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Clinical & Refractive Optometry VOLUME 28, NUMBER 5, 2017

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New Onset Rotary Nystagmus in a Patient with Chiari Malformation Transient Vision Loss: Getting to the Heart of the Problem Corneal Phlyctenule in a Steroid Responder Clinical Grading of Nuclear Sclerotic Cataracts

Clinical&Refractive Optometry

Editorial Board • Volume 28, Number 5, 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.

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Clinical&Refractive Optometry Contents • Volume 28, Number 5, 2017

CE CREDIT ARTICLES 173 New Onset Rotary Nystagmus in a Patient with Chiari Malformation Leonid Skorin Jr., OD, DO, MS, FAAO, FAOCO ABSTRACT: Malformations of the cervico-medullary junction, the connection between the brain and spine, are present in approximately one percent of live births. The most common cervico-medullary junction malformations are Chiari malformations (CMs). The majority of congenital CMs are asymptomatic, with symptoms often appearing in adolescence or later adult life and expressing wide variability depending on the involved brainstem area and the degree of pressure applied to this area. Pathogenesis is incompletely understood. Surgery is the treatment of choice to relieve functional problems with posterior fossa decompression being the most common procedure.

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Transient Vision Loss: Getting to the Heart of the Problem Oakley Hayes, OD; Nathan A. Whitaker, OD, FAAO

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ABSTRACT: Patent foramen ovale (PFO) represents a congenital defect in the wall between the atrial chambers of the heart. In the womb, the fetus relies on oxygen-rich blood from the mother which is shunted through this opening bypassing the developing lungs. In 80% of cases, the foramen closes spontaneously and is absent by birth. Herein, we report the case of a 61-year-old male who presented with transient vision loss in his right eye. After a thorough hematologic and cardiovascular evaluation, his symptoms and clinical findings were attributed to a previously undiagnosed PFO. The causes of transient vision loss are varied and the rarity of this case serves as a reminder of the importance of cardiovascular considerations among patients with similar clinical presentations.

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Corneal Phlyctenule in a Steroid Responder Michelle Steenbakkers, BSc (Hons), OD, FAAO

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ABSTRACT: The management of phlyctenulosis includes the use of topical anti-inflammatory agents; therefore the patient must be monitored for adverse drug reactions. In patients with documented steroid-induced elevation of IOP, alternative treatment for phlyctenulosis should be considered.

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Clinical Grading of Nuclear Sclerotic Cataracts Paul Varner, OD, MPH

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ABSTRACT: Widespread clinical use of grading scales facilitates patient care. Many cataract classification schema have been proposed, but without universal acceptance. Purpose: To discern why there is no consensus for grading nuclear sclerotic cataracts (NSC). Method: A NSC grading method involving anterior and posterior segment correlation was developed for clinical use. Results: This correlation method for grading NSC failed initial standardization testing. Conclusion: Current macroscopic, NSC grading scales appear unable to account for microscopic, lenticular variations, and are not useful clinically. Relevance: Newer technology will be required to achieve objective assessment for NSC.

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NEWS & NOTES

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

Courtesy of: Dr. Michelle Steenbakkers Note the area of central ulceration in the corneal phlyctenule (white arrow).

CE Credit Article Clinical & Refractive Optometry is pleased to present this continuing education (CE) article by Dr. Leonid Skorin entitled New Onset Rotary Nystagmus in a Patient with Chiari Malformation. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit, please refer to page 177 for complete instructions.

New Onset Rotary Nystagmus in a Patient with Chiari Malformation Leonid Skorin Jr., OD, DO, MS, FAAO, FAOCO

ABSTRACT Malformations of the cervico-medullary junction, the connection between the brain and spine, are present in approximately one percent of live births. The most common cervico-medullary junction malformations are Chiari malformations (CMs). The majority of congenital CMs are asymptomatic, with symptoms often appearing in adolescence or later adult life and expressing wide variability depending on the involved brainstem area and the degree of pressure applied to this area. Pathogenesis is incompletely understood. Surgery is the treatment of choice to relieve functional problems with posterior fossa decompression being the most common procedure.

cerebellar tonsils 3 to 5 mm or greater below the FM.3 When the indented bony space at the inferoposterior of the skull is smaller than normal, the cerebellum and brainstem can be pushed downward. The resulting pressure on the cerebellum can block the flow of cerebrospinal fluid (CSF).4 An undersized FM can result in similar affects.

CLASSIFICATIONS OF CHIARI MALFORMATIONS CMs are classified by both anatomical characteristics and symptom severity. Type I CM involves the cerebellar tonsils (the lower part of the cerebellum) protruding caudally into the FM, without involving the brainstem. Type I, which may not cause symptoms, is the most common form of CM and is often asymptomatic until adolescence or early

INTRODUCTION The Chiari malformation (CM) is an abnormality that affects the cerebellum at the level of the cervicomedullary junction. There are several different forms ranging from Type I, the most common form, through Type IV in order of increasing severity with Types I, II and III being the primary forms. Most cases of CM are congenital.1,2 In normal anatomy, the cerebellar tonsils are located just above the top horizontal line as illustrated in Figure 1 which identifies the level of the foramen magnum (FM). In an individual with CM, the tonsils hang below the line as illustrated in Figure 1, indicating herniation into the spinal canal. The degree to which the tonsils extend inferiorly can vary significantly.1,2 Cerebellar displacement is a fairly common finding with magnetic resonance imaging (MRI). CM Type I is radiographically defined as a simple displacement of the L. Skorin, Jr. â&#x20AC;&#x201D; Consultant, Community Division of Ophthalmology, Mayo Clinic Health System, Albert Lea, MN; Assistant Professor of Ophthalmology, Mayo Clinic College of Medicine, Rochester, MN Correspondence to: Dr. Leonid Skorin, Jr., Mayo Clinic Health System, 404 West Fountain Street, Albert Lea, MN 56007; E-mail: Skorin.leonid@mayo.edu The authors have no financial or proprietary interest in any of the material mentioned in this article. This article has been peer reviewed.

Fig. 1 Sample comparison MRI showing level of the foramen magnum (horizontal red line), herniated cerebellar tonsils and syrinx. Reprinted with permission from: Milhorat TH, Nishikawa M, Kuyla RW, Dlugacz YD. Mechanisms of cerebellar tonsil herniation in patients with Chiari malformations as guide to clinical management. Acta Neurochir (Wein) 2010; 152(7): 1117-1127.

New Onset Rotary Nystagmus in a Patient with Chiari Malformation â&#x20AC;&#x201D; Skorin Jr.

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Fig. 2 MRI of the discussed patient showing cerebellar tonsils pegged and protruding through the foramen magnum for a distance of 2.5 cm with mild ventricular dilation.

adulthood. It is often identified as an incidental finding during an examination for another condition. Type I is the only type of CM that can be acquired.5,6 Type II CM, is also called classic CM. The term Arnold-Chiari malformation, often misapplied, is specific to Type II. It involves the extension of both cerebellar and brainstem tissue into the FM. Also, the cerebellar vermis (the nerve tissue that connects the two halves of the cerebellum) may be only partially complete or absent.5 Type II is often accompanied by a myelomeningocele which usually results in partial or complete paralysis of the area below the myelomeningocele, a form of spina bifida.5,6 In Type III CM, the cerebellum and brainstem herniate through the FM and into the spinal cord area. Part of the brainâ&#x20AC;&#x2122;s fourth ventricle, the cavity that connects the superior aspects of the brain and circulates CSF, may also protrude through the opening and into the spinal cord area. In rare instances, the herniated cerebellar tissue can cause an occipital encephalocele, a pouch-like structure that protrudes out of the back of the head or the neck and contains brain matter. The covering of the brain or spinal cord can also protrude through an abnormal opening in the back or skull. Type III causes severe neurological defects.5-7 Type IV CM is characterized by an incomplete or underdeveloped cerebellum (cerebellar hypoplasia). In this rare form of CM, the cerebellar tonsils are located

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Fig. 3 Ranges of summated inferior and superior foramen magnum outlet areas stratified by etiology. Means are shown by dotted lines, 1 SD ranges are shown by boxes, and 2 SD ranges are shown by whiskers. CM-I: Chiari malformation type I; OAAJI: occipitoatlantoaxial joint instability; TCS: tethered cord syndrome; ISOL: intracranial space-occupying lesions; LPS: lumboperitoneal shunt; CM-II: Chiari malformation type II. Reprinted with permission from: Milhorat TH, Nishikawa M, Kuyla RW, Dlugacz YD. Mechanisms of cerebellar tonsil herniation in patients with Chiari malformations as guide to clinical management. Acta Neurochir (Wein) 2010; 152(7): 1117-1127.

further down the spinal canal. Prognosis for this form is very poor with death typically occurring in infancy. In Type 0 CM, there is no protrusion of the cerebellum through the FM but headache and other symptoms of CM are present.6 This form of CM is not recognized by all authorities.

RELATED CONDITIONS Syrinx, or syringomyelia, is a CSF-filled cyst that forms within the spinal cordâ&#x20AC;&#x2122;s central canal (Fig. 1). Often occurring concurrently with CM, it progressively destroys the central spinal cord, resulting in pain, weakness and stiffness in the back, shoulders, arms, or legs and may include the insensitivity to extreme hot and cold.7 Spinal curvature is a condition that often occurs in patients with syringomyelia or CM Type I. Both types: scoliosis, left or right; and kyphosis (forward bending of the spine) occur most often in children whose spinal columns are not yet fully mature.4 Hydrocephalus can result in infants having an enlarged or misshapen skull when it occurs in CMs that cause a blockage of normal CSF flow. This is most commonly associated with CM Type II and if untreated, can be fatal. Spina bifida, the incomplete development of the spinal cord occurs with CM Type II in the form of a myelomeningocele and often results in partial or complete paralysis.

Tethered cord syndrome occurs when the spinal cord attaches itself to the vertebra. This progressive disorder causes abnormal stretching of the spinal cord and can result in permanent damage to the muscles and nerves in the lower body. Additionally, this comorbidity exerts a downward force on the brainstem and brain, potentially causing or exacerbating a CM.7

neurosurgery. The patient subsequently underwent a successful cranial decompression. Two weeks post surgery showed a marked decrease in both downbeat nystagmus and left gaze nystagmus. The rotary nystagmus remained unchanged. The patient reported having a much easier time reading and working on the computer.

CLINICAL FINDINGS

CASE REPORT A 51-year-old Caucasian female presented with a chief complaint of her “eyes feeling like they move when looking down or during close work,” and images that would “jump once or twice but didn’t move constantly.” She first began noticing these specific symptoms about six months prior to her examination. Her immediate family had not noticed anything different or unusual. Further discussion disclosed the patient had been experiencing periodic unexplained non-debilitating symptoms for some years. She described not being able to tolerate walking on steep slopes in vineyards when on vacation in Italy a decade previous, and having periodic infrequent short occurrences of nausea and dizziness dating back many years as well. She was taking a single multivitamin a day together with a calcium supplement. She denied taking any other drugs, had never smoked or had any bowel or bladder control problems or any gait instabilities. There was no history of recent trauma. Her visual acuities were 6/4.5 (20/15) corrected in both eyes. A 30-2 threshold Humphrey visual field showed no evidence of defects in either eye including no scotoma or enlarged blind spot. Pupils were equal, round and reactive to light with no afferent pupillary defect. Extraocular motilities were full. Additional observations in both eyes included clockwise rotary nystagmus, horizontal endpoint nystagmus, jerk nystagmus, pendular nystagmus, significant overshoot and undershoot during saccades, refixations during pursuits, and most prominently, downbeat nystagmus accentuated on down gaze (see these observations at http://vimeo.com/26479190). She tended to sit with a slight left head tilt of which neither she nor her husband was aware. Intraocular pressures were 10 mmHg in both eyes by ICare tonometry, and the anterior segment by slit lamp examination was unremarkable other than a trace of nuclear sclerotic cataract in both eyes. Optical coherence tomography (OCT) scans of the optic nerve heads showed no nerve fiber layer depression in either eye. MRI of the head and cervical spine was obtained. The suspected CM was confirmed with the cerebellar tonsils extending approximately 2.5 mm below the FM (Fig. 2). No syringomyelia was found. The patient was referred to

The most common symptom of CM is a headache, which begins at the back of the head and neck and radiates superiorly. The pain is often made worse by various valsalva maneuvers such as coughing, sneezing or straining. As symptoms progress, visual problems become apparent. The most common visual symptoms are double vision or blurred vision. Unusual eye movements such as various types of nystagmus, especially downbeat nystagmus, are often seen clinically. Difficulties with balance, vertigo, and dizziness also may be present. Some patients may have cranial nerve compression which can result in apnea, gagging, swallowing difficulties, facial numbness or syncope. Patients may also develop muscle weakness, particularly in the upper extremities, coordination problems, and gait abnormalities.

ETIOLOGY AND PATHOGENESIS The pathogenesis of CM is incompletely understood. Current theories date to the hydrodynamic theory which relates tonsillar herniation to disordered embryonic development in the hindbrain region.8 The failure of pathways for CSF outflow from the embryological fourth ventricle to open normally results in increased pressure causing the cerebellar tonsils to migrate caudally in response to the pressure differential. Continuation of this pressure may allow for dilation of the central canal of the spinal cord, resulting in the formation of a hydromyelic cavity. Williams later proposed a theory based on pressure differential between the intraspinal and intracranial compartments.9,10 In the normal state, there should be unrestricted CSF flow between the intraspinal and intracranial compartments. In the patient with a CM there is impedance of some sort resulting in a pressure differential of the two-compartment hydrodynamic system which displaces the cerebellar tonsils down from the higher pressure intracranial compartment into the FM and the lower pressure spinal compartment. Milhorat3 correlated morphometric measurements of posterior cranial fossa with different etiologies having differing mechanisms of cerebellar tonsil herniation and found clues suggesting causal mechanisms for: (1) cranial constriction; (2) intracranial settling; (3) spinal cord tethering; (4) intracranial hypertension; and (5) intraspinal hypotension (Fig. 3).

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TREATMENT If symptoms are mild, not progressing and non-debilitating, conservative management is recommended. Supportive care such as headache and pain management, physical therapy or a reduction in activities can help manage symptoms. Surgery is the treatment of choice to correct functional problems and halt any further, potential damage to the central nervous system. More than one surgery is a possibility in more complicated cases. The most common procedure performed is a posterior fossa decompression. The neurosurgeon makes more room in the back of the head by removing small pieces of the bones of the skull. This reduces compression of the brainstem and allows the tonsils to move back into their natural position. The specific surgical techniques will vary among neurosurgeons since no consensus yet exists on the best variation of this surgical procedure.

IS THIS CONDITION HEREDITARY? Investigation into a possible genetic etiology of CM with or without syringomyelia is currently being undertaken. A genetic prevalence has been identified in some families. Researchers continue to search for the gene(s) that are responsible for producing CM. MRI is recommended for family members who have signs or symptoms of CM.

CONCLUSION The incidence of symptomatic CM is estimated to be 1:1000, common enough to be of interest to all clinicians. With the inclusion of more generalized symptoms such as periodic headaches, infrequent dizziness, subclinical balance abnormalities, and discomfort in the shoulder and neck areas, the overall incidence becomes much higher. There is no data describing the incidence of each specific type of CM. However, malformations of the

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cervico-medullary junction are present in approximately one percent of live births. The most common cervicomedullary junction malformations are CMs.11 The affected regions are: the lower brainstem which controls eye movements, swallowing, breathing, the vocal cords and sensations and movement of the arms and legs and; cerebellum which is involved in balance and that of coordinating body movements. CM symptoms are often vague and many times diagnosis of a CM is delayed, often for a prolonged period. Meanwhile, ongoing damage is occurring to the central nervous system. CMs must be considered in the differential when patients present with new onset nystagmus or other abnormal eye movements. â??

REFERENCES 1.

http://www.asap.org/index.php/disorders/chiari-malformation/ 2. http://www.ninds.nih.gov/disorders/chiari/chiari.htm 3. Milhorat TH, Nishikawa M, Kuyla RW, Dlugacz YD. Mechanisms of cerebellar tonsil herniation in patients with Chiari malformations as guide to clinical management. Acta Neurochir (Wein). 2010; 152(7):1117-1127. Published online 2010 May 4. doi: 10.1007/s00701-010-0636-3. 4. Elster AD, Chen MY. Chiari I malformations: clinical and radiologic reappraisal. Radiology. 1992; 183: 347-353. 5. http://www.ncbi.nlm.nih.gov/pubmed/20440631 6. http://www.ninds.nih.gov/disorders/chiari/detail/chiari.htm 7. Anson J, Benzel E, Awad, I, eds. Syringomyelia and the Chiari Malformations. The American Association of Neurological Surgeons, 1997: 200. 8. Gardner WJ. Hydrodynamic mechanism of syringomyelia: its relationship to myelocele. J Neurol Neurosurg Psychiatry 1965; 28: 247-259. 9. Williams B. On the pathogenesis of syringomyelia: a review. J R Soc Med 1980; 73: 798-806. 10. Williams B. Simultaneous cerebral and spinal fluid pressure recordings. Cerebrospinal dissociation with lesions at the foramen magnum. Acta Neurochir 1981; 59: 123-142. 11. http://www.pressenter.com/~wacma/milhorat.htm

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QUESTIONNAIRE New Onset Rotary Nystagmus in a Patient with Chiari Malformation Leonid Skorin Jr., DO, OD, MS, FAAO, FAOCO 1. A) B) C) D)

According to the paper, what is the prevalence of malformations of the cervico-medullary junction? 1.0% of live births 1.5% of live births 2.5% of live births 5% of live births

2. A) B) C) D)

Which of the four types of Chiari malformation (CM) is the most common? Type I Type II Type III Type IV

New Onset Rotary Nystagmus in a Patient with Chiari Malformation â&#x20AC;&#x201D; Skorin Jr.

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COPE-APPROVED CE CREDIT APPLICATION FORM

Hydrocephalus is most commonly associated with which type of CM? Type I Type II Type III Type IV

4. A) B) C) D)

In the Case Report presented, the patient noted having experienced all of the following signs and symptoms, EXCEPT: The sensation that her eyes were moving when looking down Nausea Difficulty focusing her eyes Dizziness

5. A) B) C) D)

What is the most common symptom of CM? Vomiting Gagging Difficulty swallowing Headache that begins at the back of the head and neck, radiating superiorly

6. A) B) C) D)

In the Case Report presented, which finding was not revealed by the Humphrey Visual Field Test? Absence of scotoma Various types of nystagmus Elevated intraocular pressure OU A trace of nuclear sclerotic cataract OU

7. A) B) C) D)

What is the incidence of symptomatic CM? 1:750 1:1000 1:2000 1:5000

8. A) B) C) D)

What is the most common visual symptom of CM? Floaters Intense flashes of light Excessive blinking Double/blurred vision

9. A) B) C) D)

Which of the following regions of the body is affected by CM? Cerebellum Lower brainstem Vocal cords All of the above

10. A) B) C) D)

Which of the following statements regarding CM is not true? The majority of clinical signs appear between 0 and 3 years of age Most cases are congenital Cerebellar displacement is a fairly common finding with MRI It is the most common type of cervico-medullary junction malformation

28.5:17

3. A) B) C) D)

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CE Credit Article Clinical & Refractive Optometry is pleased to present this continuing education (CE) article by Dr. Oakley Hayes and Dr. Nathan A. Whitaker entitled Transient Vision Loss: Getting to the Heart of the Problem. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit at no charge, please refer to page 184 for complete instructions.

Transient Vision Loss: Getting to the Heart of the Problem Oakley Hayes, OD; Nathan A. Whitaker, OD, FAAO

ABSTRACT Patent foramen ovale (PFO) represents a congenital defect in the wall between the atrial chambers of the heart. In the womb, the fetus relies on oxygen-rich blood from the mother which is shunted through this opening bypassing the developing lungs. In 80% of cases, the foramen closes spontaneously and is absent by birth. Herein, we report the case of a 61-year-old male who presented with transient vision loss in his right eye. After a thorough hematologic and cardiovascular evaluation, his symptoms and clinical findings were attributed to a previously undiagnosed PFO. The causes of transient vision loss are varied and the rarity of this case serves as a reminder of the importance of cardiovascular considerations among patients with similar clinical presentations.

Intraocular pressures measured 16 mmHg in each eye and anterior segment findings were normal OU. Dilated fundus examination revealed a healthy optic nerve, macula, and peripheral retina in the left eye. However, nerve fiber layer hemorrhages were noted emanating from the right optic nerve, as well as multiple cotton wool spots along the arcades (Figs. 1, 2). No associated anterior or posterior segment inflammation was present.

CASE REPORT A 61-year-old, African-American male presented with complaints of painless vision loss in the right eye of 24 hours duration. He reported no other neurological associations. Over a period of hours there had been segmental improvement in his vision. However, when comparing the right eye to the left, a subjective difference in vision persisted. His major medical diagnoses included hypertension, hyperlipidemia, and anemia. His ocular history was unremarkable. Best-corrected visual acuity measured 6/12 (20/40) OD and 6/6 (20/20) OS. Extraocular muscle functions were normal in each eye and a mild (1+) afferent pupillary defect was present in the right eye. He was unable to identify any color plates with the right eye, but properly identified all plates on the left. Visual field testing revealed a generalized depression across the entire right visual field, whereas the field was clear on the left. O. Hayes, N.A. Whitaker — Tuscaloosa Veteran’s Affairs Medical Center, Tuscaloosa, AL Correspondence to: Dr. Nathan A. Whitaker, Tuscaloosa Veteran’s Affairs Medical Center, 3701 East Loop Road., Tuscaloosa, Alabama 35404; E-mail: nathan.whitaker@va.gov

Fig. 1 Nerve fiber layer hemorrhages emanating from the right optic nerve and multiple cotton wool spots.

Fig. 2 Retinal findings in the left eye were unremarkable

Transient Vision Loss: Getting to the Heart of the Problem — Hayes, Whitaker 179

Table I Etiologies of transient vision loss1-6

Fig. 3 An embolic etiology was suspected although signs and symptoms were initially isolated to the right eye. At subsequent exams, emboli (arrow) were noted in each eye.

An initial diagnosis of ischemic optic neuropathy was made on the basis of the right eye findings and preliminary hematologic testing included: CBC, chem-7, sedimentation rate (ESR), ANA, RPR, and a lipid profile. These tests yielded no abnormalities. Carotid Doppler ultrasonography revealed 15%, hemodynamically insignificant, bilateral stenosis. Blood pressure readings were slightly elevated to 156/108 and since the primary care provider felt this to be associated with over-thecounter cold remedies, the patient was encouraged to discontinue those medications. Of particular concern was the likelihood that our patientâ&#x20AC;&#x2122;s complaints and clinical findings represented embolic phenomena as his symptoms continued to recur. A cardiovascular evaluation was arranged and a transesophageal echocardiogram (TEE) revealed a previously undiagnosed patent foramen ovale (PFO). Although the signs and symptoms were initially confined to the right eye, subsequent examinations did reveal emboli in each eye (Fig. 3). The patient has since undergone surgical repair of the PFO and his posterior segment findings and symptoms of fleeting vision loss have resolved.

DISCUSSION Transient vision loss has been associated with a wide variety of ophthalmic and systemic conditions (Table I).1-6 Among adults, the underlying etiology is typically associated with cerebral ischemia.7 Prompt recognition, as well as appropriate evaluation and referral, is essential as many of these patients are at increased risk of stroke and/or myocardial infarction.8-10 In children, the causes for transient vision loss are generally benign with

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Ocular

Dry eye Keratitis Blepharitis Iridocyclitis Hyphema Papilledema Disc drusen

Angle closure glaucoma Retinal detachment Vitreal detachment Vitreal hemorrhage Optic neuritis Vascular occlusive disease Ischemic optic neuropathy

Intraorbital

Hemangioma

Osteoma

Intracranial

A/V malformation Multiple sclerosis

Tumor Stroke

Carotid

Embolism Stenosis

Thrombosis Dissection

Cardiac

Embolism Valvular disease Endocarditis

Arrhythmia Patent foramen ovale Heart failure

Hematologic

Anemia Sickle cell disease Coagulation disorders Giant cell arteritis

Polycythemia Wegener granulomatosis Anti-phospholipid antibodies

Miscellaneous

Hypotension Raynaudâ&#x20AC;&#x2122;s syndrome Conversion reaction Sexual intercourse Drugs Head trauma

Migraine Vasospasm Malingering Exercise with demylinating disease

migraine-related auras and epilepsy representing common associations.11 Evaluation of the patient with complaints of transient vision loss should begin with a determination of whether the loss is monocular or binocular. As most patients are unfamiliar with the anatomy of the visual system, clinicians will often encounter stroke patients with homonymous hemianopsia who confuse their field loss with monocular vision loss in the eye ipsilateral to the field cut. Once laterality is confirmed, ocular causes of monocular loss should be ruled out to avoid unnecessary and costly cerebrovascular studies. Questions that address the temporal profile of vision loss (seconds, minutes, or hours) assist in differentiating causes of vision loss associated with anterior and posterior cerebral blood flow. Monocular loss in adults that recovers within a period of minutes, amaurosis fugax, is commonly associated with circulatory disturbances involving the distribution of the carotid artery and its branches.6 Of particular concern among older adults is the potential for giant cell arteritis. Among patients who developed giant cell related ocular complications such as ischemic optic neuropathy (anterior or posterior), central or cilioretinal artery occlusion, and ocular ischemic syndrome, two-thirds reported episodes of amaurosis fugax prior to the discovery of their retinal findings and

Table II Common risk factors for transient vision loss15,20-22

Table III Management of transient vision loss1,2,5,15,23

Non-Modifiable

Hematologic CBC Sedimentation rate Glucose Cholesterol Triglycerides Coagulation profile (PT, PTT)

Age Sex Race Genetic predisposition Family History Modifiable Hypertension Diabetes Hypercholesterolemia Obesity Smoking Oral contraceptives Coronary artery disease or cardiac arrhythmias Alcohol and/or drug abuse Vascular disease (polymyalgia, lupus, arteritis) Vasospasm (migraine)

Fig. 4 In the presence of increased pressure within the chest wall, blood is shunted from the right to left atrium through the PFO. Clots, or particles cross this opening, may travel to the brain causing a stroke, into a coronary artery resulting in myocardial infarction, or to the retinal arteries causing transient vision loss or retinal artery occlusion. (Photo courtesy NMT Medical)

the onset of vision loss.12,13 In 1990, the Amaurosis Fugax Study Group identified five distinct etiologies of transient monocular vision loss including: embolic, hemodynamic, ocular, neurologic and idiopathic.1 More recently, a simpler categorization including circulatory, ocular and neurological causes, was suggested by Bacigalupi.14 Brief bilateral vision loss in adults, lasting only seconds to minutes, or alternating episodes of transient loss between the two eyes, implicate the posterior cerebral circulation,

Cardiovascular Electrocardiogram - Arrhythmias

Hypercoagulability work-up - ANA - VDRL/RPR - Protein C/S deficiency - D-dimer test - Homocysteine (tHcy) - Antithrombin III (AT-III) - Fibrin degradation products (FDPs) - Serum viscosity - Lupus anticoagulant Echocardiogram - Valvular disease - Septal wall defect (PFO)

Carotid Duplex B-mode Doppler

or the vertebrobasilar distribution. Bilateral visual changes occurring with postural changes may also be encountered among those with postural hypotension or increased intracranial pressure.15 The presence or absence of concurrent neurologic symptoms must also be considered when evaluating the patient with transient vision loss. Horizontal hemifield loss with an associated afferent pupillary defect would be suggestive of pre-chiasmal optic nerve disease, whereas, quadranopsia and hemianopsia would implicate the post-chiasmal optic radiations. The onset of neurologic dysfunction among those with compromised anterior circulation is generally abrupt, with symptoms generally reaching maximal intensity within 24 hours. Cognitive dysfunction, altered mental status, difficulty with speech, unilateral weakness, poor coordination, numbness, paresthesia and loss of visual acuity and/or visual field are common among these patients. In contrast, symptoms of posterior circulation ischemia tend to not be as abrupt, and may be alternating and occur with postural changes.13 Neurological dysfunction among these patients include: hemiparesis or quadriparesis, cranial nerve deficits, nystagmus, respiratory difficulty, altered sensorium, vertigo, nausea and ataxia. When posterior circulatory compromise is suspected, symptoms frequently involve the five “D’s”: dizziness, diplopia, dysarthria, dysphagia and dystaxia. Impairment may be unilateral, bilateral or alternating.15-19 The risk factors (Table II)15,20-22 and etiologies of transient vision loss are varied and may require extensive hematologic, cardiac and vascular investigations (Table III).1,2,5,15,23 Transient monocular vision loss is an important indicator of generalized atherosclerotic disease and episodes of ischemia are generally caused by emboli that

Transient Vision Loss: Getting to the Heart of the Problem — Hayes, Whitaker 181

Table IV Signs and symptoms of ischemia reported in PFO26 • • • •

Sudden numbness or weakness in face, arm, or leg Difficulty speaking or understanding words or simple sentences Sudden blurred vision or decreased vision in one or both eyes Retinal arterial emboli or occlusion

• • • •

Difficulty swallowing Dizziness, loss of balance or coordination Brief loss of consciousness Sudden paralysis

Table V Types of echocardiograms31 Trans-thoracic echocardiogram (TTE)

Most commonly used. Views of the heart are obtained by moving the transducer to different locations on your chest.

Stress echocardiogram

Performed before and after the heart is stressed either by exercise or injecting a stimulant. Usually performed to determine if there is decreased blood flow to the heart.

Doppler echocardiogram

Images blood flow through the heart chambers and valves and through the blood vessels.

Trans-esophageal echocardiogram (TEE)

The probe is passed down the esophagus to show a clearer image of the heart.

travel into the ophthalmic circulation from either carotid or cardiac sources. Carotid artery disease generally garners the most attention by practitioners due to the frequency of association with transient ischemic events and the relative ease by which the carotid artery can be assessed. However, practitioners must be mindful of cardiac associations when hematological testing and carotid artery assessments are unequivocal. Valvular disease, intracardiac lesions (myxomas or mural thrombi), or abnormalities in the heart walls, such as patent foramen ovale, represent common cardiac sources for retinal emboli.24 Patent foramen ovale (PFO) represents a congenital defect in the wall between the atrial chambers of the heart (Fig. 4), and failure to close results in the creation of a flap or valve-like opening in the atrial wall. PFO represents the most common persistent fetal cardiac abnormality, occurring in approximately 29% of the normal adult population. Although most patients with isolated PFO remain asymptomatic, PFO does present an increased risk for migraine syndromes, transient ischemic attacks and stroke.24-27 The foramen ovale forms in the fetus as an incomplete closure in the septum between the atrial chambers of the heart and acts as a one-way valve allowing oxygenated blood from the mother to bypass the developing fetal lungs and enter the left side of the heart. The foramen typically closes by birth when the right atrial pressure declines, allowing normal blood flow through the lungs.26 Estimates suggest that one in five persons has PFO. Fortunately, less than 1% of these individuals will have stroke or other symptoms that require surgical closure.25-27 In patients who have stroke from unknown, or other unidentifiable causes (cryptogenic stroke), the prevalence of PFO approaches 40%.28 Those cases with more severe right-to-left shunting of the blood, and/or a larger septal defect, are more likely to experience paradoxical embolism and subsequent stroke.27,29,30 The signs and

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symptoms of ischemia reported among those diagnosed with PFO are non-specific and depend on whether emboli travel through the anterior or posterior cerebral vascular bed (Table IV).26 PFO can only be detected by specialized testing including: electrocardiogram (ECG or EKG), echocardiogram, cardiac magnetic resonance imaging (MRI), and angiography. Of the various echo studies that are available, the trans-esophageal echocardiogram (TEE) is most effective in evaluating patients for the presence of PFO (Table V).31 Management of PFO is conservative initially and includes pharmacological agents such as aspirin, plavix, aggrenox, and Coumadin. Surgical intervention is employed with persistent, recurring symptoms and may involve open heart surgery or cardiac catheterization to close the defect.7,27 Surgical closure is typically not performed in asymptomatic cases where PFO is discovered incidentally during a routine or screening echocardiogram.

CONCLUSION Patent foramen ovale represents the most common, persistent, congenital fetal cardiac defect. Fortunately, only 1% to 2% of individuals with a PFO experience neurological symptoms requiring intervention. Less common are ocular findings that result in a diagnosis of PFO requiring surgical intervention to alleviate symptoms. This case is unique in that regard and emphasizes the necessity of considering cardiovascular etiologies among our patients who present with transient vision loss. ❏

REFERENCES 1. 2.

Amaurosis Fugax Study Group: Current Management of Amaurosis Fugax. Stroke 1990; 21(2): 201-208. Kunimoto DY, Kanitkar KD, Makar MS: The Wills Eye Manual. Office and Emergency Room Diagnosis and Treatment of Eye Disease. 4th ed. Philadelphia: Lippincott Williams and Wilkins, 2004.

4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Benavente O, Eliasziw M, Streifler JY, et al: Prognosis after Transient Monocular Blindness Associated with Carotid-Artery Stenosis. N Engl J Med 2001; 345: 1084-1090. Levine SR, Crofts JW, Lesser GR, et al: Visual symptoms associated with the presence of a lupus anticoagulant. Ophthalmology 1998; 15: 686-692. Winterkorn JMS, Mack P, Eggenberger E: Transient Visual Loss in a 60 year-old Man. Surv Ophthalmol 2008; 53: 301-305. White MF, Kline LB. Ocular Manifestations of Carotid Artery Disease. In: Farris BK ed. The Basics of Neuroophthalmology. New York, NY: Mosby, 1991: 319-343. Brown RD, Petty GW, O’Fallon WM, et al: Incidence of transient ischemic attack in Rochester, Minnesota, 1985-1989. Stroke 1998; 29: 2109-2113. Cucchiara BL, Messe SR, Taylor RA, et al: Is the ABCD Score Useful for Risk Stratification of Patients with Acute Transient Ischemic Attack? Stroke 2006; 37: 1710-1714. Poole CJ, Russell RW. Mortality and stroke after amaurosis fugax. J Neurol Neurosurg Psychiatry 1985; 48: 902-905. Klein R, Klein BE, Jensen SC, et al. Retinal emboli and stroke: The Beaver Dam Eye Study. Arch Ophthalmol Aug 1999; 117(8): 1063-1068. Amick A, Caplan LR. Transient monocular vision loss. Compr Ophthalmol Update 2007; 8 (2): 91-100. Hayreh, et al. Ocular Manifestations of Giant Cell Arteritis. American Journal of Ophthalmology 1998;125(4): 509-519. Hayreh, et al. Occult Giant Cell Arteritis. American Journal of Ophthalmology 1998; 125(4): 520-526. Bacigalui M. Amaurosis Fugax. A Clinical Review. The Internet Journal of Allied Sciences and Practice. April 2006, Volume 4, Number 2. Graybeal LE, Whitaker NA. Visual Problems Result From Severe Stenosis. Review of Optometry 2006; 143(11): 109-117. Becker KJ. Vertebrobasilar ischemia. New Horizons 1997; 5: 305-315. Easton DJ, Fauci AS, Isselbacher KJ: Cerebrovascular Disease. In: Harrison’s Principles of Internal Medicine. New York, NY, 1998: 2325-2348.

18. Victor M. Cerebrovascular Disease. In: Adam’s and Victor’s Principles of Neurology. New York, NY: McGraw-Hill; 2000: 821-851. 19. Ferbert A, Bruckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke 1990; 21: 1135-1142. 20. American Stroke Association. Stroke Curriculum for medical students. Modules 1-6. 2000. 21. Millikan CH and the Ad Hoc Committee on Cerebrovascular Disease: A Classification and Outline of Cerebrovascular Diseases II. Stroke 1975; 6: 564-616. 22. Ingall TJ. Preventing ischemic stroke. Current approaches to primary and secondary prevention. Postgrad Med 2000; 107(6): 34-36, 39-42, 47-50. 23. Khamashta MA, Cuadrado MJ, Mujic F, et al: The Management of Thrombosis in the AntiphospholipidAntibody Syndrome. N Engl J Med 1995; 332: 993-997. 24. Clifford L, Sievers R, Salmon A, Newsom RSB: Central retinal artery occlusion: association with patent foramen ovale. Eye 2006; 20: 736-738. 25. Lechat P, Mas JL, Lascault G, et al. Prevalence of patent foramen ovale in patients with stroke. N Engl J Med 1998; 318: 1148-1152. 26. Cleveland Clinic Center for Consumer Health Information. 26 April 2004. The Cleveland Clinic Foundation. http://www.clevelandclinic.org/health/health-info/docs/ 3400/3454.asp?index=11626. 27. De Castro S, Cartoni D, Fiorelli M, et al. Morphological and Functional Characteristics of Patent Foramen Ovale and Their Embolic Implications. Stroke 2000; 31: 2407-2413. 28. Wechsler LR. PFO and stroke. What are the data? Cardiology in Review 2008; 16: 53-57. 29. Steiner MM, Di Tullio MR, Rundek T, et al. Patent foramen ovale size and embolic brain imaging findings among patients with ischemic stroke. Stroke 1998; 29: 944-948. 30. Stone DA, Godard J, Corretti MC, et al. Patent foramen ovale: association between the degree of shunt by contrast transesophageal echocardiography and the risk of future ischemic neurologic events. Am Heart J 1996; 131: 158-161. 31. Sharma S, Sharma SM, Cruess AF, et al. Transthoracic echocardiography in young patients with acute retinal arterial obstruction. RECO Study Group. Retinal Emboli of Cardiac Origin Group. Can J Ophthalmol 1997; 32: 38-41.

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QUESTIONNAIRE Transient Vision Loss: Getting to the Heart of the Problem Oakley Hayes, OD; Nathan A. Whitaker, OD, FAAO 1. According to the paper, in what percentage of cases does the foramen close spontaneously? A) 35% B) 50% C) 75% D) 80% 2. A) B) C) D)

In the Case Report presented, what was the patient’s complaint at initial presentation? Abrupt and painful vision loss over a 6-hour period Painful vision loss accompanied by migraine Painless vision loss of 24 hours’ duration Sudden blurred vision bilaterally

Clinical and Refractive Optometry 28:5, 2017

COPE-APPROVED CE CREDIT APPLICATION FORM

In the Case Report presented, dilated fundus examination revealed all of the following, EXCEPT: Healthy optic nerve Nerve fibre layer hemorrhages in right optic nerve Multiple cotton wool spots along the arcades Edema in the right macula

4. A) B) C) D)

Which of the following is not a possible etiology of transient vision loss? Stroke Myocarditis Head trauma Thrombosis

5. A) B) C) D)

In patients with transient vision loss and compromised anterior circulation, which of the following is a neurologic symptom? Altered mental status Memory loss Paresthesia Both A & C are correct

6. A) B) C) D)

In what percentage of the normal adult population does patent foramen ovale (PFO) exist? Approximately 10% Approximately 29% Approximately 30% Approximately 45%

7. A) B) C) D)

In patients with transient vision loss and posterior circulation ischemia, which of the following is a possible neurologic sign/symptom? Strabismus Ataxia Vertigo Both B & C are correct

8. A) B) C) D)

Patients with PFO are at risk for all of the following conditions, EXCEPT: Transient ischemic attack Sjögren’s syndrome Migraine syndromes Stroke

9. A) B) C) D)

In what percentage of patients with cryptogenic stroke does PFO occur? Approximately 10% Approximately 20% Approximately 30% Approximately 40%

10. A) B) C) D)

Which of the following is a common risk factor for transient vision loss? Race Oral contraceptives Diabetes All of the above

28.5:17

3. A) B) C) D)

Transient Vision Loss: Getting to the Heart of the Problem — Hayes, Whitaker 185

CE Credit Article Clinical & Refractive Optometry is pleased to present this continuing education (CE) article by Dr. Michelle Steenbakkers entitled Corneal Phlyctenule in a Steroid Responder. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit, please refer to page 191 for complete instructions.

Corneal Phlyctenule in a Steroid Responder Michelle Steenbakkers, BSc (Hons), OD, FAAO

ABSTRACT Background: Phlyctenular keratoconjunctivitis is a delayed hypersensitivity response in the cornea or conjunctiva to an antigen to which it has become sensitized. Two different types of phlyctenules exist, corneal and conjunctival, and they are differentiated by their respective location, size, clinical signs, and sequelae. Standard treatment for phlyctenulosis includes the use of topical antibiotic-steroid combination drops and thus requires the clinician to monitor for steroid-induced glaucoma. Case Report: An 18-yearold Asian man presented with a three-week history of a red right eye. Presenting visual acuities were 6/4.5 (20/15) in each eye. A sector of conjunctival injection with an associated elevated white corneal lesion was noted nasally in the right eye. The patient was diagnosed with a corneal phlyctenule and treated with a topical antibiotic-steroid combination. The phlyctenule responded to the treatment; however, the patient was subsequently managed for an increased intraocular pressure (IOP) response to the topical steroid. Conclusion: The management of phlyctenulosis includes the use of topical anti-inflammatory agents; therefore the patient must be monitored for adverse drug reactions. In patients with documented steroidinduced elevation of IOP, alternative treatment for phlyctenulosis should be considered.

INTRODUCTION Phlyctenular keratoconjunctivitis is a nonspecific delayed hypersensitivity response in the cornea or conjunctiva to an antigen to which it has become sensitized.1 Antigens M.J. Steenbakkers — University of Waterloo, School of Optometry Correspondence to: Dr. Michelle Steenbakkers, University of Waterloo, School of Optometry, 200 University Avenue West, Waterloo, ON N2L 3G1; E-mail: mjsteenb@sciborg.uwaterloo.ca This article has been peer-reviewed. The author has no financial or proprietary interest in the materials or products mentioned in this article.

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responsible for the keratoconjunctivitis include staphylococcal exotoxins, tuberculoprotein and other bacteria,2,3 fungi, parasites and chlamydial infestations.4-7 The term phlyctenula originates from the Greek word meaning blister,7 where the resulting lesion is often round and elevated. Two different types of phlyctenules exist, conjunctival and corneal, and they are differentiated by their respective location, size, presenting symptoms, clinical signs, and sequelae. One of the main treatment regimens for phlyctenulosis includes the use of topical antibiotic-steroid combination drops. Due to the propensity for exogenous steroids to incite an elevation in intraocular pressure (IOP), the clinician must monitor for steroidinduced glaucoma. The following case report concerns a patient treated for corneal phlyctenulosis secondary to staphylococcal exotoxin hypersensitivity who demonstrated steroid-induced elevation of IOP during his treatment. Due to the possibility of exacerbations of phlyctenulosis, alternative treatment options for future episodes are discussed in this report.

CASE PRESENTATION An 18-year-old Asian man presented with a chief complaint of a three-week history of a red, watery right eye. He reported no pain or photophobia and experienced minimal white ocular discharge upon waking. Previous treatment with a polymyxin B/trimethoprim ophthalmic solution (Polytrim®, Allergan) four times a day in the right eye for one week provided no improvement in the patient’s symptoms. Current treatment consisted of 0.5% moxifloxacin hydrochloride ophthalmic solution (Vigamox®, Alcon) used every 2 hours for the previous 24 hours. There was no other significant ocular history and this was the first episode of a red eye that the patient could recall. Medical history was unremarkable; the patient reported good general health with no known drug allergies. Presenting unaided visual acuities were 6/4.5 (20/15) in each eye. Ocular motility was full and unrestricted; pupils were equal, round and reactive with no afferent pupil defect noted. Anterior segment exam revealed a sector of conjunctival injection nasally in the right eye. A 1.0 mm by 0.5 mm diameter elevated white lesion with

Fig. 1 Anterior segment photograph of the initial presentation of a 1.0 mm by 0.5 mm diameter elevated corneal phlyctenule on right inferior nasal limbus. The lesion was surrounded by diffuse punctate keratitis and was located at the head of a comet of injected conjunctival blood vessels.

sharp borders was noted in the inferior nasal right peripheral cornea. The area was surrounded by diffuse punctate keratitis. The lesion stained with sodium fluorescein and demonstrated a small area of central ulceration (Figs. 1, 2). The anterior chamber was free of aqueous cells, with only trace flare present. Bilateral meibomian gland inspissation, inflamed eyelid margins and anterior blepharitis were noted. IOP by Goldmann applanation tonometry was 10 mmHg and 12 mmHg in the right and left eyes, respectively. An undilated fundus exam revealed healthy optic nerves and maculae. The patient was diagnosed with corneal phlyctenulosis secondary to staphylococcal exotoxins and 0.3%/0.1% tobramycin/dexamethasone ophthalmic suspension (TobraDexÂŽ, Alcon) four times a day in the right eye was prescribed. The patient was instructed to initiate warm compresses and eyelid hygiene for the underlying blepharitis. Two follow-up visits were scheduled over the following week and the patient reported subjective improvement at each visit. The patient was non-compliant with TobraDex and had reduced the frequency to three times a day over the previous two days. He had not initiated any eyelid hygiene, as previously recommended. Presenting acuities remained 6/4.5 (20/15) in each eye. Slit-lamp evaluation noted reduction in conjunctival injection in the right eye and a small decrease in elevation of the corneal infiltrate although the size of the lesion was unchanged from initial presentation. IOP had increased by 4 mmHg to 14 mmHg in the right eye and was unchanged in the left eye. It was decided to continue the TobraDex four times a day in the right eye and the patient was scheduled to return in one week.

Fig. 2 Note the area of central ulceration in the corneal phlyctenule (white arrow).

At the subsequent visit, the patient reported noncompliance with the TobraDex over the previous week as he had discontinued the drops for a few days as he felt his vision was blurring. Two days after cessation of the TobraDex, the redness began to return and he initiated the TobraDex twice daily in the right eye. Entering acuity was slightly reduced at 6/6+2 (20/20+2) in the right eye and 6/4.5 (20/15) in the left eye. Slit lamp examination revealed a flat non-staining white lesion in the inferior nasal cornea of the right eye. There was a mild associated sectoral hyperemia. The anterior chamber was dark and quiet. Intraocular pressures by Goldmann applanation were elevated to 24 mmHg in the right eye and 12 mmHg in the left eye. The phlyctenular keratitis was responding to the prescribed treatment; however, the patient was demonstrating a steroid-induced elevation of IOP. The TobraDex was discontinued pending ophthalmological assessment the following day. At the ophthalmological consultation, the patient was assessed as have a resolved staphylococcal infiltrate with an intraocular pressure of 30 mmHg. He was instructed to return to the optometrist for a oneweek IOP assessment. At that visit, IOP was measured to be 17 mmHg OD and 14 mmHg OS. At a follow-up visit four weeks later, the IOP was measured to be 10 mmHg in each eye. At this final visit, the patient was re-educated on the importance of managing the underlying blepharitis to reduce recurrence of the phlyctenulosis. He was instructed to return for evaluation should he experience another exacerbation.

DISCUSSION Phlyctenulosis Phlyctenular keratoconjunctivitis has been described as a nonspecific delayed hypersensitivity response in the

Corneal Phlyctenule in a Steroid Responder â&#x20AC;&#x201D; Steenbakkers

187

Table I Organisms implicated in the pathogenesis of phlyctenular keratoconjunctivitis. Bacteria

Bacillus spp. Mycobacterium tuberculosis Neisseria gonorrhoeae Staphylococcus aureus

Chlamydia

Chlamydia trachomatis

Parasites

Ancylostoma duodenale Ascaris lumbricoides Hymenlepsis nana Leishmaniasis spp.

Fungi

Candida spp. Coccidiodes immitis

Virus

Herpes simplex

cornea or conjunctiva to an antigen to which it has become sensitized.1 In the past, tuberculoprotein was thought to be the main antigen responsible for the keratoconjunctivitis; however, other antigens inciting a phlyctenular response include staphylococcal exotoxins, and other bacteria,2,3 fungi, parasites and chlamydial infestations (Table I).4-7 Two different types of phlyctenules exist, conjunctival and corneal, and they are differentiated by their respective locations. Conjunctival phlyctenules present as single or multiple elevated pinkish lesions of 0.5 mm to 3.0 mm in diameter surrounded by a zone of limbal hyperemia. These lesions often occur near the corneal limbus. The conjunctival nodule may develop a central lesion and ulcerate although it most often heals rapidly over 10 to 12 days without a residual scar. The most common presenting symptoms of phlyctenular conjunctivitis are tearing and irritation. In comparison, corneal phlyctenules appear as unilateral or bilateral localized infiltrates, measuring 0.5 mm to 2.0 mm. Initiating at the corneal limbus, often located inferiorly as in the reported case, or elsewhere in the corneal periphery, these lesions are at the head of a comet of new blood vessels. The phlyctenule may ulcerate over the first few days and some have the propensity to migrate centrally, leaving a leash of neovascular pannus.7,8 The patient presented in this case report demonstrated a small area of central ulceration in his corneal phlyctenule; however, the lesion did not migrate in his cornea. The symptoms of phlyctenular keratitis are often more severe than phlyctenular conjunctivitis. In more severe cases of phlyctenular keratitis, tuberculin protein hypersensitivity should be suspected (Table I).7,9 Differential diagnosis of phlyctenulosis includes pingueculitis, inflamed pterygium, sterile or infectious peripheral corneal infiltrates, marginal ulcers, herpes simplex keratitis, ocular cicatricial pemphigoid, acne rosacea and vernal keratoconjunctivitis.7,8

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Treatment Management of phlyctenular keratoconjunctivitis is aimed at the eradication of precipitating conditions, such as underlying eyelid margin disease, and the reduction and prevention of inflammation and anterior corneal stromal scarring. Combinations of topical antibiotics and topical steroids are often prescribed for the treatment of phlyctenular keratoconjunctivitis. Patients often note improvement in phlyctenulosis within 48 hours of initiating treatment with a topical steroid, as was noted in this case report.10 Corticosteroids (glucocorticoids) are potent antiinflammatory agents; however, they increase the risk of glaucoma by raising the intraocular pressure when administered exogenously, either topically, periocularly or systemically.11 Approximately 18% to 36% of the general population are considered steroid responders, showing a moderate increase of 5 mmHg or more in IOP after topical administration of steroids.12-14 However, 5% to 6% of the general population, including the case reported, and 46% to 92% of patients with primary open-angle glaucoma (POAG) have a significant and potentially damaging rise in IOP after topical steroid administration.12,14-17 Furthermore, it has been noted that patients over the age of 40 with certain systemic diseases or conditions, such as diabetes mellitus, high myopia or connective tissue disease, as well as relatives of patients with POAG are more vulnerable to steroid-induced glaucoma.11 Other risk factors, such as racial origin, systemic hypertension, and vasospasm are likely to be associated with a steroidinduced elevation of IOP, but have not yet been fully established.11 The patient presented in this report did not present with any of these risk factors. As the demographic of phlyctenular keratoconjunctivitis includes the pediatric population, it is important to consider that recent studies show that children below 10 years of age can manifest a rapid elevation of IOP with topical steroids and should be monitored accordingly.18-20 The proposed mechanism of steroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork (TM) and its extracellular matrix, which is responsible for nearly 90% of aqueous humor (AH) drainage from the eye.11,21 In vitro studies of dexamethasone-perfused cultured human eyes have demonstrated increased amounts of fibrillar extracellular material deposited in the trabeculae and Schlemmâ&#x20AC;&#x2122;s canal, thus increasing resistance to AH outflow compared to age-matched norms.22 Cellular debris may also accumulate in the aqueous flow channels as a result of decreased phagocytic activity of the TM cells.23, 24 Ocular hypertension after steroid administration depends on the specific drug, the dose and the frequency of administration.25 If a steroid response is suspected, the drug should be discontinued, used in a lower concentration, or substituted with a weaker topical steroid (e.g. 0.1%

fluorometholone, FML®)10 or a modified “soft” topical steroid. This last category includes 0.5% loteprednol etabonate (Lotemax®, Bausch and Lomb), which has less likelihood of increasing IOP as it undergoes hydrolysis in the cornea and AH to become an inactive derivate.26, 27 A recent study in subjects 18 years and older demonstrated that 0.5%/0.3% loteprednol etabonate/tobramycin ophthalmic suspension (Zylet®, Bausch and Lomb) was as effective as 0.3%/0.1% dexamethasone/tobramycin ophthalmic suspension (TobraDex, Alcon) in reducing the signs and symptoms of ocular inflammation associated with blepharokeratoconjunctivitis.28 The topical nonsteroidal anti-inflammatory agents, such as 0.1% diclofenac (Voltaren®, Novartis), 0.4% ketorolac (Acular-LS®, Allergan) and 0.1% nepafenac (Nevanac®, Alcon) have similar anti-inflammatory activity to 1.0% prednisolone acetate (Pred Forte®, Allergan) and have served as an alternative to topical steroids in postoperative cataract inflammation29 and may prove useful in the management of phlyctenular keratoconjunctivitis. The efficacy of other agents, such as long-term topical cyclosporine A (CsA) 2% solution, which is 40 times more concentrated than the 0.05% topical CsA preparation Restasis® (Allergan), have been demonstrated as safe and effective in treating phlyctenular keratoconjunctivitis associated with severe steroid-dependent corneal inflammation in children.30 Other alternative treatment options for phlyctenular keratoconjunctivitis have included oral antibiotics, mainly cyclines (tetracycline, doxycycline) or macrolides (erythromycin).2 In this approach, the anti-inflammatory properties of these antibiotics are utilized via their proposed inhibition of staphylococcal exotoxin-stimulated T-cell proliferation and cytokine production. In the cases where steroid therapy must be maintained, adding an IOP-lowering agent could be considered.31 In those patients who have received either a chronic or high dose administration of topical steroid, a gradual tapering dose of the steroid should be prescribed when discontinuing therapy. The tapered dosage will prevent exacerbation of the underlying condition and reduce this risk of steroid withdrawal syndrome.32 The IOP usually returns to baseline measurements within 2 to 4 weeks after discontinuation of topical steroid therapy, although there are a few reports of permanently elevated IOP requiring medical or surgical intervention.13,33 It is important to also consider the other ocular complications of steroid therapy, including posterior subcapsular cataract,34,35 delayed wound healing and corneal ulceration,36 ocular infection,37 ptosis,38 mydriasis38,39 and atrophy of the eyelid skin.37 The underlying antigenic etiology should also be considered when initiating treatment for phlyctenular keratoconjunctivitis. Education on the use of warm compresses and eyelid hygiene can improve the eyelid

margin condition. A topical antibiotic ointment, such as erythromycin, may be prescribed to alter bacterial flora of the eyelid. As a point of interest, in recalcitrant or chronic cases of phlyctenular keratoconjunctivitis, where eye lid disease is absent, the possibility of tuberculosis or a gastrointestinal parasite should be considered and evaluated.

CONCLUSION This case detailed the assessment and management of a patient with a corneal phlyctenule and blepharitis, whose steroid-induced elevation of IOP demonstrates the need for alternative treatment strategies for future exacerbations. ❏

REFERENCES 1. 2.

9. 10.

11. 12. 13.

14.

15. 16.

17.

Sorsby A. The etiology of phlyctenular ophthalmia. Br J Ophthalmol 1942; 26: 159-179. Zaidman GW, Brown SI. Orally administered tetracycline for phlyctenular keratoconjunctivitis. Am J Ophthalmol 1981; 92: 173-182. Culbertson WW. Huang AS, Mandelbaum SH, et al. Effective treatment of phlyctenular keratoconjunctivitis with oral tetracycline. Ophthalmology 1993; 100: 1358-1366. Jeffrey MP. Ocular diseases caused by nematodes. Am J Ophthalmol 1995; 40: 41-52. Al Husaini MK, Khalifa R, Al-Ansary ATA, et al. Phlyctenular eye disease is associated with Hymenolepis nana in Egypt. Br J Ophthalmol 1979; 63: 627-631. Hussein AA, Nasr ME. The role of parasitic infections in the etiology of phlyctenular eye disease. J Egypt Soc Parasitol 1991; 21: 865-868. Tabbara KF. Phlyctenulosis. In: Roy FH, Fraunfelder FW, Fraunfelder FT, eds. Current ocular therapy. 6th ed. Philadelphia, PA: Elsevier, 2008: 388-389. Neiberg MN, Sowka J. Phlyctenular keratoconjunctivitis in a patient with staphylococcal blepharitis and ocular rosacea. Optometry 2008; 79: 133-137. Rohatgi J, Dhaliwal U. Phlyctenular eye disease: a reappraisal. Jpn J Ophthalmol 2000; 44: 146-150. Roberts CM. Quick consult to diagnosing and treating ocular disease. Woburn, MA: Butterworth-Heineman, 2002; 34-35. Tripathi RC, Parapuram SK, Tripathi BJ. Corticosteroids and glaucoma risk. Drugs and Aging 1999; 15(6): 439-450. Becker B. Intraocular pressure response to topical corticosteroids. Invest Ophthalmol Vis Sci 1965; 49(2): 198-205. Francois J, Heintz-De Bree C, Tripathi RC. The cortisone test and the heredity of primary open-angle glaucoma. Am J Ophthalmol 1966; 62(5): 844-952. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics: I. The effect of dexamethasone in the normal eye. Arch Ophthalmol 1963; 70: 482-491. Becker B, Mills DW. Corticosteroid and intraocular pressure. Arch Ophthalmol. 1963; 70: 500-507. Becker B, Mills DW. Elevated intraocular pressure following corticosteroid eye drops. JAMA 1963; 185(11): 884-886. Biedner BZ, David R, Grudsky A, et al. Intraocular pressure response to corticosteroids in children. Br J Ophthalmol 1980; 64(6): 430-431.

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18. Ohji M. Kinoshita S, Ohmi E, et al. Marked intraocular pressure response to instillation of corticosteroids in children. Am J Ophthalmol 1991; 112(4): 450-454. 19. Kwok AK, Lam Ds, Ng Js, et al. Ocular-hypertensive response to topical steroids in children. Ophthalmol 1997; 104(12): 2112-2116. 20. Lam DS, Kwok AK, Chew S. Accelerated ocular hypertensive response to topical steroids in children. Br J Ophthalmol 1997; 81(5): 422-423. 21. Tripathi RC, Tripathi BJ. Functional anatomy of the anterior chamber angle. In: Tasman WW, Jaeger EA, eds, Duaneâ&#x20AC;&#x2122;s biomedical foundations of ophthalmology. Vol. 1. Philadelphia, PA: JB Lippincott Co., 1989: 1-88. 22. Clark AF, Wilson K, de Kater AW, et al. Dexamethasoneinduced ocular hypertension in perfusion-cultured human eyes. Invest Ophthalmol Vis Sci 1995; 36(2): 478-489. 23. Matsumoto Y, Johnson DH. Dexamethasone decreases phagocytosis by human trabecular meshwork cells in situ. Invest Ophthalmol Vis Sci 1997; 38(9): 1902-1907. 24. Bill A. The drainage of aqueous humor (Editorial). Invest Ophthalmol Vis Sci 1975; 14(1): 1-3. 25. Kass MA, Johnson T. Corticosteroid-induced glaucoma. In: Ritch R, Shields MB, Krupin T, eds. The glaucomas, Vol. 2. St. Louis, MO: Mosby, 1989: 1161-1168. 26. Novack GD, Howes J, Crockett RS, et al. Change in intraocular pressure during long-term use of loteprednol etabonate. J Glaucoma 1998; 7(4): 266-269. 27. Druzgala P, Wu WM, Bodor N. Ocular absorption and distribution of loteprednol etabonate, a soft steroid, in rabbit eyes. Curr Eye Res 1991; 10(10): 933-937. 28. White EM, Macy JI, Bateman KM, Comstock TL. Comparison of the safety and efficacy of loteprednol 0.5%/tobramycin 0.3% with dexamethasone 0.1%/tobramycin 0.3% in the treatment of blepharokeratoconjunctivitis. Curr Med Res Opinion 2008; 24(1): 286-296.

29. Brennan KM, Brown RM, Roberts CW. A comparison of topical non-steroidal anti-inflammatory drugs to steroids for control of post cataract inflammation. Insight 1993; 18(1): 8-9, 11. 30. Doan S, Gabison E, Gatinel D, et al. Topical cyclosporine A in severe steroid-dependent childhood phlyctenular keratoconjunctivitis. Am J Ophthalmol 2006; 141: 62-66. 31. Mindel JS, Tavitian HO, Smith Jr H, et al. Comparative ocular pressure elevation by medrysone, fluorometholone, and dexamethasone phosphate. Arch Ophthalmol 1980; 98(9): 1577-1578. 32. Swartz Sl, Dluhy RG. Corticosteroids: clinical pharmacology and therapeutic use. Drugs 1978; 16(3): 238-255. 33. Spaeth GL, Rodrigues MM, Weinreb S. Steroid-induced glaucoma: A Persistent elevation of intraocular pressure; B Histopathological aspects. Trans Am Ophthalmol Soc 1977; 75: 353-381. 34. Ticho U, Durst A, Licht A, et al. Steroid-induced glaucoma and cataract in renal transplant recipients. Isr J Med Sci 1977; 13(9): 871-874. 35. Tripathi RC, Kipp MA, Tripathi BY, et al, Ocular toxicity of prednisone in pediatric patients with inflammatory bowel disease. Lens Eye Toxic Res 1992; 9(3-4): 469-482. 36. Krupin T, LeBlanc RP, Becter B, et al. Uveitis in association with topically administered corticosteroid. Am J Ophthalmol 1970; 70(6): 883-885. 37. Cubey RB. Glaucoma following the application of corticosteroid to the skin of the eyelid. Br J Dermatol 1976; 95(2): 207-208. 38. Miller D, Peczon JD, Whitworth CG. Corticosteroids and functions in the anterior segment of the eye. Am J Ophthalmol 1965; 59: 31-34. 39. Armaly MF. Effect of corticosteroids on intraocular pressure and fluid dynamics: III. Changes in visual function and pupil size during topical dexamethasone application. Arch Ophthalmol 1964; 71: 636-644.

Call for Papers Clinical & Refractive Optometry welcomes original articles based on clinical or basic research, case reports, and review papers related to the practice of optometry. Please submit manuscripts to: Clinical & Refractive Optometry Attn: Mary Di Lemme, Managing Editor 3484 Sources Blvd., Suite 518 Dollard-des-Ormeaux, Quebec H9B 1Z9 e-mail: mdilemme@mediconcept.ca

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QUESTIONNAIRE Corneal Phlyctenule in a Steroid Responder Michelle J. Steenbakkers, BSc (Hons), OD, FAAO 1. A) B) C) D)

Which of the following forms of corticosteroids causes the greatest ocular damage? Systemic Periocular There is no distinction Topical

2. A) B) C) D)

Which clinical signs and symptoms did not present in the patient in the Case Report White ocular discharge upon awakening Conjunctival injection nasally in the right eye Pain and inflammation in the right eye Diffuses punctate keratitis in the right eye

Corneal Phlyctenule in a Steroid Responder â&#x20AC;&#x201D; Steenbakkers

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COPE-APPROVED CE CREDIT APPLICATION FORM

Phlyctenular keratoconjunctivitis can be caused by all of the following, EXCEPT: Herpes simplex virus Chlamydia trachomatis Bacillus spp. N. meningitides

4. A) B) C) D)

All of the following statements is not true. The symptoms of phlyctenular keratitis are often more severe than those of phlyctenular conjunctivitis Phlyctenular conjunctivitis commonly presents with tearing and irritation Phlyctenular conjunctivitis is self-limiting once use of the causal antigen has been suspended Corneal phlyctenules appear as unilateral or bilateral localized infiltrates

5. A) B) C) D)

Differential diagnosis of phlyctenulosis includes which of the following condition: Eye warts (HPV virus) Marginal ulcers Acne rosacea Both B & C are correct

6. A) B) C) D)

At what age are certain patients more vulnerable to steroid-induced glaucoma? Over age 25 Over age 30 Over age 35 Over age 40

7. A) B) C) D)

Which of the following is considered a steroid response? An increase of 5 mmHg or more in IOP An increase of 7 mmHg or more in IOP An increase of 10 mmHg or more in IOP An increase of 5 mmHg or more in IOP in Caucasians; an increase of 7 mmHg or more in African-Americans

8. A) B) C) D)

What of the following is not a risk factor for steroid-induced elevation of IOP? Systemic hypertension Family history of the condition Racial origin Vasospasm

9. A) B) C) D)

What of the following is an ocular complication of steroid therapy? Ocular infection Delayed wound healing Ptosis All of the above

10. A) B) C) D)

Why was the patient in this Case Report non-compliant with TobraDexÂŽ? He found it inconvenient He didnâ&#x20AC;&#x2122;t believe it would actually help his condition He felt that he was developing blurred vision It caused him ocular pain and stinging

28.5:17

3. A) B) C) D)

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CLICK HERE TO PRINT THIS CE CREDIT ARTICLE AND TEST

Clinical & Refractive Optometry is pleased to present this encore continuing education (CE) article by Dr. Paul Varner entitled Clinical Grading of Nuclear Sclerotic Cataracts. In order to obtain a 1-hour Council of Optometric Practitioner Education (COPE) approved CE credit, please refer to page 200 for complete instructions.

Clinical Grading of Nuclear Sclerotic Cataracts Paul Varner, OD, MPH

ABSTRACT Importance: Widespread clinical use of grading scales facilitates patient care. Many cataract classification schema have been proposed, but without universal acceptance. Purpose: To discern why there is no consensus for grading nuclear sclerotic cataracts (NSC). Method: A NSC grading method involving anterior and posterior segment correlation was developed for clinical use. Results: This correlation method for grading NSC failed initial standardization testing. Conclusion: Current macroscopic, NSC grading scales appear unable to account for microscopic, lenticular variations, and are not useful clinically. Relevance: Newer technology will be required to achieve objective assessment for NSC.

CLINICAL GRADING OF NUCLEAR SCLEROTIC CATARACTS Cataract remains the leading ophthalmic disease in the 21st century. Worldwide it is still the foremost cause of blindness.1 Lens and cataract procedures are the most common surgeries performed globally2 and in the US,3 and are some of the leading surgical procedures undertaken in Canada.4 Yet for such a ubiquitous ophthalmic finding, there continues to be a lack of clinical consensus regarding how to grade or classify this common entity. The need for a common ground becomes apparent on a daily basis as patients’ descriptions of “cataracts” often do not agree with those of clinicians, who in turn do not agree among themselves. P. Varner — John J. Pershing VA Medical Center, Poplar Bluff, MO Correspondence to: Dr. Paul Varner, John J. Pershing VA Medical Center, 1500 N. Westwood Blvd., Poplar Bluff, MO USA 63901; E-mail: paul.varner@va.gov Dr. Varner reports no financial conflicts of interest. The views expressed in this article are those of the author and do not necessarily represent the position of the US Department of Veterans Affairs. This article has been peer-reviewed.

The importance of objective clinical grading in medicine includes: allowance for determination of progression in clinical and pharmaceutical trials, professional concurrence in cases of litigious or disability claims, improved patient education (especially for those who move between multiple clinicians), and clearer communication between providers regarding clinical findings. This final point is especially important in the ophthalmic world where optometrists often identify patients with cataracts and then refer cases to comprehensive ophthalmologists for surgical correction. It is therefore incumbent upon optometrists and noncomprehensive ophthalmologists to correctly differentiate surgical lenses from non-surgical ones and to succinctly communicate these findings to the operating surgeons in order to streamline the referral process and to ensure that surgical procedures are obtained in the most timeeffective fashion. This is even more critical in parts of the world where access to health care is limited and surgical resources are limited. Visual acuities are the most widely-used test for visual function,5 but do not wholly assess visual disability related to cataracts,6,7 and — as a subjective test — can be tempered by depression, mood and anxiety.8,9 Ideally, a quantitative system would be used to control for subjective influence of both patients and examiners, and to remove qualitative interpretation from this process. In fact many grading systems have been developed in an attempt to standardize descriptions of the various types of cataracts, both in vitro10-13 and in vivo. For the latter case there are several subjective and objective methods described for assessment in the clinic (Table I14-34). To date, no “preferred” grading system has emerged from the ophthalmic community regarding usage of any of these scales. Description of mixed lenticular opacities as N02/NC3/C2 according to LOCS III criteria, for example, is not part of the lingua franca of the ophthalmic world outside research settings.

WHY IS THERE NO CONSENSUS? The answer to this seemingly innocuous question is surely multifactorial and involves any or all of the following components.

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Table I Cataract grading scales Subjective Methods

Date

Via

Oxford Clinical Cataract Classification and Grading System Johns Hopkins (Wilmer) Grading System Color Matching Technique New Dehli Cataract Classification Lens Opacity Rating System Japanese Cooperative Cataract Epidemiology Study Group Wisconsin System for Classification of Cataracts Lens Opacities Classification System (LOCS) III Age-Related Eye Disease Study (AREDS) System World Health Organization (WHO) Simplified Cataract Grading System

1986 1988 1988 1989 1989 1989 1990 1993 2001 2002

Slit lamp & diagrams14 Slit lamp & photographs15 Slit lamp & color samples16 Slit lamp & direct ophthalmoscope17 Slit lamp & photographs18 Slit lamp & photographs19,20 Photograph & standard photos21 Slit lamp & standard photos22 Photographs & standard photos (AREDS)23 Slit lamp & standard photographs24

National Eye Institute (NEI) Scheimpflug Cataract Imaging System Lens Opacity Meter Oxford Modular Cataract Image Analysis System (Case 2000 CCD Method)

1987 1990 1990

Digital Analyzer Lens Absorption Monitor Modified NEI Scheimpflug Cataract Imaging System Laser Slit Lamp Method Anterior Segment Optical Coherence Tomography Computer-Aided Nuclear Cataract Diagnosis System Optical Quality Analysis System

1991 1993 1993 1999 2009 2010 2011

Lens densitometry25 Modulated light source26 Slit lamp & retro-illuminated photos, computer-graded lenticular auto-fluorescence images27 Anterior segment camera/computer28 Video-based images29 Lens densitometry30 Laser slit lamp digital images31 Lens density measurement32 Computer-graded slit lamp images33 Double-pass measure of optical aberrations and light scatter34

Objective Methods

No cataract grading scale has proven to be generalizable. Providers seem unable to agree on the clinical grading of cataract. Inter-observer reliability for grading cataracts has been studied, but found to be poor.35,36 This is unfortunate, considering that confirming inter-observer reliability for cataract evaluation is expensive and time-consuming.37 Head-to-head comparison of subjective grading methods has found both correlation38,39 and poor agreement40 between various scales in the clinical setting. Adequate agreement between subjective and objective classification systems has also been reported in clinical setting,41 although has not translated into widespread professional consensus.

Cataractogenesis remains enigmatic and inevitable. Currently, the exact nature of cataractogenesis remains poorly understood.42 The eye’s lens thickens and turns yellow with age, eventually progressing to opacification (i.e., cataractogenesis).43,44 Cataract development is an unavoidable part of “aging” and will eventually develop in all humans whose longevity permits the natural course of events to unfold. As such perhaps there is little financial impetus to study the natural course of the disease.

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There is no prophylactic treatment against cataract formation, and the only treatment that is available is very successful. There is no prophylactic intervention proved to deter cataract development.44,45 Unlike many other ophthalmic conditions, there is currently only one treatment available for cataracts: surgical removal with prosthetic lens implantation.46 This highly-successful procedure has a 95% success rate, with a 0.001% risk of permanent vision loss.47 With such successful outcomes, cataract surgery is being performed at earlier stages in the disease,7,48 even for “clear-lens” extractions. It is possible that clinicians feel that this situation precludes the wide-spread need for accurate clinical assessment by formalized grading systems (i.e., it’s not a 6/6 (20/20) lens, it can be fixed surgically, end of story).

Cataract is not difficult to understand — no need to complicate the matter. Perhaps cataracts are so ubiquitous and conceptually easy to understand that that the topic is overlooked in the interest of teaching complexities of cornea, glaucoma, uveitis and retinal disease to trainees within the constraint of curricular demands. It is not unexpected that more time is

while some individuals with better vision/moreobvious cataract show little subjective visual improvement following lens extraction/implantation procedures. After a review of the above confounders surrounding cataract evaluation, it should not be surprising that clinical grading scales are not widely used. There is no easy answer to the initial question of why consensus has not been achieved for grading cataracts, and this conundrum has not been specifically addressed in the ophthalmic literature to date.

BACK TO BASICS Fig. 1 White nuclear sclerotic cataract (NSC)

devoted to refraction and contact lens fitting techniques than objective grading scales for cataract. 5.

Unavailability of technology for grading systems. Some objective grading systems rely on photographic or ancillary technology that is not widely available. Unlike automated perimeters or ocular coherence tomographs, Scheimpflug (algorithm for correcting distortions in photographs) and other computer-based technologies used in cataract research are not widely available or used in clinical settings.

Psychometric effects of grading scales. Perhaps proposed grading scales are too coarse for accurate interpretation by clinicians. In the absence of evenlyspaced benchmarks, finer scaling may be required to attain meaningful clinical grading of cataracts.49

Clinical non-correlation of lenticular opacities to visual acuity. Or is non-consensus in grading cataracts due to inconsistencies apparent in correlating lenticular opacities with best-corrected visual acuities? All clinicians have seen best visual acuities that do not correlate well with lenticular opacities (in the absence of other ophthalmic pathology). Occasional patients with advanced lenticular opacities still retain moderately “good” vision, while others with minimal cataract have unexpectedly-poor visual acuity — even considering the psychological state of the patient8,9 — regardless of the grading scale used to evaluate these subjects. It is a frustration to all clinicians when patients with poorer visual acuity/minimal lenticular opacities are found to have greatly improved vision following cataract surgery;

Although seemingly trivial, it is important to remember what a cataract is and is not. A cataract is an opacity of the lens.43,44,50 There are several types of lens opacities, with nuclear sclerotic, posterior subcapsular and cortical varieties being the most common clinically.24 In general, posterior subcapsular and cortical cataracts do not seem clinically difficult to describe — either the opacities are on-axis and visually-significant (symptomatic to patients) or off-axis and visually-insignificant (asymptomatic to patients). Subjective patient symptoms, best-corrected visual acuities and the degree of lens opacities correlate well enough clinically as to prevent frequent miscommunication between patients and providers for the management of these types of lenticular opacities. However, the continuum of nuclear sclerosis and nuclear sclerotic cataracts (NSC) is not so clear-cut. Nuclear sclerosis (i.e., hardening and loss of pliability of lens fibers) is a senescent process that is very commonly associated with yellow discoloration of the lens. The appearance of yellowing of the lens nucleus is readily apparent long before there is an effect on visual acuity or other measures of visual function: binocularity, contrast sensitivity, color desaturation, motion threshold, visual field, etc. It should be emphasized that varying degrees of nuclear sclerospresence of 6/6 (20/20) visual acuity (VA) should not be termed a “cataract.”44 The term cataract is only appropriate when opacification of the lens precludes 6/6 (20/20) VA, the most commonly used clinical measure of visual function. When not accompanied by opacification, nuclear sclerosis is simply an incidental, normal, age-related exam finding. (Advising patients with 6/6 (20/20) VA and nuclear sclerosis that they have “cataracts” — and the psychological implications of this practice for patients — is beyond the scope of this discussion, but is encountered on a daily basis in some patient populations.) It is equally important to recall that nuclear sclerosis is not always associated with yellowing of the lens. “White cataracts” (Fig. 1) occur with opacification of the lens nucleus in the absence of lens discoloration, and, in

Clinical Grading of Nuclear Sclerotic Cataracts — Varner

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NS Cataract Grading Scale 6/6 (20/20)

6/12 (20/40)

6/24 (20/80)

Clear Pseudophkic, or trace NS

1+ NSC

2+ NSC

6/48 (~20/150)

6/120 (~20/400)

>6/120 (>20/400)

No views of fundus

3+ NSC

4+ NSC

Mature Cataract

Fig. 2 Correlated anterior/posterior segment grading scale (representative views from right eyes purposely rotated 180 degrees to maintain consistent views for grading purposes)

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Fig. 3 Paradoxical correlation between lenticular opacity and fundus view

early stages, can be easily overlooked when evaluating a patient with subjective visual symptoms, decreased visual acuities, and a seemingly normal ocular health examination. Conversely, lens brunescence is more readily clinically apparent as a brown-colored appearance of the lens — an atypical form of nuclear sclerosis. The extreme presentations of white, yellow or brunescent lenticular opacities are often described as a “mature cataract.” Early stages of these variant clinical presentations may offer paradoxical challenges to clinicians accustomed to the clinical picture of typical lenticular yellowing and nuclear sclerotic opacification.

IS THERE A BETTER CLINICAL SOLUTION? Non-use of available subjective or objective cataract grading scales suggests an unanswered clinical problem, and opens the possibility of development a new clinicallyrelevant grading scale. Perhaps the answer is a grading scale that includes the appearance of lenticular opacities within the context of ocular fundus views. Figure 2 provides a chart correlating visual acuities, anterior segment photos of different degrees of nuclear sclerotic opacities, the corresponding fundus views taken through those same lenticular opacities, and an equivalent grade. For these images, all eyes either had 6/6 (20/20) VA prior to the development of lens opacities or attained 6/6 (20/20) VA postoperatively following cataract extraction procedures. All vertical columns are intended to be interchangeable: that is, a grade of 2+ NSC should correspond to approximately 6/24 (20/80) VA and the depicted view of the fundus; or a patient with roughly 6/24 (20/80) VA and the associated fundus view would be expected to have lenticular opacities consistent with the picture of grade 2+ NSC. (Incidentally, grades of “2” or “2-” (“two minus”) are not routinely used in medicine. The reasons may be lost to time, but it could be surmised that use of the + superscript was a quick way to distinguish handwritten

numbers from letters, and to prevent errors related to poor penmanship.) The gradations (e.g., 1+ to 2+) are intended to reflect a doubling of the visual angle [e.g., 6/12 (20/40) to 6/24 (20/80)]. It should be emphasized, based on this algorithm, that if there is no direct correlation between best-corrected visual acuity (BCVA) and the degree of lenticular opacity, then the cause for decreased VA should not be solely ascribed to “cataract.” The aim is to create a consistent measure of lens opacity and its effect on visual acuity. Thus a provider should be able to predict BCVA based on lenticular or fundus appearance and vice versa, and the matching grade assigned to a case would provide a standard for communication. Ultimately, this anterior segment-posterior segment, correlated grading scale failed to provide a consistent evaluation of nuclear cataracts during preliminary use. Many exceptions to these gradations were immediately revealed during initial applications of the scale, and it was quickly discovered that many lenticular opacities remain inconsistent with reported visual acuities. Figure 3 provides an example of a case with what should be a 3+ NSC lens, but with reasonable fundus view and visual acuity of 6/12 (20/40). Because lens grading and fundus views did not show a consistent relationship with best-corrected visual acuity, this grading scale also failed to provide a useful clinical tool, and must, too, be relegated to the growing pool of ineffective cataract grading scales.

DISCUSSION It may be inferred that the reason for the discrepancies found for this cataract grading method rests in the microscopic variations found within the lens matrices. Microscopic morphological features such as waterclefts, vacuoles and retrodot opacities have the potential to degrade vision,51 although they may not be readily apparent via biomicroscopy. Higher-order optical aberrations are not directly “observable” during clinical examination, but their presence may also explain non-correlation of subjective, “poorer” visual acuities with clinical examination of the lens.52-54 As lens opacification develops, it is likely an irregular process on the microscopic level of the lens proteins. It may be conjectured that tiny, clear areas remain juxtaposed to opaque ones, resulting in localized pinhole effects that are unobservable by direct examination. Thus, random irregularities within the opacified lens proteins may create optical pinhole effects, which account for visual acuities that are “better” than would be predicted based strictly on biomicroscopic observation of the lenses themselves. Conversely, mildly opacities directly obscuring the eye’s nodal points may result in a VA “worse” than

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might be predicted by direct lens and fundus observations. In the final analysis, it may be surmised that the lack of clinical consensus on existing cataract grading scales is a culmination of lenticular factors at the microscopic level, and may serve to answer the question “why aren’t published grading scales used widely in clinical settings?” Surely future grading systems may redefine cataract in terms of events at the microscopic — rather than macroscopic — level.

CONCLUSION Perhaps a re-formulation of the question at hand is indicated: Are reliable cataract grading scales achievable for clinical use? Given the limits of current cataract grading scales, it appears that clinicians will require newer technology to objectively quantify lens opacification. Recently, use of an Objective Scatter Index was reported to correlate with severity of cataract and visual acuity.7 This technology quantifies optical aberration and light scatter in an objective way. Future study will determine if this method provides sound clinically-useful data. Scanning laser algorithms, aberrometry, and optical coherence tomographs, or a combination of these technologies, are possible avenues for future exploration, although there currently seems to be little incentive to drive these research questions. As such, at least for the present, it appears that reliable quantification of NSC will remain elusive due to higher-order aberrations and localized pinhole effects within lens protein matrices. Ultimately, we are left with a clinical challenge. Clinicians should be aware of these shortcomings in their attempts to quantify and communicate severity of nuclear sclerotic cataracts. Providers must continue to critically view lenticular opacities, but must still consider subjective reports of visual disability to guide decisions of ophthalmic surgical care. ❏ Acknowledgements: The author would like to thank Antonia Varner for the preparation of the Figures and Table.

REFERENCES 1.

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World Health Organization. Visual impairment and blindness. 2013. http://www.who.int/mediacentre/ factsheets/ fs282/en/. Accessed 01 Jul 2014. Kohnen T, Baumeister M, Kook D, et al. Cataract surgery with implantation of an artificial lens. Dtsch Arzteblt Int 2009; 106: 695-702. US Department of Health & Human Services, Agency for Healthcare Research and Quality (AHRQ). Ambulatory surgery in US hospitals, 2003. http://www.ahrq.gov/data/ hcup/factbk9/factbk9b.htm. Accessed 01 Jul 2014. Canadian Institute for Health Information. Waiting for health care in Canada: what we know and what we don't know. 2006. http://secure.cihi.ca/cihiweb/products/ WaitTimesReport_06_e.pdf. Accessed 07 Feb 2014.

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25. Datiles MB, Edwards PA, Trus BL, Green SB. In vivo studies on cataracts using the Scheimpflug slit lamp camera. Invest Ophthalmol Vis Sci 1987; 28: 1707-1710. 26. Flammer J, Bebie H. Lens opacity meter: a new instrument to quantify lens opacity. Ophthalmologica 1987; 195: 69-72. 27. Sparrow JM, Phelps Brown NA, Shun-Shin GA, Bron AJ. The Oxford modular cataract image analysis system. Eye 1990; 4: 638-648. 28. Adamsons I, Taylor KI, Enger C, Taylor HR. A new method for documenting lens opacities. Am J Ophthalmol 1991; 111: 65-70. 29. Johnson CA, Howard DL, Marshall D, Shu H. A noninvasive video-based method for measuring lens transmission properties of the human eye. Optom Vis Sci 1993; 70: 944-955. 30. Vivino MA, Chintalagiri S, Trus B, Datiles M. Development of a Scheimpflug slit lamp camera system for quantitative densitometric analysis. Eye 1993; 7: 791-798. 31. Hall NF, Lempert P, Shier RP, et al. Grading nuclear cataract: reproducibility and validity of a new method. Br J Ophthalmol 1999; 83: 1159-1163. 32. Wong AL, Leung CK-S, Weinreb RN, et al. Quantitative assessment of lens opacities with anterior segment optical coherence tomography. Br J Ophthalmol 2009; 93: 61-65. 33. Li H, Lim JH, Mitchell P, et al. A computer-aided diagnosis system of nuclear cataract. IEEE Trans Biomed Eng 2010; 57: 1690-1698. 34. Vilaseca M, Romero MJ, Arjona M, et al. Grading nuclear, cortical and posterior subcapsular cataracts using an objective scatter index measured with a double-pass system. Br J Ophthalmol 2012; 96: 1204-1210. 35. Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham eye study monograph: an ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration and visual acuity in a general population of 2631 adults, 1973-1975. Surv Ophthalmol 1980; 24(Suppl): 335-610. 36. West S, Rosenthal F, Newland HS, Taylor HR. A comparison of methods for typing and grading lens opacities for field surveys. ARVO Abstracts. Invest Ophthalmol Vis Sci 1985; 26: 119. 37. West SK, Rosenthal F, Newland HS, Taylor HR. Use of photographic techniques to grade nuclear cataracts. Invest Ophthalmol Vis Sci 1988; 29: 73-77. 38. Taylor HR, Lee JA, Wang F, Muñoz B. A comparison of two photographic system for grading cataract. Invest Ophthalmol Vis Sci 1991; 32: 529-532. 39. Hall AB, Thompson JR, Deane JS, Rosenthal AR. LOCS III versus the Oxford Clinical Cataract Classification and Grading System for the assessment of nuclear, cortical and posterior subcapsular cataract. Ophthalmic Epidemiol 1997; 4: 179-194.

40. Tan ACS, Wang JJ, Lamoureux EL, et al. Cataract prevalence varies substantially with assessment systems: comparison of clinical and photographic grading in a population-based study. Ophthalmic Epidemiol 2011; 18: 164-170. 41. Robman LD, McCarty CA, Garrett SKM, et al. Comparison of clinical and digital assessment of nuclear optical density. Ophthalmic Res 1999; 31: 119-126. 42. Andjeli S, Hawlina M. Cataractogenesis. Zdrav Vestn Suppl (Slovenian Medical Journal) 2012; 1: I122-I132. 43. Hart WM, ed. Adler’s Physiology of the Eye. St Louis: Mosby-Year Book, Inc, 1992: 348. 44. Snell RS, Lemp MA. Clinical Anatomy of the Eye. Boston: Blackwell Scientific Publications, 1989: 184. 45. Robin AL, Thulasirag RD. Cataract blindness. Arch Ophthalmol 2012; 130: 1452-1455. 46. de Silva SR, Riaz Y, Evans JR. Phacoemulsification with posterior chamber intraocular lens versus extracapsular cataract extraction (ECCE) with posterior chamber intraocular lens for age-related cataract. Cochrane Database Syst Rev. 2014, Issue 1. Art. No.: CD008812. DOI: 10.1002/ 14651858. CD008812.pub2. 47. National Health Service. Cataract surgery. 2013. http://www.nhs.uk/Conditions/Cataract-surgery/Pages/ Results.aspx. Accessed 07 Feb 2014. 48. Klein BEK, Howard KP, Lee KE, Klein R. Changing incidence of lens extraction over 20 years. Ophthalmology 2014; 121: 5-9. 49. Bailey IL, Bullimore MA, Raasch TW, Taylor HR. Clinical grading and the effects of scaling. Invest Ophthalmol Vis Sci 1991; 32: 422-432. 50. Duke-Elder, S. System of Ophthalmology, Vol XI. St Louis: The CV Mosby Company, 1969: 63. 51. Holden R, Hesler J, Forbes J, Phelps Brown NA. Visual performance and objectively measured grades of cataract. A correlation of methods designed for use in longitudinal trials. Optom Vis Sci 1993; 70: 982-985. 52. Donnelly WJ 3rd, Pesudovs K, Marsack JD, et al. Quantifying scatter in Shack-Hartmann images to evaluate nuclear cataract. J Refract Surg 2004; 20: S515-S522.53. Rocha KM, Nosé W, Bottós K, et al. Higher-order aberrations of age-related cataract. J Cataract Refract Surg 2007; 33: 1442-1446.54. Lee J, Kim MJ, Tchah H. Higher-order aberrations induced by nuclear cataract. J Cataract Refract Surg 2008; 34: 2104-2109. 53. Rocha KM, Nosé W, Bottós K, et al. Higher-order aberrations of age-related cataract. J Cataract Refract Surg 2007; 33: 1442-1446. 54. Lee J, Kim MJ, Tchah H. Higher-order aberrations induced by nuclear cataract. J Cataract Refract Surg 2008; 34: 21042109.

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QUESTIONNAIRE Clinical Grading of Nuclear Sclerotic Cataracts Paul Varner, OD, MPH 1. A) B) C) D)

What is the foremost cause of blindness worldwide? Glaucoma Cataract Macular edema Stroke

2. A) B) C) D)

All of the following statements are true, EXCEPT: Cataract is an unavoidable part of “aging” A recently-developed grading scale for cataracts has proved to be generalizable There is no prophylactic treatment against cataract formation Visual acuities are the most widely-used test for visual function

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A) B) C) D) 4.

Surgical cataract removal with prosthetic lens implantation has been successful in what percentage of patients? 60% 75% 80% 95%

A) B) C) D)

What is the risk of permanent vision loss with surgical cataract removal with prosthetic lens implantation? 0.001% 0.003% 0.05% 0.5%

5. A) B) C) D)

All of the following statements about cataract are true, EXCEPT: Yellowing of the lens nucleus is apparent long before visual acuity is affected Nuclear sclerosis is associated with yellowing of the lens in 100% of cases Nuclear sclerosis is not always associated with yellowing of the lens “Mature cataracts” may have extreme presentations of white lenticular opacities

6. A) B) C) D)

All of the following are evidence of cataract, EXCEPT: Family history of the condition Best-corrected visual acuities Subjective patient symptoms The degree of lens opacities

7. A) B) C) D)

All of the following objective methods for assessment in the clinic used lens densitometry or lens density measurement, EXCEPT: National Eye Institute (NEI) Scheimpflug Cataract Imaging System Modified NEI Scheimpflug Cataract Imaging System Digital Analyzer Anterior Segment Optical Coherence Tomography

8. A) B) C) D)

What are the most common surgeries performed globally? Coronary bypass Hip replacement Coronary stents Lens and cataract procedures

9. A) B) C) D)

All of the following statements about cataract are true, EXCEPT: Agreement between subjective and objective classification systems has been inadequate Inter-observer reliability for grading cataracts has been found to be poor Visual acuities do not wholly assess visual disability related to cataracts Unavailability of technology for grading systems has been an impediment

10. A) B) C) D)

According to the paper, visual acuities can be tempered by all of the following, EXCEPT: Depression Medication Anxiety Mood

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News and Notes Mount Sinai Researchers Use Breakthrough Technology to Further Understand Eye Damage from Eclipse In a first-of-its-kind study, Mount Sinai researchers are using adaptive optics (AO) to analyze retinal eye damage from the August solar eclipse on a cellular level. The research could help doctors develop a deeper understanding of this rare condition, called solar retinopathy, which has no currently accepted treatment. Adaptive optics is a sophisticated technology that allows clinicians to examine microscopic structures of the eye in living patients with extreme detail in real time. Before the development of AO, researchers could only see this level of detail on glass slides with a microscope. A team of scientists from the New York Eye and Ear Infirmary of Mount Sinai (NYEE) and the Icahn School of Medicine at Mount Sinai used this state-of-the-art imaging technology to get a precise view of how much individual cellular damage resulted from the solar eclipse, something that has never been done before. The findings were published in the December 7 online issue of JAMA Ophthalmology. “We have never seen the cellular damage from an eclipse because this event rarely happens and we haven’t had this type of advanced technology to examine solar retinopathy until recently,” said lead investigator Avnish Deobhakta, MD, Assistant Professor of Ophthalmology at the Icahn School of Medicine at Mount Sinai. “NYEE is one of the few sites in North America with access to this technology, and using this to get an exact look at this retinal damage on such a precise level will help clinicians better understand the condition.” Mount Sinai investigators used AO imaging on a patient who looked at the sun during the eclipse for 21 seconds without protective eyewear. Four hours later, the patient developed blurry distortion in both eyes and could only see the color black. NYEE specialists examined her three days later and found she had burned a hole in her retinas and diagnosed her with solar retinopathy and photochemical burns. Using this technology, researchers obtained high-resolution images of the damaged photoreceptors, which may provide a deeper understanding of the condition that could one day lead to the development of treatments. “It’s exciting to be able to see such a correlation between the patient’s symptoms and the photoreceptor injury on a cellular level. Hopefully this research allows us to potentially develop future therapies for solar retinopathy and other forms of photic injury to the retina,” said Chris Wu, MD, a resident physician at New York Eye and Ear Infirmary of Mount Sinai. “This study can prepare doctors and patients for the next eclipse in 2024, and make them more informed of the risks of directly viewing the sun without protective eyewear.”

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