurring PSS. Measurements of disc area, cup area, cup/disc ratio, rim area, cup volume, rim volume, and cup depth were taken during PSS attacks and after remission (average time interval after remission was 38.5 days). When IOP was reduced in PSS attacks, they found a corresponding decrease in optic nerve cup volume and increase in rim area and rim volume.14 Darchuk et al conducted a similar study. They analyzed the dynamics of optic nerve head blood flow by retinal confocal tomography and Scanning Laser Doppler Flowmetry. Optic nerve rim volume, rim area, cup volume, and cup area were analyzed before, during, and after PSS attacks. In a group of four patients, it was shown that PSS produced a decrease in rim volume and rim area and an increase in cup volume and cup area during ocular hypertensive attacks. However, the changes were transient, harmless, and reversed when the attacks subsided.15 Additionally, they found that there was no visual field damage due to the hypertensive episodes. It is not certain what the mechanism is that causes optic nerve topographical changes, but there is support that the changes may be due to an IOP-related anterior repositioning of a posteriorly-displaced lamina cribrosa.14 The relationship between PSS and the primary open-angle glaucoma (POAG) has been studied. Kass et al studied a group of 11 patients with diagnosed attacks of PSS over a 13 year period. Five of the 11 were later diagnosed with bilateral POAG secondary to glaucomatous visual field defects. Interestingly, four of the patients also had a positive glucose tolerance test or overt diabetes.12 Considering the high prevalence of diabetes mellitus in patients with POAG, the authors suggested that a relationship is possible between diabetes, POAG, and PSS. Furthermore, they suggested that all patients with PSS should undergo a glucose tolerance test.12 In a retrospective study of 53 patients with PSS, Jap et al found that 26.4% developed glaucomatous damage (visual field loss and/or optic nerve cupping) due to repeated attacks. The risk for developing glaucoma was

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proportional to the length of time of having the syndrome.

Patients with the disease for longer than 10 years had a 2.8 times higher risk for developing glaucoma. They recommended that all patients with PSS be carefully examined for evidence of glaucoma even in the absence of POAG.8 Ocular hypertension in PSS generally will subside in a few weeks if left untreated, but the risk of long-term optic nerve or visual field damage warrants immediate treatment.10 The ocular hypertension is highly responsive to aqueous suppressive medical therapy. Muthusamy described two cases of PSS in which the IOPs were treated with apraclonidine 1%. Both showed a drop in IOP within one hour of application of the drops.11 When treating PSS, IOP-lowering medications such as beta-blockers and -adrenergic agonists should be used.7 Hong and Song suggested that apraclonidine may be the medication of choice due to the possible mechanism of prostaglandinmediated hypotensive effects.16 Miotics are ineffective and are contraindicated.1,6 The clinician should be wary about using prostaglandin-analogues such as latanaprost 0.005% due to paradoxical IOP-increasing effects. While prostaglandin-analogues generally decrease IOP, they may increase the blood-aqueous barrier permeability and increase the IOP in this particular syndrome.7 Topical corticosteroids are effective for treating the mild iritis10,17 and topical cycloplegics are effective for alleviating mild pain.17 There is also support for surgical intervention for the treatment of recurrent attacks of PSS. In their study of 53 patients with PSS, Jap et al described nine eyes that underwent glaucoma filtering surgery. 80% of them were successful in preventing IOP spikes during cyclitic attacks. Furthermore, the severity of the cyclitic attacks was reduced, suggesting that improvement of aqueous outflow may contribute to egression of inflammatory mediators.8 This theory was also supported by a case presented by Dinakaran and Kayarkar. They described a case of recurrent, bilateral PSS that was treated with trabeculectomy. The patient had no IOP spikes or recurrent uveitis in the subsequent 4-year follow-up.18 PSS is a unique condition in that it is inflammatory but causes hypertensive effects. Normally, ocular inflammation results in a decreased IOP secondary to inflammatory damage to the ciliary body, thus lowering the production of aqueous humor.7 However, IOP elevation may occur due to inflammatory damage to the trabecular meshwork, clogging of the trabecular meshwork with inflammatory debris, or an increase in aqueous viscosity due to the presence of inflammatory byproducts.7 However, these conditions usually occur in chronic inflammation, whereas PSS is an acute condition. The differential diagnoses for PSS should include conditions that cause dramatic changes in IOP as well as glaucoma secondary to inflammation.

Angle closure causes a unilateral increase in IOP as well as corneal edema in the involved eye. The patient will have acute pain, blurred vision, frontal headache, and nausea. The anterior chambers of both eyes will be shallow. The pupil in the involved eye will be fixed and dilated.19 Pigment dispersion syndrome can cause erratic variations in IOP, resulting in pigmentary glaucoma.

IOP spikes can be acute and the patient will be asymptomatic or mildly symptomatic to blurred vision or eye pain.

The typical patient profile is a young adult, myopic male.

Critical signs of this condition are the presence of iris pigment on the inferior corneal endothelium (Krukenberg’s spindle) and heavy pigment deposition in the trabecular meshwork when viewed gonioscopically.19 Various uveitic conditions can cause an increase in IOP. Fuch’s heterochromic iridocyclitis is a chronic condition that produces a unilateral low-grade anterior uveitis and increased IOP that does not resolve with treatment of the inflammation alone. Therefore, treatment should be aimed at lowering IOP and not managing the inflammation.20 Critical signs of this condition include the presence of non-granulomatous keratic precipitates and diffuse iris atrophy (which may appear as a hypopigmented iris) without synechiae.20 Herpes simplex virus can cause uveitic glaucoma. These patients may show keratic precipitates underlying areas of dendritic keratitis.20

REFERENCES 1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

11.

12.

13.

14.

CONCLUSION The case presented illustrates that glaucomatocyclitic crisis is a diagnosis that can be made clinically. The clinician must be keen on the patient’s minimal symptoms and thorough upon ocular health examination to detect the minimal signs it presents with. There are several differential diagnoses, although careful examination should accurately diagnose PSS. Patients with PSS should be monitored closely over their life for recurring attacks and the development of open-angle glaucoma. While surgical intervention has been shown to prevent IOP spikes and reduce cyclitic episodes, the best management of this condition is medical therapy as necessary to treat attacks and control the development of glaucoma.

Additionally, the clinician must be mindful of the peculiar relationship between the herpes virus and PSS. ❏

15.

16.

17.

18.

19.

20.

Posner A, Schlossman A. Syndrome of unilateral recurrent attacks of glaucoma with cyclitic symptoms. Arch Ophthalmol 1948; 39: 517-35.

Kanski JJ. Clinical Ophthalmology. 6th Ed. Edinburgh: Butterworth-Heinemann 2007.

Yamamoto S, Tada R, Yamamoto R, et al. Possible role of herpes simplex virus in the origin of Posner-Schlossman syndrome. Am J Ophthalmol 1995; 199: 796-798.

Teoh S, Thean L, Koay E. Cytomegalovirus in aetiology of Posner-Schlossman syndrome: evidence from quantitative polymerase chain reaction. Eye 2005; 19(12): 1338-1340.

Hirose S, Ohno S, Matsuda H. HLA-Bw54 and glaucomatocyclitic crisis. Arch Ophthalmol 1985; 103: 1837-1839.

DeRoetth A. Glaucomatocyclitic crisis. Am J Ophthalmol 1970; 69: 370-371.

Harrington J. Posner-Schlossman syndrome: a case report.

J Am Optom Assoc 1999; 70: 715-723.

Jap A, Sivakumar M, Med M, Chee S. Is Posner Schlossman syndrome benign? Ophthalmology 2001; 108: 913-918.

Green R. Posner-Schlossman syndrome (glaucomatocyclitic crisis). Clin Exp Optom 2007; 90: 53-56.

Hung P, Chang J. Treatment of glaucomatocyclitic crises.

Am J Ophthalmol 1974; 77: 169-172.

Muthusamy P. Apraclonidine in the management of glaucomatocyclitic crisis. Eye 1994; 8: 367-368.

Kass M, Becker B, Kolker A. Glaucomatocyclitic crisis and primary open-angle glaucoma. Am J Ophthalmol 1973; 75: 668-673.

Knox D. Glaucomatocyclitic crises and systemic disease: peptic ulcer, other gastrointestinal disorders, allergy, and stress. Trans Am Ophthalmol Soc 1988; 86: 473-495.

Park K, Hong C. Reversal of optic disc topography in patients with glaucomatocyclitic crisis after remission of attack. J Glaucoma 1998; 7: 225-229.

Darchuk V, Sampaolesi O, Lopez Mato O, et al. Optic nerve head behavior in Posner-Schlossman syndrome.

Int Ophthalmol 2001; 23: 373-379.

Hong C, Song K. Effect of apraclonidine hydrochloride on the attack of Posner-Schlossman syndrome. Korean J Ophthalmol 1993; 7: 28-33.

Malinovsky V. Glaucomatocyclitic crisis. J Am Optom Assoc 1983; 54: 1069-1070.

Dinakaran S, Kayarkar V. Trabeculectomy in the management of Posner-Schlossman syndrome. Ophthalmic Surg Lasers 2002; 33: 321-322.

Rhee D, Pyfer M. The Wills Eye Manual. Third Edition.

Philadelphia: Lippincott, 1999.

Kaiser P, Friedman N, Pineda R II. The Massachusetts Eye and Ear Infirmary Illustrated Manual of Ophthalmology 2nd Ed. Philadelphia: Saunders 2004.

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QUESTIONNAIRE Glaucomatocyclitic Crisis: A Case Report and Review Rex B. Villegas, OD, FAAO 1.

(A) (B) (C) (D)

Glaucomatocyclitic crisis is characterized by which of the following?

Gradual loss of visual acuity Elevated intraocular pressure Acute pain Chronic, intermittent pain

2.

(A) (B) (C) (D)

Which of the following statements best describes glaucomatocyclitic crisis?

It is usually unilateral It typically occurs in elderly men Females are usually affected more than males Recurrence is unlikely

Clinical and Refractive Optometry 28:4, 2017

COPE-APPROVED CE CREDIT APPLICATION FORM

In the Case Report presented, all of the following describe the patient at initial presentation, EXCEPT: Absence of photophobia Intermittent pain in the left eye Normal vision Redness in the left eye

4.

(A) (B) (C) (D)

In the Case Report presented, the initial oculo-visual examination revealed that: Pupils were reactive to light Near vision was markedly reduced Confrontational fields were full to finger counting OU Both A & C are correct

5.

(A) (B) (C) (D)

Which of the following is NOT a characteristic of glaucomatocyclitic crisis?

Elevation in intraocular pressure Complete angle closure Minimal pain or absence thereof No evidence of retinal vasculitis

6.

(A) (B) (C) (D)

Which of the following statements about glaucomatocyclitic crisis is incorrect?

Patients may be asymptomatic Corneal edema may be present The patientâ&#x20AC;&#x2122;s vision is rarely affected Episodes of attacks may occur without apparent cause

7.

(A) (B) (C) (D)

All of the following statements regarding Posner-Schlossman syndrome (PSS) are true, EXCEPT: Individuals with PSS are at risk for glaucoma Episodes of attacks may occur without apparent cause Family history of the disease is a possible risk factor It may be an autoimmune condition

8.

(A) (B) (C) (D)

According to this paper, glaucomatocyclitic crisis may be bilateral at different times in what percentage of patients?

30% 40% 50% 60%

9.

(A) (B) (C) (D)

Which of the following is a symptom of angle closure?

Blurred vision Nausea Acute pain All of the above

10.

(A) (B) (C) (D)

Which of the following best describes the patient profile for pigment dispersion syndrome?

18-year-old myopic female 22-year-old myopic male 40-year-old myopic female 55-year-old myopic male

28:4, 17

3.

(A) (B) (C) (D)

Glaucomatocyclitic Crisis: A Case Report and Review â&#x20AC;&#x201D; Villegas

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CLICK HERE TO PRINT THIS CE CREDIT ARTICLE AND TEST

Clinical & Refractive Optometry is pleased to present this continuing education (CE) article by Dr. Melissa Contreras and Dr. Steven Ferrucci entitled Adult Onset Coats’ Disease. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit, please refer to page 155 for complete instructions.

Adult Onset Coats’ Disease Melissa Contreras, OD, MPH, FAAO Steven Ferrucci, OD, FAAO

ABSTRACT Coats’ disease is a condition involving retinal telangiectasias and retinal vessel aneurysms causing subretinal and intraretinal exudation and lipid accumulation in healthy individuals. It is found to occur most frequently unilaterally in young males. In the case of two Latino male patients diagnosed with adult onset Coats’ disease, non-macular peripheral exudation and telangectasias were evident. Fortunately, due to lesion location, both maintain good central vision. Current treatment options for Coats’ include laser photocoagulation, steroid injection and intravitreal anti-vascular endothelial growth factor (VEGF) injections. Careful evaluation of location and severity of lesions must be assessed prior to determination of treatment modality.

INTRODUCTION Coats’ disease, first described in 1908 by ophthalmologist George Coats’,1 involves idiopathic retinal telangiectasias and aneurysms of retinal blood vessels that result in vascular leakage, hemorrhaging, capillary dropout, and exudation into surrounding tissues in the absence of vitreoretinal traction.2-5 In Coats’ disease, retinal vessels exhibit hyperpermeability and a breakdown of the blood retinal barrier.6 This is thought to be caused by high levels of vascular endothelial growth factor (VEGF) consistent with a deficiency in the protein product norrin in the eye, suggesting its association as a causative factor in the M. Contreras — Assistant Clinic Director, University Eye Center, Ketchum Health, Los Angeles, CA; Assistant Professor, Southern California College of Optometry, Fullerton, CA; S. Ferrucci — Chief of Optometry, Sepulveda Ambulatory Care Center, Sepulveda, CA; Professor, Southern California College of Optometry, Fullerton, CA Correspondence to: Dr. Steven Ferrucci, Chief of Optometry, Sepulveda Ambulatory Care Center, 16111 Plummer Street, #112e, Sepulveda, CA, 91343; E-mail: Steven.Ferrucci@va.gov The authors have no financial or proprietary interest in any material mentioned in this article.

This article was peer-reviewed.

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disease.7-10 VEGF is necessary for normal vascular development and angiogenesis because of its high selectivity for vascular endothelial cells, but in diseased states it is secreted by hypoxic retinal pigment epithelial (RPE) cells. As a result, aberrant neovascularization develops in eyes with elevated levels of VEGF.11 Often the progression of exudation and lipid deposition7 can lead to a total exudative retinal detachment.12 Patients may be asymptomatic or present with decreased visual acuities, blindness, leukocoria, strabismus, pain, and/or nystagmus.4,12,14 In the case of the two Latino male patients diagnosed with adult onset Coats’ disease, non-macular peripheral exudation and telangectasias were discovered on a routine comprehensive exam.

CASE 1 A 49-year-old male Latino patient presented to clinic for a comprehensive eye exam with no entering complaints.

His past medical history was significant for elevated liver function tests, depression and osteoarthritis. On examination his best-corrected visual acuity was 6/6 (20/20) OD and OS with a plano DS and +0.25 DS correction, respectively. Pupils were normal, round and equally reactive to light, extraocular muscle movements were full OU, confrontation visual fields were full to finger count both eyes, and he was orthophoric in primary gaze. Anterior segment evaluation of both eyes was found to be within normal limits. Intraocular pressures were 19 mmHg OD and 18 mmHg OS with Goldmann applanation tonometry. Blood Pressure was found to be 127/83 mmHg The dilated fundus examination revealed clear media, mild arteriovenus nicking OS, and a cup to disc ratio of 0.30 round with distinct margins and healthy rim tissue OU. A drance hemorrhage was noted OS (Fig. 1A,B). Both maculas were found to be flat and avascular. The left eye was notable for extensive exudative material temporally from 1 to 5 o’clock, denser inferotemporally bordering a large intraretinal hemorrhage. The right eye was notable for inferotemporal telangectasias and micro aneurysms without exudation. The left eye was also significant for 2+ arterial sheathing and large areas of temporal lipid exudates with subretinal fluid outside the macula.

Fig. 1 (A) Color fundus photography showing an unremarkable OD. (B) Color fundus photography showing a drance hemorrhage OS.

Fig. 2 (A) Color fundus photography showing peripheral retinal exudation and hemorrhages OS. (B) Fluorescein angiography showing late leakage oftelangiectasias OS.

Findings were confirmed on follow-up by fluorescein angiography showing focal areas of capillary dropout, telangectasias and capillary changes with mild hyperflourescence in the affected area suggestive of a slow mild leakage with no obvious neovascularization along with an area of hyperflourescence continuous with a macroaneurysm and an area of blocked fluorescence from the subretinal heme. (Fig. 2A,B) Optical coherence tomography (OCT) was not attempted given the lesion’s peripheral location. A preliminary diagnosis of Coats’ disease was made.

The patient was referred to his primary medical provider to rule out diabetes, thromboembolic disease, blood pressure control, renal function tests, carotid ultrasounds, echocardiogram, and electrocardiogram given the unlikely hemorrhage finding along with exudation. All

exams returned normal making idiopathic Coats’ disease the primary working diagnosis. A consultation with our retinal specialist confirmed the diagnosis, and recommended quadrantic panretinal photocoagulation (PRP) in the left eye. The patient underwent a single session, 714 spots of PRP OS in the temporal retina, with no complications. The patient did not return for the second session of PRP and presented again 3 years later with no evidence of exudation or hemorrhage. Vision remained stable at 6/6 (20/20) OD, 6/4.8 (20/16) OS, and he continues to be followed on an annual basis.

CASE 2 A 47-year-old Latino male presented to clinic with a complaint of decreased vision at near through his current

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Fig. 3 (A) Color fundus photography OS without visible telangiectasias. (B) Fluorescein angiography showing late staining temporally OS.

Fig. 4 (A) Color fundus photography of peripheral retinal exudation OS. (B) Fluorescein angiography of the same area showing no active leakage OS.

glasses. His previous medical history was significant for hypertension, hyperlipidemia, hepatitis B carrier, and positive PPD. The patient’s best corrected visual acuity was 6/6 (20/20) in the right eye with a -0.25 DS correction and 6/6 (20/20) in the left eye with a plano -0.50 x 120 correction. Pupils were normal, extraocular muscles were full OU, and confrontation fields were full to finger count each eye. Anterior segment evaluation revealed pingueculae OU with all other findings within normal limits.

Intraocular pressures were 14 mmHg OU with Goldmann applanation tonometry. Blood pressure was found to be 127/83 mmHg. Dilated posterior segment evaluation revealed clear media, cup to disc ratios of 0.20 round OD and OS with disc margins distinct and rims tissue pink and healthy.

Maculas were flat and avascular both eyes. The peripheral retinal exam was significant for possible peripheral

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vasculitis with exudates inferior and inferior temporally in the left eye without hemorrhages as well as temporally along superior arcades.

Findings were confirmed on follow-up with fluorescein angiography (Figs. 3A,B; 4A,B) exhibiting an area of late staining superiotemporally with a window defect and no vascular leakage or vasculitis. Recent blood work ruled out diabetes. A diagnosis of adult onset idiopathic Coats’ disease OS was made with a recommendation for a wide field fluorescein angiography to be completed to further assess the peripheral aspects of the lesion to make appropriate recommendations for treatment. The patient did not return for the fluorescein angiography and has since been lost to follow-up.

DISCUSSION Coats’ is a non-hereditary disease of mosaic phenotype8,10 with no racial predilection.6 It manifests predominantly

Table I Five stages of Coats’ disease Stage 1: Retinal telangiectasias Stage 2: Telangiectasias and exudation A: Extra foveal B: Foveal Stage 3: Exudative retinal detachment A: Subtotal detachment 1. Extra foveal 2. Foveal B: Total retinal detachment Stage 4: Total retinal detachment and glaucoma Stage 5: Advanced end stage disease

unilaterally in young males in the first decade of life,6 although a small percentage of patients do not present with symptoms until adulthood.6 A 2010 study by Morris et al found the estimated incidence to be at least 0.09 per 100,000.13 According to some authors, the disease has an association with some systemic conditions such as Turners syndrome and familial renal retinal dystrophy,3 while others argue there is no direct correlation to any systemic disease, stating that abnormal retinal telangiectasias with systemic associations do not technically qualify as Coats’ disease which is strictly idiopathic.3 Pathogenesis of vessel leakage begins with weakened artery walls and fewer pericytes, leading to telangiectasias, microaneurysm, and sausaging of vessels.3 Resulting poor blood flow can lead to macular ischemia and neovascularization.3 Retinal and vitreous hemorrhages are typically uncommon in Coats’ disease although they may be found at a higher rate in adult onset Coats’.1,4 In adult onset Coats’ vascular abnormalities generally occur in peripheral and equatorial regions consistent with both cases presented.14 George Coats’ originally described variations of these retinal vascular anomalies as three different diseases but later went on to merge the first two as variations of the same disease3 and the last was later defined as Von Hippel-Landau angiomas.5 More recently, Shields et al classified the disease into five stages that are useful clinically for documentation (Table I).4,6 Differential diagnoses are many and include: retinopathy of prematurity,4 familial exudative vitreoretinopathy and idiopathic juxtafoveal telangiectasias, as well as age-related macular degeneration, diabetes, hypertension, and hyperlipidemia.4 As late stages of Coats’ disease may sometimes mimic retinoblastoma, it is important to rule out this out as a diagnosis given its potential for morbidity.6 Clinical diagnosis is based on location and appearance. A careful fundus exam with condensing lenses, funds photography, OCT, and fluorescein angiograph are often necessary to accurately classify a lesion with active leakage requiring treatment.

Telangectasias show early hyperflourescence along with late leakage while exudates hypoflouresce.1 Fluorescein

angiography may also help identify areas of capillary nonperfusion and macular edema. An extra-foveal inactive lesion can be followed regularly without immediate treatment when indicated.

Complications resulting from Coats’ disease include capillary non-perfusion, neovascular glaucoma, cystoid macular edema, and retinal detachment from exudative accumulation in the subretinal space. Therefore, individualized considerations to determine the treatment modality best fit for the patient are necessary.3,4,15 Historically Coats’ was treated with enucleation when presenting in children due to its similarity to retinoblastoma in appearance and to prevent progression into neovascular glaucoma.5,6,16 In such cases computed tomography (CT) scan, magnetic resonance imaging (MRI), B scan ultrasonography to identify a mass or a fine needle biopsy confirming the absence of cancer cells should be performed to rule out a tumour and save the eye whenever possible.5,16 The high levels of vascular endothelial growth factor in the eye associated with vascular permeability are decreased by laser photocoagulation; more recently, severe cases have been treated with cryopexy and pan-retinal photocoagulation.17 In cases with resultant retinal detachment, scleral buckle is employed to prevent or repair the detachment.16 Lastly, if salvage is not possible, enucleation of the eye remains an option.

Prognostic visual outcome has been shown to depend on macular involvement9 and level of vision at presentation, and not specifically on treatment modality.16 Most recently, in addition to surgical and laser treatments, abnormal telangiectasias can be treated with the help of anti-VEGF intravitreal injections if diagnosed early.9 Medications such as bevacizumab,18,19 (pegaptanib sodium)8 and ranibizumab which bind and neutralize active forms of VEGF in the eye,11 may reduce the angiogenic factors, resulting in stability or resolution of retinal exudation.20 In addition, the corticosteroid triamcinolone acetate has been shown in studies to increase the reabsorbtion of subretinal fluid when used in conjunction with other treatment modalities.20 Patients who exhibit limited responsiveness to laser treatment may be good candidates for these alternatives to reduce exudates, macular edema and sub-retinal fluid due to their effectiveness against microangiopathy.20 As with any treatment option, complications are always a factor that must be taken into consideration. With the use of fluorescein angiography and more recently OCT, more detailed views of vessel leakage can be defined and localized, and are useful tools for follow-up and documentation of treatment outcomes.9

CONCLUSION Coats’ disease can commonly progress or reoccur; therefore, follow-up is necessary throughout life.3,21

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Luckily for the patients with adult onset Coats’ presented here, the disease appeared to be generally less aggressive with a limited area of involvement.21 With ever-changing research and advancements in technology, we continue to gain better understanding of Coats’ disease with new discoveries aiding in diagnosis and in treatment modalities that will provide the best quality of care for patients. ❏

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2.

3.

4.

5.

6.

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9.

Coats’ G. Forms of retinal disease with massive exudation.

R Lond Ophthal Hosp Rev 1908; 17: 440-525.

Jones J, Kroll A, et al. Coats’ disease. Int Ophthalmol Clin 2001; 41(4): 189-198.

Shields JA, Shields CL, et al. Clinical variation and complications of Coats’ disease in 150 cases. The 2000 Stanford Gifford memorial lecture. Am J Ophthalmol 2001; 131: 561-571.

Char DH. Coats’ syndrome: long-term follow-up. Br J Ophthalmol 2000; 84: 37-39.

Rubin MP, Mukai S. Coats’ disease. Int Ophthalmol Clin 2008; 48: 149-158.

Margolis R, Folgar F, et al. Diffuse retinal capillary leakage in Coats’ disease. Retinal cases and brief reports. Published ahead of print. Post-author corrections, August 9, 2011.

Sun Y, Jain A, et al. Elevated vascular endothelial growth factor levels in Coats’ disease: rapid response to pegaptanib sodium. Graefe’s Arch Clin Exp Ophthalmol 2007; 245: 1387-1388.

Alverez-Riviera LG, Abraham-Marin ML, et al. Coats’ disease treated with bevacizumab. Arch Soc Esp Oftalmol 2008; 83: 329-332.

Graeme C, Black M, et al. Coats’ disease of the retina (unilateral retinal telangiectasias) caused by somatic mutation of the NDP gene: a role for norrin in retinal angiogenesis. Human Molecular Genetics 1999; 8: 2031-2035.

10. Kim R. Introduction, mechanism of action and rationale for anti-vascular endothelial growth factor drugs in age-related macular degeneration. Indian J Ophthalmol 2007; 55: 413-415.

11. Shienbaum BS, Tasman W. Coats’ disease: a lifetime disease. Retina 2006; 26: 422-424.

12. Morris B, Foot B, Mulvihill A. A population based study of Coats’ disease in the United Kingdom. In: Epidemiology and clinical features at diagnosis. Eye (London, England) 2010; 24(12): 1797-1801.

13. Vasquez PN, Liliana Santamaria JL. Adult onset of recurrent Coats’ disease. Arch Soc Esp Oftalmol 2007; 82: 555-558.

14. Schefler A, Berrocal M, et al. Advanced Coats’ disease: management with repetitive aggressive laser ablation therapy. Retina 2008; 23(3): S38-S41.

15. Adam R, Kertes P, et al. Observations on the management of Coats’ disease: less is more. Br J Ophthalmol 2000; 84: 37-39.

16. Tarkkanen A, Laatikainen L. Coats’ disease: clinical, angiographic, histopathologic findings and clinical managements. Br J Ophthalmol 1983; 67: 766-776.

17. Yu-Guang H, He Y, Wang H, et al. Elevated vascular endothelial growth factor level in Coats’ disease and possible therapeutic role of bevacizumab. Graefe’s Arch Clin Exp Ophthalmol 2010; 248: 1519-1521.

18. Goel N, Kumar V, et al. Role of intravitreal bevacizumab in adult onset Coats’ disease. Int Ophthalmol 2011; 31: 183-190.

19. Othman I, Moussa M, Bouhaimed M. Management of lipid exudates in Coats’ disease by adjuvant intravitreal triamcinolone: effects and complications. Br J Ophthalmol 2010; 94(5): 606-610.

20. Smithen LM, Brown GC, Brucker AJ, Yannuzzi LA, et al.

Coats’ disease diagnosed in adulthood. Ophthalmology 2005; 112: 1072-1078.

21. Andonegui J, Arangueren M, et al. Coats’ disease of adult onset. Arch Soc Esp Oftalmol 2008; 83: 117-120.

28:4, 17

COPE-APPROVED CE CREDIT APPLICATION FORM

INSTRUCTIONS FOR 1 HOUR OF

CE CREDIT

This course is valid for 1 hour of COPE-approved CE credit, to be taken no later than November 1, 2020.

If you score 70% or more on the test questionnaire, a COPE CE Credit Certificate will be sent to you.

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TO TAKE AND SUBMIT THIS TEST OFFLINE If you are a Pre-Paid test subscriber, download a copy of this form, fill in the information requested below in the IDENTIFICATION section, and then answer each of the 10 multiple choice questions in the QUESTIONNAIRE section. Please mail this form to the address shown below.

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Name: First______________________________ Last___________________________________ Address:________________________________________________________________________ Number

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QUESTIONNAIRE Adult Onset Coats’ Disease Melissa Contreras, OD; MPH, FAAO; Steven Ferrucci, OD, FAAO 1.

(A) (B) (C) (D)

All of the following statements regarding Coats’ disease are true, EXCEPT: It is usually unilateral There is a higher incidence among African Americans It usually occurs in young males It is not hereditary

2.

(A) (B) (C) (D)

Which of the following treatments is not effective for Coasts’ disease?

Steroid injections Laser photocoagulation Photodynamic therapy (PDT) Intravitreal anti-VEGF injections

Adult Onset Coats’ Disease — Contreras, Ferrucci

155

COPE-APPROVED CE CREDIT APPLICATION FORM

Which of the following is a clinical sign or symptom of Coats’ disease?

Hyperosmolarity Leukocoria Elevated IOP Diplopia

4.

(A) (B) (C) (D)

Stage 4 of Coats’disease consists of: Advanced end stage disease Telangiectasias and exudation Total retinal detachment and glaucoma Exudative retinal detachment

5.

(A) (B) (C) (D)

Which of the following findings describe the patient in Case 1?

High blood pressure Pupils dilated Pupils equally reactive to light Decreased vision OD

6.

(A) (B) (C) (D)

Which of the following is more common in adult onset Coats’?

Pain Loss of visual acuity Retinal and vitreous hemorrhage Exudation

7.

(A) (B) (C) (D)

In which stage does exudative retinal detachment occur?

Stage 1 Stage 2 Stage 3 Stage 5

8.

(A) (B) (C) (D)

Which finding does not describe the patient in Case 2?

Excellent visual acuity Increased intraocular pressure OD Extraocular muscles full OU Confrontational fields full to finger count each eye

9.

(A) (B) (C) (D)

Which of the following statements regarding Coats’ disease is not true?

It can reoccur following treatment It progresses, rather than remaining static Prognostic visual outcome depends, in part, on macular involvement A watchful waiting approach is appropriate in the majority of cases

10.

(A) (B) (C) (D)

Which of the following was the patient’s complaint in Case 2 of the paper presented?

Decreased vision at near Decreased vision upon awakening Floaters Foreign body sensation

28.4:17

3.

(A) (B) (C) (D)

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Clinical and Refractive Optometry 28:4, 2017

CLICK HERE TO PRINT THIS ENCORE CE CREDIT ARTICLE AND TEST

Clinical & Refractive Optometry is pleased to present this encore continuing education (CE) article

by Drs. Stacey Chong, Patricia Hrynchak, Michelle Steenbakkers, Derek Ho, Natalie Hutchings and Nadine Furtado entitled Blind Spot Mapping: A Case Report, which was originally published in Clinical & Refractive Optometry 27:2. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit, please refer to page 163 for complete instructions.

Blind Spot Mapping: A Case Report Stacey Chong, OD, MSc, BSc; Patricia K. Hrynchak, OD, MScCH(HPTE); Michelle J. Steenbakkers, BScH, OD, FAAO; Derek Y. Ho, MD; Natalie Hutchings, MCOptom, PhD; Nadine M. Furtado, OD, MSc, FAAO

ABSTRACT The blind spot is an essential element in static perimetry as the absolute scotoma produced is used to ensure that the patient is fixating steadily throughout the test.

If the optic nerve is anomalous, the scotoma might not be in the predicted location. This case outlines a few potential pitfalls in perimetry in a patient with an anomalous optic nerve head.

INTRODUCTION Visual field reliability indexes are essential to ensuring the validity of the test.1 The reliability indices are monitored throughout an automated Humphrey visual field test and include fixation losses, false positives and false negatives. Fixation is monitored to determine if the patient is shifting their point of gaze. False positives occur when a patient has responded when a stimulus was not presented.

False negatives occur when the patient does not respond to a stimulus brighter than the predetermined threshold.

It has been found that when reliability criteria are compared between normal patients and those with glaucoma, 30% and 45%, respectively had unreliable fields as determined by a failure to meet the criterion outlined by the manufacturer of the Humphrey Visual Field Analyzer (HFA).2 The manufacturer has indicated that fixation losses should not be greater than 20%, and false positives and negatives should not be greater than 33%. Nearly half of the instances where fixation losses were greater than 20% were caused by technical artifacts including improper initial determination of the blind spot and high false positives.3 Re-plotting the blind spot during testing has the potential to decrease the frequency S. Chong, P.K. Hrynchak, M.J. Steenbakkers, D.Y. Ho, N. Hutchings, N.M. Furtado â&#x20AC;&#x201D; University of Waterloo, School of Optometry and Vision Science, Waterloo, ON Correspondence to: Dr. Stacey Chong, 85 Finch Avenue East, Toronto, ON M2N 4R4; E-mail: stacey.chong.od@gmail.com The authors have no financial interests.

This article has been peer reviewed.

of unreliable test results secondary to excessive fixation losses from 33% to 14%.3 The blind spot of the patient is plotted at the start of visual field testing. Fixation losses are monitored throughout testing by presenting a suprathreshold stimulus in the area of the predetermined blind spot. If the stimulus is detected, it is assumed the patient has lost fixation. When fixation losses are high, re-plotting of the blind spot may address the issue. Determination and tracking of the blind spot as a reliability index are used in both in kinetic perimetry and static perimetry.

CASE REPORT A 46-year-old Egyptian man presented for a full eye exam with the complaint of intermediate blurred vision.

Medical history and family ocular history were unremarkable. He was not taking any systemic medications and he had no known drug allergies. Ocular history included bilateral LASIK surgery performed in Egypt in 2002.

Pre-surgical refractive error was approximately -11.00 DS with -2.00 D of astigmatism in each eye, as reported by the patient.

Best-corrected visual acuities were 6/6 (20/20) in the right (-0.25 -1.75 x 160) and left eye (+0.75 -1.50 x 015) for distance and near. Cover test was normal, eye movements were unrestricted and confrontation fields were full to finger counting in each eye. Pupils were round and reactive to light with no relative afferent pupillary defect detected. Slit lamp biomicroscopy was unremarkable.

Intraocular pressures (IOPs, at 3:20 pm), measured with Goldmann applanation tonometry, were 20 mmHg in the right eye and 23 mmHg in the left eye. Gonioscopy revealed that the angles in both eyes were open to posterior trabecular meshwork in all quadrants. Pupils were dilated using one drop of 1% tropicamide and one drop of 2.5% phenylephrine. Dilated fundus exam revealed mild nuclear sclerosis. Asymmetric optic nerve cupping was noted with vertical cup-to-disc ratios (C/D) of 0.45 in the right eye and 0.60 in the left eye; C/D assessment was difficult due to a large tilt of the nerves. The optic nerve in the right eye followed the ISNT rule and there was a suspicion of thinning of the inferior rim of the left nerve.

In addition, the right nerve was rotated 40 degrees clockwise and the left nerve 30 degrees counterclockwise.

There was no evidence of pallor or edema of the neuroretinal rim in either eye. The vasculature of the fundus

Blind Spot Mapping: A Case Report â&#x20AC;&#x201D; Chong et al

157

Fig. 1 First Humphrey visual field of the right eye with a temporal defect.

Fig. 2 First Humphrey visual field of the left eye showing a temporal defect along with a superior nasal defect.

was normal and there were no holes, tears or breaks of the retina in either eye.

Baseline Humphrey (740i, Carl Zeiss Meditec, Dublin, CA) automated 30-2 threshold SITA-standard visual fields (Figs. 1, 2) were carried out with good reliability (right: fixation losses 3/19, false positives 2%, false negatives 0%; left: fixation losses 2/22, false positives 1%, false negatives 0%). The right eye was within normal limits and the left eye was outside normal limits as determined by the Glaucoma Hemifield Test, which compares sectors of static threshold visual field results from above and below the horizontal meridian for symmetry based on the anatomy of the retinal nerve fiber layer.4 A temporal defect was found in the right eye and a temporal as well as superior nasal defect was found in the left eye. The mean deviations (MD) were -4.97 dB (right) and -8.54 dB (left), indicating the overall depression of the field from the normative database.5 The pattern standard deviations (PSD) were 3.13 dB (right) and 3.59 dB (left), representing the degree of difference between the measured visual field pattern and the normal hill of vision.5 The visual field index (VFI) was 92% (right) and 83% (left), referring to the estimation of the rate of change of glaucoma as a percentage of field loss relative to a group of normal observers.6 The diagnosis of tilted optic discs was made. A tilted optic nerve does not insert at a 90-degree angle into the eye, but rather obliquely, and typically is accompanied by a rotation along the anterior-posterior axis.7 Sequelae of tilted discs typically include myopia and astigmatism, as well as a temporal visual field loss that does not respect the midline, both of which were present in this patient.7 The differential diagnoses included glaucoma, a tumor of the anterior visual pathway and papilledema. The optic nerves did not show any signs of edema or papilledema, color vision was normal and the visual field defects did not respect the midline as would be expected with tumor involvement. The patient was also diagnosed as a glaucoma suspect due to the following risk factors: high myopia,

asymmetric C/D ratios, small optic nerve head with large cupping, rim tissue that did not follow the ISNT rule (left eye), and high IOPs (likely underestimated due to thin corneal tissue or decreased corneal hysteresis secondary to LASIK correction). A repeat Humphrey visual field 30-2 SITA standard test, Spectralis Optical Coherence Tomography (OCT; Heidelberg Engineering, Carlsbad, CA) of the optic nerve and macula, and pachymetry were ordered to further evaluate the risk of glaucoma.

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Follow-Up #1 (2 Weeks Later) A follow-up appointment revealed IOPs to be 19 mmHg in the right eye and 18 mmHg in the left eye at 2:45 pm.

The slight asymmetry of the vertical optic nerve cupping was confirmed by a different clinician with stereoscopic fundus exam and photography (Figs. 3, 4). Humphrey visual field testing (Figs. 5, 6) showed good reliability of the right eye and 19/19 fixation losses in the left eye (gaze tracker was turned off). Similar although smaller defects on the visual field tests were found and the defects were much less dense than previous testing. A repeat visual field was scheduled, along with pachymetry and OCT. Follow Up #2 (10 Weeks Following the First Assessment) The IOPs, by Goldmann tonometry, at 5:13 pm were 24 mmHg in the right eye and 26 mmHg in the left eye; pachymetry was 496 Âľm in the right eye and 495 Âľm in the left eye. The vertical C/D ratios were judged to be 0.7 in the right eye and 0.8 in the left eye by a third clinician and verified with stereoscopic fundus photos. Humphrey visual field testing (Figs. 7, 8) of the right eye continued to be reliable, while the left eye once again showed high fixation losses of 5/19 (26%) and low reliability, despite re-plotting of the blind spot midway through the test.

Humphrey visual field analysis over the three visits showed a consistent temporal defect in the right eye that became smaller and less dense over time and with practice. The left eye also showed a consistent temporal

Fig. 3 Stereo photos of the patient’s right optic nerve. Note the large tilt (40 degrees clockwise) of the optic nerve and no evidence of pallor or edema of the neuroretinal rim.

Fig. 4 Stereo photos of the patient’s left optic nerve. Again, note the tilt (30 degrees counterclockwise) of the optic nerve and no evidence of pallor or edema of the neuroretinal rim.

Fig. 5 Second Humphrey visual field of the right eye showing a mild temporal defect.

Fig. 6 Second Humphrey visual field of the left eye showing a temporal defect. The previously noted nasal defect was not found. Note gaze tracking turned off and high fixation losses (19/19).

defect, along with what was thought to be a superior nasal defect that became less apparent over time.

Imaging with the Heidelberg Retinal Tomography (HRT; Heidelberg Engineering, Carlsbad, CA) and OCT were attempted. Due to the axial length of the patient’s eye and the tilt of the optic nerve, HRT imaging was not possible. The OCT using the Heidelberg Spectralis (Fig. 9) was accomplished with fairly good quality (right: Q = 24, left: Q = 22). The OCT revealed bilateral small optic nerve heads (right: 1.30 mm2, left: 1.44 mm2). The nerve fiber layer thickness plots (TSNIT plots) demonstrated the general shape of two large peaks, although positioned closer together than average for each eye. The positioning of the peaks caused the nerves to be classified as outside normal limits (when compared to the Caucasian database) with thin superior and inferior rim tissue relative to the normative database. When the TSNIT plots were directly compared between the right and left eye, they were quite symmetrical and the height of each peak would have fallen in the normal range had the peaks been recorded in the appropriate location.

When comparing the physical appearance of the optic nerve rim (structure) to the trend of visual field

defects detected by the three tests performed to this point (function), the temporal defects detected corresponded to tilted nerves. The left eye initially (first field) showed the start of an arcuate defect superiorly which would align with the initial speculation that there was inferior thinning of the left optic nerve. The suspected defect was not repeatable, although reliability of the tests was low due to high fixation losses. The OCT showed thinning of the superior nerve fiber layer (NFL) in the left eye and potentially both superior and inferior temporal thinning for both eyes. The latter would potentially correspond to an inferior field defect as well as nasal defects, which were not demonstrated by the visual field tests of the patient.

Follow Up #3 (5 Months Later) At a fourth appointment, plotting of the blind spot (Octopus 900; Haag Streit, Mason, OH) using static perimetry (Fig. 10) showed only two absolute defects corresponding to the patient’s blind spot (right eye) that were not within the shaded area for the typical optic nerve, but were shifted closer to the fovea. The minimum number of points that may encompass the average optic nerve (blind spot) with this method was 11, which is

Blind Spot Mapping: A Case Report — Chong et al

159

Fig. 7 Third Humphrey visual field of the right eye with a temporal defect.

Fig. 8 Third Humphrey visual field of the left eye with a temporal defect.

High fixation losses (5/19) causing test to have low reliability.

of the blind spot indicated that it was located at (right eye) and/or just below (left eye) the horizontal meridian.

Visual field testing (Figs. 12, 13) was repeated with the Octopus 900 and the right eye was performed reliably with a temporal defect. The test of the left eye was also reliable with a temporal defect and scattered nasal defects.

DISCUSSION

Fig. 9 OCT using the Heidelberg Spectralis showing symmetrical TSNIT plots with shifted peaks, although the nerves were classified as outside normal limits.

far greater than the two points that were absolute defects for this patient. In the left eye, the absolute defect was also closer to the fovea than the outlined normal optic nerve and there was only one spot that defined the patient’s blind spot. However, the majority of the points had a relative defect. When using the kinetic module (Octopus 900, Fig. 11) for plotting the blind spot, it was found to be less than a few degrees round in both the right and left eye, as well as shifted towards the foveae in each eye. The speed of the target was slightly higher than that typically used and this could account for the small size of the nerve, although this finding was consistent on both tests, static and kinetic. Both tests for determining the size

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The patient was being monitored for glaucoma due to his risk factors that included high myopia, high IOPs, large cupping in a small disc and loss of the ISNT rule of the neuroretinal rim. Visual fields are integral for monitoring glaucoma progression and can be quite difficult to interpret when the results are unreliable. Fixation losses are a common cause of poor reliability and can be attributed to the patient’s ability to perform the test or due to technical artifacts.2 In this case, they were likely due to the patient’s very small blind spot from which fixation was monitored.

When the test was set up accurately (Figs. 1, 2) and the patient was able to maintain fixation, there was good reliability. If not positioned correctly, fixation losses were high (Fig. 6), although the depth of the defects was shown to decrease slightly. By re-plotting the blind spot mid-way through testing, the fixation losses decreased but results were still unreliable (Fig. 8). Fixation losses, measured using the Heijl-Krakau method, can occur for other reasons than unsteady gaze, such as the initial blind spot plotted at the edge of a scotoma, a head tilt or an alteration in head position.8 It is suggested that when fixation losses are high, the other reliability indices should be taken into consideration to determine whether the visual field should be included for analysis.8 The assertion that the small blind spots were causing high fixation losses was hypothesized due to the severity of the patient’s tilted disc on fundus exam. The patient’s optic nerves were found to be structurally smaller than average by OCT, which was confirmed functionally when the blind spots were found to be smaller and closer to the fovea using the static and kinetic perimetry available on the Octopus 900. The OCT measurements of the optic

Fig. 10 Mapping of the blind spot using static perimetry, left and right eye.

Fig. 11 Mapping of the blind spot using static perimetry on the Octopus 900, left and right eye showing very small areas of absolute defect corresponding to the blind spot.

Fig. 12 First visual field using the Octopus 900 of the right eye showing a temporal defect.

Fig. 13 First visual field using the Octopus 900 of the left eye showing a temporal defect with scattered nasal defects.

disc surface area were 1.30 mm2 in the right eye and 1.44 mm2 in the left eye, which is much smaller than the average optic disc surface of 2.69 mm2.9 Re-plotting of he blind spot multiple times throughout testing may be necessary to ensure a reliable test result.

The patient performed the initial Humphrey visual field well but fixation losses on every additional field were very high and caused the field to be labeled unreliable. The variability could be attributed partially to the difference in skill between technicians administering the tests. The visual field carried out on the Octopus did not indicate any fixation losses but this was due to the type of fixation monitoring system used. The Octopus 900 has a monitoring system that includes fixation control and automated eye tracking to detect and compensate for patient’s blinking, and an automatic chin rest adjustment to account for a patient’s movement during testing. The HFA used was equipped with a gaze tracking system but the newer models (HFAII-i 750i) also have eye tracking that includes the ability to automatically align the head and eye as well as a vertex monitor to indicate if the patient has moved too far away. Older HFA models use the HeijlKrakau method that initializes a point for the blind spot and continues to check the same spot periodically throughout testing.8

Overall, the visual field tests performed by this patient demonstrated temporal defects as well as inconsistent nasal defects. The temporal defects did not respect the midline, which made a neurological etiology less likely. The defects were becoming more distinct and smaller over a period of time, which could be attributed to the patient’s learning curve with the test. When reviewing MD and the PSD for the right and left eyes separately, they were fairly consistent between visits and between the two different visual field units used. The average MD, from the Humphrey visual fields, for the right eye (Figs. 1, 5, 7) was -4.27 ± 1.21 dB (± standard deviation) and the average PSD was 2.87 ± 0.23 dB (± standard deviation). These values were very similar to those found on the Octopus visual field, MD of -4.20 dB and PSD of 3.40 dB (Fig. 12). The average MD from the Humphrey visual fields for the left eye (Figs. 2, 6, 8) was -7.70 ± 1.02 dB (± standard deviation) and the average PSD was 3.19 ± 0.39 dB (± standard deviation). These values were also very similar to those found on the Octopus visual field, MD of -7.00 dB and PSD of 4.00 dB (Fig. 13). The PSD values on both units were quite similar between the eyes and the asymmetry of the MD was consistent on both units. This depression may be due to a reduction in retinal sensitivity due to a potentially diffusely hypoplastic nerve that occurs with a tilted disc.7

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161

Of note, the blind spots were missing on all the grey scales of the Humphrey visual fields.

The OCT images confirmed that the patient’s optic nerves were small which correlated well with the small blind spots on perimetry. The normative databases of the OCT are not useful when analyzing an atypical optic nerve head and nerve fiber layer, which was the case for this patient. It is referred to as “red disease” when an area is marked as abnormal and said to be outside the range of the database due to a misinterpretation.10 When the OCT was further analyzed including the average thicknesses of the superior and inferior nerve fiber layer, a slightly different pattern of the TSNIT plot than normal was found, although symmetry was noted between the right and left eye which appeared to indicate that the patient likely did not have glaucoma. Upon investigation, the peaks on our scan, the OCT misinterpreted the NFL thickness and included a blood vessel in its calculation. Retinal blood vessels create a barrier on the OCT scan so that imaging cannot be done on tissue located beyond the blood vessel; it appears as if there is only white space below the blood vessel. The peaks of tissue for our patient corresponded to the areas where blood vessels are found. This accounts for the initial symmetry that was noted and does not correctly identify the NFL. Of note, the OCT NFL scan has a standard 3.4 mm diameter circle location. The position of the scan circle can have an effect on the measurements of the thickness of the NFL and the peaks, which typically indicate the thickest area of NFL can be shifted and will not align with that of the printout.11 The nature of the scan would create peaks that fell further apart than the normative database with a small optic nerve head and closer together for a large optic nerve head. Ultimately the OCT did not definitively indicate the thickness of the patient’s NFL. However, since the OCT will most likely continue to scan this patient in the same manner on each visit, it can still be used as a tool for monitoring change in apparent thickness of the NFL. This patient had several risk factors for glaucoma, including high myopia, high IOPs (potentially higher than recorded because of the altered cornea post-LASIK) and large C/D ratios in small optic nerves. The patient’s recorded IOP values were in the upper range of normal (18 to 26 mmHg). This actually may have been underestimated due to the decrease in corneal hysteresis, a biomechanical property of the cornea or the difference in the bending properties as the pressure is assessed using applanation also known as the elasticity.12 Studies have shown that a decreased corneal hysteresis is commonly associated with a decreased central corneal thickness.

Both are risk factors for the development of glaucoma, independent of IOP, because they may represent weakness in the structure of the eye which could encompass the lamina cribrosa.12 This patient did not have a family history of glaucoma and had no systemic risk factors. Both the visual field defects and the OCT findings were attributed

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to the patient’s tilted optic nerve anatomy. The absence of a blind spot on the HFA was likely due to the small size of the optic nerve combined with the tilt of the optic disc, confirmed by blind spot mapping using the Octopus visual field and OCT imaging. This patient has not yet been diagnosed with glaucoma, but due to the risk factors, warrants close monitoring. Comparisons with the patient’s own data (rather than with normative data) will be the best way to establish the presence of glaucomatous changes, which will include both serial visual field and OCT measurements. Both visual field and OCT measurements are expected to remain stable in a patient with a tilted disc, but are expected to progress in the presence of glaucoma.

If visual field tests continue to be unreliable, serial OCTs may be the best tool for monitoring. A diurnal measurement of IOPs should also be considered to determine the extent of pressure fluctuation.

CONCLUSION It is important to remember that there can be anomalies identified by technology that defy typical interpretation, especially when the patient does not fall within the parameters defining normative databases. The information that we obtain from our various instruments should be critically analyzed and integrated to extract the necessary valuable information. ❏

REFERENCES 1.

Newkirk MR, Gardiner SK, Demirel S, Johnson CA. Assessment of false positives with the Humphrey Field Analyzer II perimeter with the SITA Algorithm. Invest Ophthalmol Vis Sci 2006: 47(10): 4632-4637.

2. Katz J, Sommer A. Reliability indexes of automated perimetric tests. Arch Ophthalmol 1988; 106(9): 1252-1254.

3. Sanabria O, Feuer WJ, Anderson DR. Pseudo-loss of fixation in automated perimetry. Ophthalmology 1991: 98(1); 76-78.

4. Asman P, Heijl A. Glaucoma Hemifield Test. Automated visual field evaluation. Arch Ophthalmol 1992; 110(6): 812-819.

5. Yaqub M. Visual fields interpretation in glaucoma: a focus on static automated perimetry. Community Eye Health 2012; 25(79-80): 1-8.

6. Artes PH, O’Leary N, Hutchison DM, Heckler L, et al.

Properties of the Statpac Visual Field Index. Glaucoma 2011; 52(7): 4030-4038.

7. Witmer MT, Margo CE, Drucker M. Tilted optic disks. Surv Ophthalmol 2010; 55(5): 403-428.

8. Nema HV, Nema N. Diagnostic Procedures in Ophthalmology.

New Delhi: Jaypee Brothers Medical Publishers, 2003.

9. Jonas JB, Gusek GC, Naumann GO. Optic disc, cup and neuroretinal rim size, configuration and correlations in normal eyes.

Invest Ophthalmol Vis Sci 1988; 29(7): 1151-1158.

10. Chong GT, Lee RK. Glaucoma versus red disease: imaging and glaucoma diagnosis. Curr Opin Ophthalmol 2012; 23(2): 79-88.

11. Gabriele ML, Ishikawa H, Wollstein G, Bilonick RA, et al.

Optical coherence tomography scan circle location and mean retinal nerve fiber layer measurement variability. Invest Ophthalmol Vis Sci 2008; 49(6): 2315-2321.

12. Abitbol O, Bouden J, Doan S, Hoang-Xuan T, et al. Corneal hysteresis measured with the Ocular Response Analyzer® in normal and glaucomatous eyes. Acta Ophthalmologica 2010; 88(1): 116-119.

28:4, 17

COPE-APPROVED CE CREDIT APPLICATION FORM

INSTRUCTIONS FOR 1 HOUR OF

CE CREDIT

This encore course is valid for 1 hour of COPE-approved CE credit, to be taken no later than April 1, 2019.

If you score 70% or more on the test questionnaire, a COPE CE Credit Certificate will be sent to you.

TO TAKE AND SUBMIT THIS TEST ONLINE Begin by clicking <HERE> and follow the onscreen instructions.

If you are a Pre-Paid test subscriber, you will automatically be directed to the test questionnaire. Once successfully completed, you will automatically be forwarded a personalized 1-Hour COPE CE credit certificate by email.

If you are not a Pre-Paid test subscriber, you will automatically be directed to PayPal inorder to purchase this test. Following payment, you will automatically be directed to the test questionnaire.

TO TAKE AND SUBMIT THIS TEST OFFLINE If you are a Pre-Paid test subscriber, download a copy of this form, fill in the information requested below in the IDENTIFICATION section, and then answer each of the 10 multiple choice questions in the QUESTIONNAIRE section. Please mail this form to the address shown below.

If you are not a Pre-Paid test subscriber, download a copy of this form, fill in the information requested below in the IDENTIFICATION section, and then answer each of the 10 multiple choice questions in the QUESTIONNAIRE section. Please mail this form to the address shown below along with a cheque for $25 made payable to Mediconcept Communications.

Mail to: CRO 3484 Sources Blvd., Suite 518, Dollard-Des-Ormeaux, QC H9B 1Z9, Canada

IDENTIFICATION Name: First______________________________ Last___________________________________ Address:________________________________________________________________________ Number

Street

Suite

_______________________________________________________________________________ City

Province

Professional License Number:_______________ Office Phone: (

Postal Code

) _______________________

E-mail: ________________________________________________________________________

QUESTIONNAIRE Blind Spot Mapping: A Case Report Stacey Chong, OD, et al 1.

(A) (B) (C) (D) 2.

(A) (B) (C) (D)

When comparing normal patients and those with glaucoma, what percentage had unreliable fields as determined by a failure to meet the criterion outlined by the manufacturer?

15% and 35%, respectively 20% and 40%, respectively 30% and 45%, respectively 45% and 50%, respectively With the Humphrey Visual Field Analyzer (HFA), where fixation losses were greater than 20%, what amount was caused by technical artifacts?

Nearly one-quarter Nearly one-third Nearly half Nearly three-quarters

Blind Spot Mapping: A Case Report â&#x20AC;&#x201D; Chong et al

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(A) (B) (C) (D) 4.

Re-plotting the blind spot during testing has the potential to decrease the frequency of unreliable test results secondary to excessive fixation losses by what amount?

From 25% to 10% From 33% to 14% From 35% to 13% From 40% to 10%

(A) (B) (C) (D)

The manufacturer of the HFA has stated that false positives and negatives should not be greater than what amount?

15% 20% 25% 33%

5.

(A) (B) (C) (D)

All of the following clinical signs describe the patient in the Case Report presented, EXCEPT: Abnormal cover test Unrestricted eye movements No relative afferent pupillary defect Unremarkable slit lamp biomicroscopy

6.

(A) (B) (C) (D)

In the Case Report presented, dilated fundus exam revealed all of the following, EXCEPT: Mild nuclear sclerosis Left nerve was rotated 40 degrees clockwise Asymmetric optic nerve cupping Right nerve was rotated 40 degrees clockwise

7.

(A) (B) (C) (D)

In the Case Report presented, what was the patientâ&#x20AC;&#x2122;s visual field index (VFI)?

75% (right) and 63% (left) 82% (right) and 75% (left) 90% (right) and 73% (left) 92% (right) and 83% (left)

8.

(A) (B) (C) (D)

The Case Report presented revealed all of the following optic nerve findings, EXCEPT: Abnormal color vision No signs of edema No signs of papilledema Normal color vision

9.

(A) (B) (C) (D)

In follow-up #2 in the Case Report presented, Humphrey visual field testing revealed what percentage of fixation losses?

22% 25% 26% 28%

10.

(A) (B) (C) (D)

The manufacturer of the HFA has stated that fixation losses should not be greater than what percentage?

10% 15% 18% 20%

28:4, 17

COPE-APPROVED CE CREDIT APPLICATION FORM

3.

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Clinical and Refractive Optometry 28:4, 2017

Case Consultations CRO is pleased to present this second case in the Case Consultations Series by Dr. Henry Reis. The patient is a controlled diabetic with untreated Rosacea presenting with complaints of “gritty eyes” for which he has been self-medicating without success using Visine. Six randomly selected optometrists from across the country have been asked to review this case and recommend a specific treatment plan for this patient based entirely on their anecdotal experience. Their unedited recommendations have been reproduced below exactly as they were received. Please let us know how they compare to yours.

Refraction/BCVA • OD: -4.75/sph 20/20 J1; OS: -4.50/sph 20/20 J1 Slit Lamp Examination • Moderate MGD, Demodex [-], LWE [+] • Mild conjunctival injection; diffuse SPK 1+/4+ present • No other abnormalities seen

Henry Reis, MD Burnaby, BC CASE DESCRIPTION RMS, is a 33-year-old software programmer presenting with a chief complaint of gritty, red eyes, mostly at work for the last year. He has been using Visine Red Eyes p.r.n., without much relief.

Ocular History • Blepharitis – chronic; has used warm compresses intermittently over the last month • No history of contact lens wear • Happy with current glasses (-4.50/sph OU providing 20/20 J1)

Dilated Fundus Examination • ONH: 0.40x0.30 OD; 0.35x0.35 OS • Vitreous: OU floaters • Macula: OU clear • Posterior pole: OU clear • Peripheral retina: OU clear and flat, no holes/breaks Tear Osmolarity (i-Pen) • OD: 322 mOsm/L; OS: 318 mOsm/L SM Tube • OD: 2 mm; OS: 1 mm Oculus Keratograph • NIKBUT 3s OD; 4s OS • Abnormal lipid layer (irregular pattern) • Receded meibomian glands with drop-out OU 2+/4+

Medical History • DMI – controlled with Insulin • Rosacea – not being treated at the moment Allergies • NKDA; no environmental allergies

Questions for the Case Consultations Panel 1.

2.

3.

4.

5.

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What type of treatment regimen would you recommend for this patient and would that treatment regimen include the regular use of an eye drop?

Do you usually recommend a specific type of eye drop, or do you usually leave the choice of a specific eye drop up to the patient?

If you do recommend a specific type of eye drop, what essential ingredients do you want that eye drop to contain and why?

From your experience, is compliance with an eye drop regimen an issue; and if yes, what do you feel are the main reasons for noncompliance?

Do you usually schedule a return-to-clinic visit in order to assess your patient’s progress; and if you do, in what time interval?

Clinical and Refractive Optometry 28:4, 2017

Ben Barrus, OD Calgary, AB The treatment regimen I would recommend for this patient is: 1) stop use of Visine; 2) i-drop hyaluronate artificial tear stabilizing drops to improve tear retention time, increase TBUT and reduce dry eye discomfort; 3) 4-5 g re-esterified Omega-3 targeting more than 1500 mg EPA daily; and 4) prescribe topical ivermectin 1% and/or metronidazole 1% daily for 3 months to manage Demodex induced meibomian gland dysfunction (MGD) and anterior blepharitis.

I prescribe an unpreserved artificial tear in all cases.

In instances of rapid tear breakup I prefer a hyaluronatebased drop. If TBUT is good, then using a saline drop to improve osmotic balance is helpful.

Hyaluronate is my preferred stabilizing agent.

There are several stabilizing additive drops on the

market but I find that they provide less consistent results than i-drop. My second choice is Hylo. I do not use Hylo-Dual.

From my experience, I do not feel compliance is an issue. Showing the patient the results and explanation using images or photos generally creates very good compliance.

I see patients back for dry eye follow-up on a 3-month re-visit schedule. When treating Demodex infection I often see them back in 6 weeks to ensure compliance and clinical signs are improving. Following Demodex eradication I assess MGD for improvement from baseline. If improvement is not sufficient, then referral for LipiFlow or IPL treatment is arranged. In the case presented above I would anticipate that the patient would have facial rosacea and as such I would anticipate and educate the patient with an eye towards referring him for IPL at our 3-month visit.

Susana Sebestyen, OD, FAAO Oakville, ON My short treatment regimen for this patient would be to replace Visine with an artificial tear such as i-drop Pur, Hylo, or Hyabak which not only builds up the lipid layer and tear volume but also has an anti-inflammatory property. I would also add Thealoz to help restore the epithelium and address the lid wiper epitheliopathy. I would address the blepharitis in the short term with i-lid ’n lash pads and Bruder Mask compresses followed in 3-4 weeks with BlephEx/debridement treatment.

For long-term treatment, I would prescribe Doxycycline Hyclate 100 mg per day for 1 month, and then drop this down to 50 mg for another month, and continue every other day for another 2 months as maintenance. I would also ask the patient to start taking Omega-3 triglyceride supplements at 2000-3000 mg per day. I always try to emphasize to my patients that symptomatic relief will not cure dry eye disease or meibomian gland dysfunction, but that effective treatment will protect their ocular surface and help maintain clear and comfortable vision.

I always prescribe a specific eye drop. I find that when I let the patients select their own drops they tend to be less compliant. They sometimes start mixing and matching different commercial eye drops, and in turn that can compromise the effectiveness of the prescribed treatment regimen. I prefer non-preserved drops, containing hyaluronate and lipid building ingredients such as i-drop Pur, i-drop Pur Gel and Hylo Gel for nighttime use.

I’ve found that compliance becomes a significant issue when patients become less symptomatic. When that happens, I point out that dry eye disease is a vision disease, and when I feel that it’s necessary to reinforce that point, I challenge my patients to keep their eyes open for a full minute to see if it affects their vision, and it always does.

As for follow-up visits, I tend to call patients back in as little as 1-2 weeks. If the treatment protocol is working well and I feel that the patient is compliant, I may schedule the next follow-up visit in 6 months. I hardly ever leave it longer than that, even if it’s just to re-educate the patient or to enhance their treatment regimen with other possibilities.

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Edward Chow, OD Markham, ON My treatment plan would be the following: 1) discontinue Visine immediately as it may exacerbate his dry eye; 2) perform an in-office hot compress and manual gland expression; 3) prescribe Lotemax Gel q.i.d. x 2 weeks and b.i.d x 2 weeks; 4) lipid based emulsions such as Systane Balance q.2h; 5) preservative-free artificial tears with hyaluronan such as i-drop Pur q.i.d.; 6) Bruder heating mask at home q.d. x 8 mins; 7) triglyceride-based omega-3 fatty acid q.d.

(1,800 mg EPA+DHA); 8) consider doxycycline 50 mg p.o. q.d. but in Ontario, we are limited to 14 days of oral antibiotic treatment. I would refer him to his family physician to treat for the rosacea as indicated.

I always recommend specific eye drops to my patients as patients are indecisive.

I recommend preservative-free eye drops as preservatives are known to promote inflammation and reduce cellular viability. I also recommend hyaluronate as it is the only natural substance found within the eye that has viscoadaptive and corneal regenerative properties. For the very severe dry eye, I use a bioprotectant such as trehalose or ectoine to prevent osmotic degradation.

Compliance is always an issue because we all know that life gets in the way and patients forget to use eye drops. The key to proper compliance is patient education.

I schedule a follow up after 2 weeks to ensure compliance and to check for progress and tailor the treatment accordingly.

Jules Plante, OD, MSc, FAAO Montreal, QC This patient is demonstrating a potentially severe mixed dry eye condition, as shown by the highly positive tear osmolarity measure, short tear break-up time and diffuse superficial punctate keratitis. Clinical signs are pointing toward both aqueousdeficient dry eye (SM Tube reduced and signs of lid wiper epitheliopathy) and evaporative dry eye (meibomian gland drop-out, abnormal lipid layer) possibly aggravated by chronic blepharitis and rosacea. Considering his rather young age, his environment (intensive computer usage) and the fact that he is affected by diabetes, I would go for an aggressive treatment plan to avoid long-term exacerbation of his ocular condition.

The meibomian gland dysfunction component has to be treated either with warm compresses or thermopulsation (LipiFlow) and daily Omega-3 (2000 mg to 3000 mg). Inflammation needs to be controlled with a soft

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steroid (Lotemax Gel) t.i.d. for 2 weeks and b.i.d. for another 2 weeks. The aqueous deficiency has to be treated by lubricant unpreserved eye drops composed of sodium hyaluronate (i-drop Pur and/or i-drop Pur Gel) used 4 times daily and cyclosporine A 0.05% b.i.d.

(Restasis). The patient should also use lid scrubs and warm compresses on a daily basis.

I usually prescribe sodium hyaluronate nonpreserved drops for its viscoelastic properties and I encourage the patient to be compliant with the scheduled regimen. I also stress the importance of using nonpreserved eye drops and explain to the patient that all eye drops are not equal.

I believe that the main reasons for noncompliance are misunderstanding of the condition and poor relief of the ocular irritation. To avoid this, I usually prefer to prescribe a moderately viscous gel drop, for which the residency time is longer than traditional eye drops.

Finally, I schedule a follow-up within 3 months to confirm the treatment effectiveness.

Francis Gaudreault, OD Quebec City, QC

Krista Flynn, OD Kingston, NS

The primary defect in ocular rosacea is the meibomian gland inflammation leading to meibomian gland dysfunction (MGD) and gland atrophy. These result in eyelid margin erythema, telangiectasia, inspissated meibomian gland orifices and blepharitis.

Chronic inflammation will also cause a loss of lacrimal gland secretions.

Both quantitative and qualitative abnormalities of the tear film should cause hyperosmolarity. Every patient with ocular rosacea like this patient should have a long-term therapy because of the chronicity of the condition. Consider LipiFlow to clear the blocked glands and restore normal function of the residual meibomian glands. Treat the inflammation with a topical steroid such as Lotemax Gel q.i.d. x 14 days and b.i.d. x 1 month. Start topical cyclosporine (Restasis) twice daily for long term. The anti-inflammation effect of Restasis on the ocular surface associated with tear production augmentation will improve the signs and symptoms of this patient. Lid hygiene and Omega-3 supplements (Systane Vitamins) would also be recommended every day. Warm compresses like Bruder Moist Heat Eye Compress should be done two to three times a week to maintain the effect of the LipiFlow. The use of an eye drop should be as needed.

I always recommend a specific eye drop depending if it’s an aqueous tear deficiency or an evaporative dry eye.

Every drop has a different function and is more effective depending on the type of disorder. i-drop Pur Gel is preservative free, it hydrates and stabilizes the tear film very well in mostly all cases. Refresh Optive Fusion preserved with gentle Purite is good for aqueous deficiency and against hyperosmolarity. I also use Refresh Optive Advanced for patients who need a lipid-based tear.

Ideally, I use preservative-free eye drops. If not, I use drops with a gentle preservative such as Purite. Hyaluronic acid is an essential ingredient. Also, viscoelastic properties ensure a superior moistening and a long-lasting comfort.

Some patients will not be compliant if we don’t take enough time to explain the real benefits of theses eye drops and why it’s so important for their condition. They will return to a less expensive eye drop.

The patient should have a 3-month follow-up.

Consider oral doxycycline if needed. Apprilon 40 mg once daily for 2 months is my first choice.

The primary goal would be to start this patient on a regime that will focus on treating their chronic meibomian gland dysfunction (MGD). This would consist of warm compresses (Bruder) 10 min q.d., lid wipes (i-lid ’n lash Plus) daily and Omega-3 supplementation (Ascenta EPA+).

Because of the increased osmolarity and low tear volume, I would start them on an artificial tear containing sodium hyaluronate t.i.d. and reassess in 6 weeks. Adding Maxitrol ung to lid rims q.h.s OU x 1 month would be considered if significant blepharitis and inflammation remained at follow up.

My preference is to recommend a specific eye drop to patients based on the findings of their examination. For patients with a higher osmolarity (>320) or eyes that appear more inflamed with any level of MGD, I prescribe a tear containing sodium hyaluronate (Refresh Fusion, Hylo or i-drop Pur Gel). I prefer non-preserved artificial tears for patients that require a t.i.d.+ dosing. I will recommend a lipid-based tear (Refresh Optive Advanced or Systane Balance) to those patients who have a lower osmolarity with mild to moderate MGD. In my experience, compliance can become an issue for patients who: experience stinging on insertion, who feel the drops are not helpful, or once they become symptom free. To improve compliance, I usually schedule multiple follow-up visits from 6 weeks.

Summary of Treatment Recommendations For Meibomian Gland Dysfunction Bruder Mask Omega-3 LipiFlow Manual Gland Expression For Inflammation Lotemax Restasis For Hyperosmolarity i-drop Hylo Systane Refresh Essential Eye Drop Ingredient Hyaluronate Is Compliance an Issue?

Yes No Next Scheduled Follow-Up Visit In 2 Weeks In 6 Weeks In 12 Weeks

6 out of 6 6 out of 6 3 out of 6 1 out of 6 3 out of 6 2 out of 6 6 out of 6 3 out of 6 2 out of 6 2 out of 6 6 out of 6 5 out of 6 1 out of 6 2 out of 6 1 out of 6 3 out of 6

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News and Notes Lyndon Jones named as a Fellow of the Canadian Academy of Health Sciences Lyndon Jones, a Professor at the School of Optometry and Vision Science, and Director of the Centre for Contact Lens Research at the University of Waterloo, has been awarded a Fellowship of the Canadian Academy of Health Sciences (CAHS).

Induction as a Fellow is “considered one of the highest honors within Canada’s academic community.

CAHS Fellows, who serve as unpaid volunteers, are nominated by their institutions and peers and selected in a competitive process based on their internationally recognized leadership, academic performance, scientific creativity and willingness to serve.”

Lyndon is also a Fellow and Diplomate of the American Academy of Optometry (AAO), and he has been awarded a number of national and international awards.

“The CAHS is a prestigious organization with people from many sectors of health science and I feel very honored to be inducted as a Fellow. This fellowship is a reflection of not only my own achievements, but also those of my former graduate students, postdocs and colleagues who I have had the privilege of working with over the past 25 years, particularly my colleagues within the Centre for Contact Lens Research and the School of Optometry and Vision Science at the University of Waterloo,” said Lyndon.

Congratulations Lyndon and thank you for your leadership and dedication! We wish you continued success from everyone at the UWaterloo School of Optometry and Vision Science.

Bausch + Lomb Introduces Ocuvite Eye Vitamin Adult 50+ Formula Minigels Bausch + Lomb recently announced the launch of Ocuvite® Adult 50+ Formula Minigel daily eye vitamins that help replenish vital nutrients that eyes can lose as they age. The new minigels, which will replace the currently offered Ocuvite Adult 50+ soft gels, now include highly concentrated fish oil, helping to make them 25% smaller and easier to swallow.

“I often recommend Ocuvite Adult 50+ Formula as a supplement for my patients who want to take a more proactive role in supporting their eye health. I’ve found that some patients are unaware of the benefits of an eye vitamin, while others claim pill size and difficulty swallowing as reasons why they won’t take them,” said Jeffry Gerson, an optometrist from Grin Eye Care in Leawood, Kansas. “People take vitamins to maintain their overall health, but often don’t think that vitamins have a role in eye health. With the introduction of Ocuvite Adult 50+ Formula Minigels, I will have the opportunity to convince my otherwise skeptical patients to begin taking an eye vitamin.”

For more information on Ocuvite Adult 50+ Vitamins, visit www.bausch.ca.

SEE additional safety information on page 170

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