DOCSLIB.ORG

Doctor, Why Can't I See? Evaluation of the Patient Uncorrectable to 20/20

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Doctor, Why Can't I See? Evaluation of the Patient Uncorrectable to 20/20 8/26/2019 Speakers Bureau for Aeri, Allergan, Bausch & Lomb, Glaukos, Ivantis, Optovue, Reichert Robert P. Wooldridge, O.D., F.A.A.O. Always be able to account for a patient’s VA Always be able to account for a patient’s VF Always be able to account for a patient’s C/O LOV ◦ vague complaint Anatomical Approach Refractive How to Evaluate Media opacity/distortion Refraction Macula problem ◦ Retinoscopy-lost skill look for scissors/distorted reflex Optic nerve/Neurologic Pinhole VA Amblyopia High order aberrations Hysteria/malingering 1 8/26/2019 Tear film Grade the View! Cornea VA vs View ◦ PEK, Central Cloudy Dystrophy of Francois (CCDF) Anterior Chamber 20/80 ◦ Careful evaluation for C/F hem, etc Lens ◦ Milky white NS vs yellow brown NS; vacuoles Vitreous 20/20 ◦ Hemorrhage ◦ Clarity: variable, cloudy ◦ Punctate Keratopathy Slit Lamp exam PEK, SPK Tear BUT ◦ Opacity: Oculus Topographer Scar Epithelial edema Stromal edema Central Cloudy Dystrophy of Francois (CCDF) Slit Lamp exam Keratoconus Corneal topography Pellucid Marginal Retinoscopy Degeneration (PMD) Pachymetry Post LASIK/PRK ◦ Ultrasonic Post PKP ◦ OCT CL induced 2 8/26/2019 Unusual cause of Nuclear sclerosis (NS) unclear media ◦ Milky white vs. Careful slit lamp brunescent yellow/brown NS exam ◦ Vacuoles ◦ Cells/flare Cortical cataract ◦ RBC’s ◦ Anterior (ACC) Turn the SL light ◦ Posterior (PCC) up high! Posterior Subcapsular (PSC) Easier to see with dilated pupil Myopic shift is a good hint of cataract progression! Slit Lamp exam 50yo WM referred as Glaucoma suspect Direct and Retro VA 20/20 OU illumination C/O occasional cloudy vision OD Contrast Sensitivity ◦ Without glare H/O RD repair 1981 ◦ With glare 18yo WF referred: VA uncorrectable to 20/20 Patient unsure of course of VA Wears DWSCL MH: mild congenital hear defect FH: Father has poor VA cc BVA R 20/25- L 20/40 low myopia Pupils, SLE Normal OU CT: Orthophoric Stereo 5/9 SLE NL OU DFE: OD NL OS mild RPE change in macula 3 8/26/2019 Amsler grid Color Vision Corneal Topography Fluorescein Angiogram OCT Disc OCT Macula ERG/EOG MRI Brain and orbits Fundus Flavimaculatus Autosomal recessive Early stage may show little/no visible retinal signs Fluorescein angiogram often diagnostic ERG may be NL 4 8/26/2019 VA R 20/30 L 20/40 38 yo Nepalese Male moved to US in 1996 Referred for glaucoma evaluation H/O good VA as a child ◦ Began to have decreased vision with light at 18yo ◦ First glasses in 1996; not diagnosed with glaucoma ◦ Has been on glaucoma drops x 1 year ◦ Using Travatan-Z, Cosopt, Alphagan-P OU Medical history: NL FH: 5 siblings; sister has similar symptoms VAsc R 20/200 L 20/100 NI with refraction Pupils, motility NL OU CT: Orthophoric SLE NL OU with mild hyperemia OU; ◦ lenses clear IOP R 18 L 16 CCT R 542 L 542 Color vision R 2/15 L 2/15 Fundus as seen 5 8/26/2019 Glaucoma Other optic nerve disease Media opacity Macular problem Amblyopia Neurological problem Corneal Topography Fluorescein Angiogram OCT Disc OCT Macula ERG/EOG MRI Brain and orbits 6 8/26/2019 VEP’s very poor OU mfERG’s abnormal outside central macular area Full field ERG: ◦ Very attenuated photopic responses ◦ Normal scotopic responses No diagnosis given Referred to neuro-ophthalmology for second opinion who then referred him to retinal specialist for third opinion Retinal Cone Dystrophy 42yo WM Life-long H/O poor VA OU Diagnosed as amblyopia OU since childhood VA R20/30 L 20/30 Pupils NL Neg. APD CT:orthophoric SLE NL OU DFE NL but thin macular RPE, ◦ No foveal reflex Bilateral amblyopia No strabismus No uncorrected refractive error/astigmatism No H/O ocular surgery 7 8/26/2019 SL with: ◦ HH lens, fundus CL BIO Direct O-scope Amsler Grid OCT Photo Fundus Autofluoresence (FAF) Fluorescein Angiography (FA) Multifocal ERG 2009 Congenital Dystrophies 65yoWF C/O Acquired diseases distorted VA OS ◦ Age-related Macular Degeneration (AMD) ◦ Diabetic retinopathy VA 20/20- OU ◦ Edema Pupils, VF NL ◦ Epi-retinal Membrane (ERM) A Grid ◦ Hole ◦ OD Nl ◦ Hypoplasia ◦ OS distorted ◦ Toxicity-drug SLE 1+ NS OU ◦ Vascular disease/event ◦ Inflammatory diseases Trauma 5/05/2011 5/06/13 20/20-20/25 20/20-20/25 8 8/26/2019 Pre-retinal membrane VERY common Usually due to PVD causing tear in ILM ◦ Glial cells proliferate on retinal surface May also be associated with diabetic retinopathy and other retinopathies Treatment is PPV/membrane peel if visually significant ◦ VA criteria variable 60yo WF referred with VA uncorrectable to 20/20 Previous exam showed no apparent cause VA R 20/20 L 2030 Minimal distortion on A grid OS Pupils, CVF NL OU Cover test orthophoric OU SLE NL OU 9 8/26/2019 66 yo WM C/O “barrel distortion” OD ◦ X1 week; constant, notices at near only ◦ No complaints OS VA R 20/80 L 20/20 A. Grid +distortion OD only Pupils NL SLE 1+ NS OU Larry Pre PPV/MP Larry Post PPV/MP PPV/MP 12/05/12 Last visit July 2013 VA R 20/80 L 20/25 Still has some distortion OD SLE OD 3+ NS OS 1+ NS DFE OD: Mild RPE change OS 2+ ERM 10 8/26/2019 68 yo WF treated for glaucoma Visual Acuity OS? VA R 20/20 L 20/25 Measured in 2013 as R 20/15 L20/15- with PTMH present ERM PTMH 20/20- OU 11 8/26/2019 PTMH FTMH Patient may be asymptomatic Patient usually symptomatic VA may be good/excellent 20/15-20/30 VA usually 20/70-20/400 ERM and/or PVD often co-existent Treatment: PPV/gas bubble No treatment indicated 73yo WF 6 weeks postop. phaco patient C/O decreasing VA for past 2 weeks 12 8/26/2019 1995 20/20 OU no complaints; NL exam Young adult 2002 vertical diplopia: LSO; MRI shows UBO’s Males> females ◦ No specific systemic diagnosis made Unilateral 2005: VA R 20/20-25 L 20/25-30 ◦ Central oval RPE change OU noted ◦ Attempted FA; could not find vein ◦ Retinal specialist noted mild macular pigmentary changes, no need to WU further, mfERG if desired ◦ mfERG=Normal 2007: FA at JMEC confirms parafoveal telangiectasia 2012 OD 20/30 OS 20/50-70 S/P multiple Avastin injections 13 8/26/2019 68yo WF C/O poor VA OU S/P phaco/IOL OD Sep. 2009;poor VA since then; no reason given VA R 20 25- L 20/50 Pupils, color VA, CT NL OU SLE: OD 2+ PCO OS Cataract DFE:“Trace central sensory retinal change OU” 28yo WM C/O blurred VA OD x 3 months Corneal topography MH No medical illnesses or complaints OCT macula VAsc R 20/70 L 20/20; NI with refraction OCT disc Pupils NL Neg APD Visual field CVF FTFC OU Fluorescein angiogram Motilities full OU; CT orthophoric MRI brain/orbits Color VA R 4/14 L 13/14 ERG/EOG/VEP Amsler grid OD IT paracentral scotoma; OS nl SLE, DFE completely NL OU OCT macula is normal VF has some bitemporal flavor Plan: MRI/MRA brain and orbits c/s contrast 14 8/26/2019 Had pituitary tumor resected Jan. 22 VAsc R 20/15 L 20/15 Color Vision R 15/15 L 15/15 Pupils NL Last seen in 2012: all findings normal Slit lamp with hand-held lens Visual Evoked Potential (VEP) Direct ophthalmoscope MRI/CT Fundus photography Ultrasound ◦ Fundus autofluoresence Fluorescein angiography OCT HRT Visual field Pupil reactions Color vision Glaucoma Arcuate bundle defect Optic Neuritis Does NOT respect vertical midline ◦ Anterior NO early CENTRAL scotoma ◦ Retro-bulbar ◦ But paracentral possible! Optic nerve drusen Nasal usually worse than temporal Papilledema Temporal to blind spot last to go Ischemic Optic Neuropathy (AION) Remember to correlate with cupping! 15 8/26/2019 57yoWF referred with poor VA OS, cause BVA R 20/25+ L 20/70 unknown Pupils NL Neg APD ◦ Thought to have some AMD OS Motility full; CT orthophoric 3 mos ago pat. was looking at Amsler grid IOP R 13 L 14 with friends at home and noted distortion OS Amsler grid OD NL OS paracentral distortion ◦ Does not know if onset was sudden or gradual SLE NL; lenses clear OU ◦ No VA complaint OD ◦ H/O seeing 20/20 OU in past years DFE as seen MH: Normal, no medical illnesses ◦ 8 children (post traumatic stress??) ◦ No significant HA’s or other complaints Normal Tension glaucoma Anterior ischemic optic neuropathy Optic atrophy Intracranial mass Prostaglandin QHS OU MRI CBC, ESR, CRP ◦ reveals Pituitary adenoma Fluorescein angiogram OCT macula Tumor resected MRI brain/orbits 16 8/26/2019 Confrontation VF are Not Enough!! Just Another Day With the Wooldridge Teens Mental disorder that impairs physical Conscious attempt to deceive for personal functions with no physiological basis; sensory gain motor symptoms include seizures, paralysis, temporary blindness; increase in stress or avoidance of unpleasant responsibilities may precipitate Subconscious response Patient believes he/she has a real problem But may have something to gain 17 8/26/2019 Patient has a true organic disease/problem Hysteria: But also has a functional component ◦ Young: 9-13yo most common Adults possible ◦ Female Malingering ◦ Late teens to adults Loss of Vision Reads every line at same slow speed, letter by ◦ Monocular or binocular letter ◦ Central or peripheral Ambulates well despite C/O severe LOV ◦ Usually sudden in onset Severely constricted CVF Can be dated/connected to an event ◦ Sometimes vague, uncertain NO APD despite severe unilateral LOV Careful history 1.
Load more

Recommended publications
  • Treacher Collins Prize Essay the Significance of Nystagmus
    Eye (1989) 3, 816--832 Treacher Collins Prize Essay The Significance of Nystagmus NICHOLAS EVANS Norwich Introduction combined. The range of forms it takes, and Ophthalmology found the term v!to"[<xy!too, the circumstances in which it occurs, must be like many others, in classical Greece, where it compared and contrasted in order to under­ described the head-nodding of the wined and stand the relationships between nystagmus of somnolent. It first acquired a neuro-ophthal­ different aetiologies. An approach which is mological sense in 1822, when it was used by synthetic as well as analytic identifies those Goodl to describe 'habitual squinting'. Since features which are common to different types then its meaning has been refined, and much and those that are distinctive, and helps has been learned about the circumstances in describe the relationship between eye move­ which the eye oscillates, the components of ment and vision in nystagmus. nystagmus, and its neurophysiological, Nystagmus is not properly a disorder of eye neuroanatomic and neuropathological corre­ movement, but one of steady fixation, in lates. It occurs physiologically and pathologi­ which the relationship between eye and field cally, alone or in conjunction with visual or is unstable. The essential significance of all central nervous system pathology. It takes a types of nystagmus is the disturbance in this variety of different forms, the eyes moving relationship between the sensory and motor about one or more axis, and may be conjugate ends of the visual-oculomotor axis. Optimal or dysjugate. It can be modified to a variable visual performance requires stability of the degree by external (visual, gravitational and image on the retina, and vision is inevitably rotational) and internal (level of awareness affected by nystagmus.
    [Show full text]
  • WSPOS Worldwide Webinar 16: Amblyopia - How and When
    Answers to Audience Questions - WSPOS Worldwide Webinar 16: Amblyopia - How and When WWW 16 Panellists Anna Horwood Celeste Mansilla David Granet Krista Kelly Lionel Kowal Susan Cotter Yair Morad Anna Horwood (AH), Celeste Mansilla (CM), Krista Kelly (KK), Lionel Kowal (LK), Susan Cotter (SC), Yair Morad (YM) 1. How do you maintain attained iso visual acuity after successful amblyopia treatment? AH: Intermittent monitoring. If they have regressed previously, I might carry on very intermittent occlusion (an hour or two a week) until I was sure it was stable. CM: With gradual and controlled reduction of the treatment, for example: if the patient had 1 hour of patch per day, I leave it with 1 hour 3 times a week during a month. I do a check and if the visual acuity was maintained, I lower patches to 2 times a week. I keep checking and going down like this until I suspend the treatment. If at any time I detect worsening visual acuity, I return to the previous treatment. SC: Best way is attainment of normal binocular vision. I do not worry about ansiometropic amblyopes who have random dot stereopsis post-treatment. If have constant unilateral strabismus, I can do some limited part-time patching, decreasing patching dosage over time given no regression of VA. YM: repeat examination every 6 months. If I see regression, I will prescribe patching for 30 min a day. 2. How do you plan for very dense amblyopes? AH: I very rarely see them because, with screening, they are picked up early and usually do well.
    [Show full text]
  • Pediatric Ophthalmology/Strabismus 2017-2019
    Academy MOC Essentials® Practicing Ophthalmologists Curriculum 2017–2019 Pediatric Ophthalmology/Strabismus *** Pediatric Ophthalmology/Strabismus 2 © AAO 2017-2019 Practicing Ophthalmologists Curriculum Disclaimer and Limitation of Liability As a service to its members and American Board of Ophthalmology (ABO) diplomates, the American Academy of Ophthalmology has developed the Practicing Ophthalmologists Curriculum (POC) as a tool for members to prepare for the Maintenance of Certification (MOC) -related examinations. The Academy provides this material for educational purposes only. The POC should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed at obtaining the best results. The physician must make the ultimate judgment about the propriety of the care of a particular patient in light of all the circumstances presented by that patient. The Academy specifically disclaims any and all liability for injury or other damages of any kind, from negligence or otherwise, for any and all claims that may arise out of the use of any information contained herein. References to certain drugs, instruments, and other products in the POC are made for illustrative purposes only and are not intended to constitute an endorsement of such. Such material may include information on applications that are not considered community standard, that reflect indications not included in approved FDA labeling, or that are approved for use only in restricted research settings. The FDA has stated that it is the responsibility of the physician to determine the FDA status of each drug or device he or she wishes to use, and to use them with appropriate patient consent in compliance with applicable law.
    [Show full text]
  • Strabismus, Amblyopia & Leukocoria
    Strabismus, Amblyopia & Leukocoria [ Color index: Important | Notes: F1, F2 | Extra ] EDITING FILE ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ ​ Objectives: ➢ Not given. Done by: Jwaher Alharbi, Farrah Mendoza. ​ ​ Revised by: Rawan Aldhuwayhi ​ Resources: Slides + Notes + 434 team. ​ ​ NOTE: F1& F2 doctors are different, the doctor who gave F2 said she is in the exam committee so focus on her notes Amblyopia ● Definition Decrease in visual acuity of one eye without the presence of an organic cause that explains that decrease ​ ​ in visual acuity. He never complaints of anything and his family never noticed any abnormalities ​ ● Incidence The most common cause of visual loss under 20 years of life (2-4% of the general population) ● How? Cortical ignorance of one eye. This will end up having a lazy eye ​ ● binocular vision It is achieved by the use of the two eyes together so that separate and slightly dissimilar images arising in each eye are appreciated as a single image by the process of fusion. It’s importance 1. Stereopsis 2. Larger field If there is no coordination between the two eyes the person will have double vision and confusion so as a compensatory mechanism for double vision the brain will cause suppression. The visual pathway is a plastic system that continues to develop during childhood until around 6-9 years of age. During this time, the wiring between the retina and visual cortex is still developing. Any visual problem during this critical period, such as a refractive error or strabismus can mess up this developmental wiring, resulting in permanent visual loss that can't be fixed by any corrective means when they are older Why fusion may fail ? 1.
    [Show full text]
  • Assessment and Management of Infantile Nystagmus Syndrome
    perim Ex en l & ta a l ic O p in l h t C h f Journal of Clinical & Experimental a o l m l a o n l r o Atilla, J Clin Exp Ophthalmol 2016, 7:2 g u y o J Ophthalmology 10.4172/2155-9570.1000550 ISSN: 2155-9570 DOI: Review Article Open Access Assessment and Management of Infantile Nystagmus Syndrome Huban Atilla* Department of Ophthalmology, Faculty of Medicine, Ankara University, Turkey *Corresponding author: Huban Atilla, Department of Ophthalmology, Faculty of Medicine, Ankara University, Turkey, Tel: +90 312 4462345; E-mail: [email protected] Received date: March 08, 2016; Accepted date: April 26, 2016; Published date: April 29, 2016 Copyright: © 2016 Atilla H. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract This article is a review of infantile nystagmus syndrome, presenting with an overview of the physiological nystagmus and the etiology, symptoms, clinical evaluation and treatment options. Keywords: Nystagmus syndrome; Physiologic nystagmus phases; active following of the stimulus results in poor correspondence between eye position and stimulus position. At higher velocity targets Introduction (greater than 100 deg/sec) optokinetic nystagmus can no longer be evoked. Unlike simple foveal smooth pursuit, OKN appears to have Nystagmus is a rhythmic, involuntary oscillation of one or both both foveal and peripheral retinal components [3]. Slow phase of the eyes. There are various classifications of nystagmus according to the nystagmus is for following the target and the fast phase is for re- age of onset, etiology, waveform and other characteristics.
    [Show full text]
  • Amblyopia HANDOUT ACES
    AMBLYOPIA CORNEA PUPIL CATARACT IRIS LENS RETINA MACULA OPTIC NERVE The eye on the right is at risk for all three types of AMBLYOPIA. Rays of light enter the normal eye on the left, are bent by the cornea and the lens and are focused one the most precise part of the retina called the macula. Light entering the right eye is disrupted by a congenital cataract (deprivational amblyopia). Since the right eye is shorter than the left, light doesn't focus on the retina due to unequal far-sightedness(refractive amblyopia). Since the left eye is crossed (esotropia-type strabismus), incoming light fails to align on the macula (strabismic amblyopia). ye doctors and orthoptists want each child to grow frequently suppresses or "turns off" the brain image from up with the healthiest visual system possible. the non-dominant eye. Strabismic amblyopia can be E This goal requires the close cooperation of treated by combinations of drops, glasses, patching parents, pediatricians, primary doctors, optometrists, and/or eye muscle surgery. school nurses and health aids and the professionals who DETECTION: Within the first days after birth, deal with visually impaired babies. part of each baby's first physical exam is the "red reflex" an abnormality of which could indicate cataract or tumor. At birth, a normal infant has relatively poor vision in the range A part of routine pre-school pediatric check-ups is of 20/2000! Under normal conditions, the visual system improves so that observations of red reflex by photoscreen and Brückner 20/20 vision might be attained by school age and retained after age 10 years.
    [Show full text]
  • 6269 Variation of the Response to the Optokinetic Drum Among Various Strain
    [Frontiers in Bioscience 13, 6269-6275, May 1, 2008] Variation of the response to the optokinetic drum among various strains of mice Oliver Puk1, Claudia Dalke1, Martin Hrabé de Angelis2, Jochen Graw1 1 GSF-National Research Center for Environment and Health, Institute of Developmental Genetics, D-85764 Neuherberg, Germany, 2GSF-National Research Center for Environment and Health, Institute of Experimental Genetics, D-85764 Neuherberg, Germany TABLE OF CONTENTS 1. Abstract 2. Introduction 3. Materials and methods 3.1. Animals 3.2. Vision test protocol 3.3. Statistical analysis 3.4. Funduscopy 3.5. Electroretinography 3.6. Histology 4. Results 4.1. Head-tracking behavior 4.2. Electroretinography, funduscopy and histology of DBA/2 and BALB/c mice 4.3. Linkage analysis of BALB/c 5. Discussion 6. Acknowledgement 7. References 1. ABSTRACT 2. INTRODUCTION The mouse is currently an established The optokinetic drum has become an appropriate mammalian model for studying hereditary disorders, which tool to examine visual properties of mice. We performed have an effect on eye structure and function. In order to baseline measurements using mice of the inbred strains select and characterize mouse mutants suffering from C3H, C57BL/6, BALB/c, JF1, 129 and DBA/2 at the age of ocular defects, a variety of test systems are well 8-15 weeks. Each individual C57BL/6, 129 and JF1 mouse established, like slit lamp analysis for detecting lens was reliably identified as non-affected in vision by opacities, iris and corneal abnormalities (1-3), funduscopy determining head-tracking responses. C3H mice were used for abnormalities of the retinal fundus, reflecting retinal as negative control because of their inherited retinal degeneration, vascular problems and optic disc alterations degeneration; as expected, they did not respond to the (4), or electroretinography for functional disorders of the moving stripe pattern.
    [Show full text]
  • Human Amblyopia
    Human Amblyopia • “Lazy Eye” • Relatively common developmental visual disorder (~2%) • Reduced visual acuity in an otherwise healthy and properly corrected eye • Associated with interruption of normal early visual experience • Most common cause of vision loss in children • Well characterized behaviorally, not neurologically • Treated by patching in children Visual Deficits in Amblyopia • Reduced monoc. visual acuity - defining feature – Usually 20/30 - 20/60 • Impaired contrast sensitivity – Prominent at high spatial frequencies Contrast Sensitivity Sensitivity Contrast – Central visual field is generally most affected Spatial Frequency • Moderate deficits in object segmentation/recognition and spatial localization • Severe deficits in binocular interactions Subtypes of Amblyopia • Anisometropic – Unequal refractive error between the two eyes • Strabismic – Deviated eye that may or may not have unbalanced refraction • Deprivation – Congenital cataract; corneal opacity; eyelid masses Mechanisms of Amblyopia 1. Form deprivation . Sharp image is not formed at the retina 2. Abnormal binocular vision . Binocularity is often changed or lost in amblyopia Models of Amblyopia • Competition hypothesis originated with experiments in kittens in the 1960s by Hubel and Wiesel • Monocular deprivation of retinal input during ‘critical’ developmental periods leads to striking abnormalities in the physiology of visual cortical neurons • Binocular deprivation actually leads to less severe abnormalities • Amblyopia may be a form of activity-dependent deprivation,
    [Show full text]
  • Eye Care for EB Patients Debra.Org
    Eye Care for EB Patients Strategies to prevent blistering, scarring and vision loss DEBRA Care Conference 7.23.18 Vicki M. Chen, MD Assistant Professor of Ophthalmology New England Eye Center Tufts Medical Center / Floating Hospital for Children Boston, MA Financial Disclosures • None relevant Lecture Outline 1. What EB related problems can occur in the eye? 2. How can we prevent these problems? 3. Can we do more to reduce pain and vision loss? 4. Is research for EB related eye problems moving forward? What EB related problems can occur in the eye? • The most common problem is corneal abrasion • Cause is: dryness, injury, blister, erosion Missing epithelium… Infection Standard of care is to see patients every 2-3 days until abrasion is healed Why do abrasions occur in EB? • The surface of the eye is similar to skin • It has collagen VII and laminin-332 (5) which form an anchoring complex Corneal basement membrane ...similar to skin What other problems can occur? • Infected abrasion = ulcer • Scarring is common • Severe scars are white and block vision Infection Mild scar Severe scar Astigmatism can lead to amblyopia • Astigmatism causes distortion of images • In young children (under 10 years) astigmatism causes amblyopia • Amblyopia: poor vision development, can be permanent Left eye Right eye Vision does not develop in the eye with high astigmatism = Amblyopia Another common problem is blepharitis OIL NO OIL • Scarring closes oil glands, causes dryness • Dry eyes are more likely to erode • Inflammation due to mild bacterial infection • BKC: severe dryness causes corneal scarring and abnormal blood vessels to grow (seen in non-EB patients) Other eye problems… Tear drainage system bands of conjunctiva (symblepharon) watery eyes from clogged tear duct (obstruction) When do these problems start? JEB H + nH RDEB-HS • Typically JEB and RDEB patients are at higher risk for eye problems • Some start as early as 4-6 months of age • 30% of JEB and 10% of RDEB patients scar within first 10 years which is the critical time of vision development Graph from: J.D.
    [Show full text]
  • Keratoconus Into Focus
    SEPTEMBER 2019 # 37 In My View In Practice Profession Sitting Down With Musings of a prospective The amblyopia app making Why the fight for female Stefanie Schmickler: business- glaucoma patient screening accessible to all leadership is far from over minded, patient-focused 12 – 13 32 – 35 46 – 49 50 – 51 Bringing Keratoconus into Focus Sharpening up our response to this underdiagnosed condition 14– 26 NORTH AMERICA www.theophthalmologist.com FOR ROTATIONAL STABILITY, THERE’S NO COMPARISON1,2 1. Lee BS, Chang DF. Comparison of the rotational stability of two toric intraocular lenses in 1273 consecutive eyes. Ophthalmology. 2018;0:1-7. 2. Potvin R, et al. Toric intraoclar lens orientation and residual refractive astigmatism: an analysis. Clin Ophthalmol. 2016;10:1829-1836. Please see Important Product Information on the adjacent page. AcrySof®IQ Toric ASTIGMATISM-CORRECTING IOL © 2018 Novartis 7/18 US-TOR-18-E-1605 105064 US-TOR-18-E-1605 TO.indd 1 1/30/19 4:04 PM ACRYSOF® IQ TORIC IOL IMPORTANT PRODUCT INFORMATION CAUTION: Federal (USA) law restricts this device to the sale by or on the order of a physician. INDICATIONS: The AcrySof® IQ Toric posterior chamber intraocular lenses are Image intended for primary implantation in the capsular bag of the eye for visual correction of aphakia and pre-existing corneal astigmatism secondary to removal of a cataractous lens in of the adult patients with or without presbyopia, who desire improved uncorrected distance vision, reduction of residual refractive cylinder and Month increased spectacle independence for distance vision. WARNING/PRECAUTION: Careful preoperative evaluation and sound clinical judgment should be used by the surgeon to decide the risk/benefit ratio before implanting a lens in a patient with any of the conditions described in the Directions for Use labeling.
    [Show full text]
  • Prolonged Pursuit by Optokinetic Drum Testing in Asymptomatic Female Carriers of Novel FRMD7 Splice Mutation C.1050 ؉5GϾA
    OPHTHALMIC MOLECULAR GENETICS SECTION EDITOR: JANEY L. WIGGS, MD, PhD Prolonged Pursuit by Optokinetic Drum Testing in Asymptomatic Female Carriers of Novel FRMD7 Splice Mutation c.1050 ؉5GϾA Arif O. Khan, MD; Jameela Shinwari, MSc; Latifa Al-Sharif, BSc; Dania S. Khalil, BSc; Nada Al Tassan, PhD Objective: To determine the genotype underlying sus- was identified in the 2 affected brothers and in the 3 asymp- pected X-linked infantile nystagmus in a family and to tomatic women only. Allele sharing analysis further con- correlate genotype with clinical examination in poten- firmed that the aunt’s phenotype was not related to the tial female carriers. FRMD7 variant, which was absent in 246 ethnic controls. Her phenotype was also not related to mutation in known Methods: Ophthalmic examination (ophthalmic, or- CFEOM genes (KIF21A, PHOX2A, TUBB3). thoptic, optokinetic [OKN] drum, and electrophysi- ologic when possible) and candidate gene analysis. Conclusions: Prolonged pursuit responses during OKN drum testing in asymptomatic female carriers is consis- Results: Two affected brothers had infantile nystagmus tent with the concept of infantile nystagmus being an ab- with no evidence of associated visual or neurological normally increased pursuit oscillation. Further studies disease. The symptomatic maternal aunt had infantile are required to determine the reproducibility of this po- nystagmus in addition to congenital fibrosis of the ex- tential female carrier sign. Rather than being FRMD7 re- traocular muscles (CFEOM) (bilateral hypotropia, exo- lated, nystagmus in the maternal aunt represented a sec- tropia, ptosis, almost complete ophthalmoplegia, and ond disease in this family, likely related to CFEOM. poorly reactive pupils). A sister, the mother, and the ma- ternal grandmother—all 3 of whom were asymptomatic— Clinical Relevance: Clinicians can use the OKN drum had delayed corrective saccades (prolonged pursuit) dur- to assess obligate female carriers in a family suspected ing OKN drum testing.
    [Show full text]
  • Presbyopia, Anisometropia, and Unilateral Amblyopia
    REFRACTIVE SURGERY COMPLEX CASE MANAGEMENT Section Editors: Karl G. Stonecipher, MD; Parag A. Majmudar, MD; and Stephen Coleman, MD Presbyopia, Anisometropia, and Unilateral Amblyopia BY MITCHELL A. JACKSON, MD; LOUIS E. PROBST, MD; AND JONATHAN H. TALAMO, MD CASE PRESENTATION A 45-year-old female nurse is interested in LASIK. She the AMO WaveScan WaveFront System (Abbott Medical does not wear glasses. She says there has always been a large Optics Inc.) for the patient’s right eye calculated a pre- difference in prescription between her eyes and that she scription at 4 mm of +2.20 -4.22 X 9 across a 5.75-mm rarely wore glasses in the past. Her UCVA is 20/200 OD, cor- pupillary diameter. This had a corresponding higher-order recting to 20/30 with +1.75 -4.25 X 180. Her UCVA is 20/40 aberration root mean square error of 0.20 µm. The OS, correcting to 20/15 with -0.75 -0.25 X 30. The patient is patient’s left eye had a calculated prescription of -0.56 right-handed, and her left eye is dominant. Central ultra- -0.21 X 31, also at 4 mm. The pupillary diameter of her left sound pachymetry measures 488 µm OD and 480 µm OS. eye was 5.25 mm, and the higher-order aberration root Figure 1 shows TMS4 (Tomey Corp.) topography of the mean square error was determined to be 0.17 µm patient’s right and left eyes, respectively. Both the (Figure 2). Klyce/Maeda and Smolek/Klyce Keratoconus Screening How would you counsel this patient regarding her suitability Systems are highlighted.
    [Show full text]