Examining the Retina
Assess the optic nerve Clinical Decisions in Retina What is the cup to disc ratio Is there good coloration and perfusion Mark T. Dunbar, O.D., F.A.A.O. Is it flat Choroidal or scleral crescent
Mark Dunbar: Disclosure Examining the Retina Consultant for Allergan Pharmn What is the caliber of the retinal vessels Optometry Advisory Board for: Make sure you look and consciously take not of what the caliber is Allergan Carl Zeiss Meditec Narrowing of the vessels requires checking Alcon Nutritional the blood pressure Advisory Board Mark Dunbar does not own stock in any of the above companies Normal A/V ratio is 2/3, ¾ ArticDx What about the arterial light reflex?
Examining the Retina Examining the Retina
Don’t forget to look at the anterior vitreous The Macula Needs to be done on every dilated patient Is there a foveal light reflex (FLR)? Done at the slit lamp, looking posterior to Is it flat? the lens Is there any fluid, hemorrhage, or exudate Retroillumination may help if you suspect Presence of drusen vitreous cell RPE mottling More on this later Examining the Retina PVD
The peripheral retina 65% of individuals > 65 have PVD It has to be done through a dilated pupil More common in women Don’t substitute imaging for indirect ophthalmoscopy More common following intraocular surgery Use Imaging as a compliment, but not substitute More common following Be systematic in your examination inflammation You should be able to see ora on “all” gazes More common in aphakes It’s all about technique
59 y/o White Male PVD
Retinal tears occur 8-15% CC of new onset flashes RE X 3 wks of eyes with symptomatic See’s them only at night PVD 90% are superior Does not seem to affect is vision VH occurs in 13-19% of VA: Best-corrected 20/20 (-3.50 OU) symptomatic PVD’s Motility, CVF, Pupils – all normal VH + PVD -> 70% will have a retinal break Anterior Segment – unremarkable PVD No VH -> 2-4% will Posterior Segment - have retinal break
Exam of a Pt with 59 y/o White Male Symptomatic PVD
Should have a high suspicion of detecting What are you suspicious of? Weis ring What are you looking for? Should have a high index of suspicion of a possible retinal break Posterior Vitreous Detachment Clinical exam should be conducted with these suspicions Clinical Exam of a Patient with Management of Acute PVD A Symptomatic PVD With Symptoms All the testing and procedures that you would normally do with any patient Educate about the Si/Sx of RD Dilated fundus exam Look specifically at the anterior vitreous Note presence or absence of pigment or cells in Return in 4-6 weeks, then 3-4 months, then the anterior vitreous -> tobacco dust, schafer’s annually sign Peripheral extended ophthalmoscopy including scleral depression
PVD NOT Seen PVD is Seen but has symptoms… What is your management? What is your management? Do you bring him back for follow up? Return with in 3-4 weeks
Management of Acute PVD Lattice Degeneration as a Routine Finding? No Symptoms
Educate about the Si/Sx of RD Is this any cause for concern?
How do you manage it? Return in 1 yr Indications for Prophylactic Lattice Degeneration Treatment of Peripheral Retinal Tears and Holes in Asymptomatic Patients Present 5-20% of the general population Phakic Highly Fellow Eye Myopic (RD in other) Localized area of Atrophic Holes No No Rarely retinal thinning Operculated No Rarely Rarely associated with a fluid Holes pocket in the overlying Lattice with or No Rarely Sometimes cortical vitreous without Holes Flap Tears Sometimes Sometimes Usually
Lattice Degeneration and 48 y/o Asymptomatic Pilot Risk of RD
RD develop in 0.7% of eyes with lattice VA 20/15 OU degeneration followed for 10.8 yrs Anterior Segment: Eyes with lattice that developed tractional Unremarkable retinal tears Fundus 40% occurred in areas not associated with lattice…normal-appearing retina
Byer NE. Ophthalmology. 1989; 96:1401-1402
Indications for Prophylactic Treatment of Peripheral Retinal Tears and Holes in Symptomatic Patients
Treat Horseshoe tears Yes Dialysis Usually Operculated holes Rarely Atrophic holes No Choroidal Nevi Management
< 3 mm elevation Flat choroidal nevi: follow < 3 DD in size yearly
95% are less than 2 Suspicious nevi: DD photo Slate gray follow in 6 wks, 3 mo, then 6 mo Drusen evidence of growth -> SRF associated with early melanoma drusen Lesions > 3 mm thickness: CNVM probably early melanoma
Features Suggesting Nevi Do any of the medications that Drusen I am taking affect my eyes? Overlying neurosensory detachment Choroidal neovascular membrane Circinate exudate “I am having blurry vision – Bony pigment spiculing could this be from any of the Zones of RPE atrophy medications that I am taking?”
Choroidal Melanoma Systemic Interactions
At least 76 classes of systemic drugs have been >3 mm elevation associated with ocular side effects Drug can interact with and disrupt any step of the Variable pigment biochemical process resulting in deleterious effects to Multiple areas of orange pigment the ocular tissues (lipofuscin) Drugs may incite an exaggerated immune response within the eye Serous fluid (detachment) in absence of drusen Uveitis or retinitis Penetration by certain systemic meds may cause ¾ Unequivocal evidence of growth deposition of the solidified form of the molecule Ethambutol Toxic Systemic Interactions Neuropathy Medications may cause alteration of the pigment st Plaquenil -> Bull’s eye maculopathy 1 described by Leibold in the 1960’s Pharmacologic toxicity can occur leading to cell Dose dependent death and loss of function Can affect the optic nerve Risk is 6-18% for pts with dose > 30 Patient variability may influence and cause mg/kg/day (18% at 35 mg/kg/day) unexpected effects Develops in 1-3% at dose 15-25 mg/kg/day Pharmaceutical studies provide statistical evidence supporting appropriate dosage for meds, however individual variation can result in unexpected results
57 y/o White Female
What are your/our obligations in Presented on 2/29/08 with decreased vision, deciding if certain medications that near > distance 2o CC: can my medicine affect my eyes? a patient is taking are affecting the LEE: 1970’s patients vision?
Ethambutol Patient History
TB regimens begin at either 50 mg/kg/day Meds Social Hx (maximum 4 grams) for 2 weeks or 25-30 1 pack/day tobacco mg/kg/day (maximum 2 grams) for 3 weeks, Pegasys and then maintained at 15-20 mg/kg/day (max usage X 40 yrs Copegus 2 grams) Visine prn For MAC regimens the maintenance dose is 15 20 drinks/day x 40 yrs, mg/kg/day (maximum 2.5 grams). quit 2007 in AA Depending on the species of mycobacteria pts, Family Hx may be treated with a loading dose of 25 IV drug usage X 10 yrs, mg/kg/day for the first two months of therapy None (Mandell et al., 2005; Micromedex 2007). quit 1970 What are your obligations for Interferon Retinopathy managing a patient on plaquenil?
1990: Ikebe reported the first case What is the risk of having ocular problems from plaquenil? 1992: IFN therapy widely used in Japan for hepatitis C patients What testing is necessary? How often do you need to follow her? 1993: Ocular complications from IFN increasingly reported from Japan
1998: Review of early reports by Hayasaka
Review of Early Reports Plaquenil Typical Findings (Hydroxychloroquine) Prescribed in 200 mg tablets CWS Dose is 200mg or 400mg daily Hemorrhages: flamed shaped or white centered Risks for macular damage include Posterior pole or around the optic disc Cumulative dose of 1000g 5-7 years or more of use Occurred alone or together ¾1% risk after 1000g total dose (7 years) Unilateral or bilateral Renal or hepatic dysfunction (both) Subjective complaints are uncommon Pre-existing macular pathology Visual acuity not usually impaired Short stature / obesity Age
Plaquenil Screening: 57 y/o Hispanic Female Traditionally Was told by her rheumatologist to have Baseline macula photos her eyes checked Color vision testing He wants to put her on a new medication but told her it can affect her eyes. Amsler grid Medical history of severe rheumatoid 10-2 Visual fields arthritis Yearly exams Currently on Prednisone 20 mg/day
Wants to start her on plaquenil Revised Recommendations on Feb 2011 Screening for Plaquenil Toxicity
• SD-OCT can show localized thinning of the parafoveal retinal layers confirming toxicity – May be unable to see with TD-OCT – Changes maybe visible prior to VF defects • FAF may reveal subtle RPE defects with reduced autofluorescence • MF-ERG can objectively document localized paracentral ERG depression in early retinopathy
Revised Recommendations on Revised Recommendations on Screening for Plaquenil Toxicity Screening for Plaquenil Toxicity
• Amsler grid testing removed as an acceptable Parafoveal loss of visual sensitivity may appear screening technique before changes are seen on fundus evaluation – NOT equivalent to threshold VF testing Many instances where retinopathy was • Strongly advised that 10-2 VF screening be unrecognized for years as field changes were supplemented with sensitive objective tests dismissed as “non-specific” until the damage such as: was severe – Multifocal ERG 10-2 VF should always be repeated promptly when central or parafoveal changes are observed – Spectral domain OCT to determine if they are repeatable – Fundus autofluorescence
Revised Recommendations on Mild Retinopathy Screening for Plaquenil Toxicity
Tests Not Recommended for Screening: Fundus photography Time domain OCT Fluorescein angiography Full-field ERG Amsler grid Color vision screening Rodriguez‐Padilla, J. A. et al. Arch Ophthalmol 2007;125:775‐780. EOG Revised recommendations on Isolated/Flame Hemorrhages screening for retinopathy Isolated Cotton Wool Spot
Older literature focused on daily dose/kg Management Implications Newer literature emphasizes cumulative dose as the most critical factor Initial baseline ¾Within 1 year of beginning medication
Then screening for toxicity should be initiated no later than 5 years after starting the medication
HIGH RISK PATIENTS 26 y/o Asian Female Factors Increasing Risk of Retinopathy
Duration of use > 5 years 2nd Year Med Student Cumulative Dose > 1000 g (total) = 400x365X7 yr Healthy Daily Dose > 400 mg/day Age Elderly Routine exam – no complaints Systemic Disease/high BMI Kidney or liver dysfunction
Ocular Disease Retinal disease or maculopathy 6 mo ago, nonspecific episodes weakness and not feeling right Previously believed highest risk of maculopathy was based on low body mass was 6.mg/kg/day Myopic – 20/20 OU
26 y/o Asian Female Assessment and Plan?
What is your management of an isolated CWS in absence of anything else?
Are you obligated to work it up? Cotton Wool Spots The Moral of the Story Brown et al. Retina. 1985 Fall-Winter;5(4):206-14
24 consecutive patients presenting with multiple or single What’s common….is common CWS were worked up - Known diabetic patients excluded Make sure you LOOK at the retinal vessels 5 patients were found to be 1 SLE Note the caliber and the presence of crossing undiagnosed diabetes 1 Polyarteritis nodosa 5 patients HTN changes 1 Leukemia 2 pts with cardiac valvular Blood pressures are important disease 1 AIDS 2 pts with radiation ret 1 Purtscher's retinopathy You have the potential to save lives 1 Metastatic carcinoma, 2 pts with severe carotid You would be surprised how many people artery obstruction 1 IV drug abuse, 1 Dermatomyositis are out there with dangerously high BP
Cotton Wool Spots Brown et al. Retina. 1985 Fall-Winter;5(4):206-14 Systemic workup failed to reveal an underlying cause in only 1 patient The Diabetic Patient
The presence of even 1 CSW spot in an What are the questions that you ask otherwise normal fundus necessitates an yourself when examining a diabetic? investigation to ascertain systemic etiologic factors
Basic Work Up for CWS The Diabetic Patient
Look at the disc – specifically look for subtle HTN NVD Fasting blood glucose Are there hemorrhages or microaneurisms? CBC Exudated, cotton wool spots? ANA Look for the presence of NVE, traction, or HIV testing VH Macular involvement? Risk for Developing PDR in 1 yr
What is the extent of the Mild NPDR: 5% involvement? Moderate NPD: 12% Severe NPDR: 52% That is the basis for classification Very Severe NPDR 72%
Diabetic Retinopathy Is there Macular Involvement? Classification Mild to Moderate Nonproliferative Are there hemorrhage or exudates in close (NPDR) proximity to the macula? Hemorrhages, microaneurysms Is it within 500 µ (1/3 DD)? Hard exudate Is there associated retinal thickening? Cotton wool spots (CWS) Minimal venous beading/IRMA By definition – that is clinically significant Macular edema macular edema (CSME)
Severe Nonproliferative CSME Diabetic Retinopathy
4-2-1 Rule Retinal thickening within 500 microns from the center of the FAZ Hemorrhages & Ma in 4 quadrants -or- Hard exudates associated with retinal thickening 500 microns from center of FAZ Significant venous beading in 2 Zones of retinal thickening > 1 DD in area, quadrants -or- any part of which is 1 DD from the center of the fovea IRMA in 1 quadrant Diabetic Retinopathy
Clinically significant macular edema How Does Macular Edema (CSME) Manifest Itself? Retinal thickening which involves or threatens the center of the macula In what forms can macular edema present?
Diabetic Macular Edema
It can’t be diagnosed with a direct ophthalmoscope You need a 3D view of the macula
Diabetic Retinopathy
Pathologic process Microaneurysms Is there CSME? Vascular If yes – referal to retinal specialist permeability is recommended Ischemia Proliferation Cicatrization Optometric Management of Diabetic Patient Asymptomatic Hollenhorst Plaques When do you initiate a work up? No diabetic retinopathy
Educate and follow yearly 1. Never Early or moderate NPDR 2. Always Establish presence of CSME 3. Only when symptoms such as TIA’s or ¾If CSME refer to retina specialist amaurosis fugax No CSME ¾Educate ¾Follow yearly
Optometric Management Asymptomatic Hollenhorst Plaques of Diabetic Patient Important Questions to Ask Severe NPDR Any TIA’s? Follow every 4 Occurs in 30-50% of pt with severe CAD months 50-75% of stroke pts have had TIA’s Any amaurosis fugax? PDR: refer to Retinal TIA’s retina specialist Lasts up to 2 minutes (can be up to 2 hrs) Numbness/weakness in parts of their body
Proliferative Retinopathy Work Up of Retinal Plaques PDR Progress in Retinal Eye Research 24 (2005) 493-519 Misconception: Vitreous hemorrhage That Asymptomatic plaque(s) in retinal arteries NVD do not require a detailed evaluation NVE SS Hayreh: “This misconception may result in a patient later Fibrovascular proliferation developing retinal artery occlusion and visual Retinal detachment loss, or a cerebral vascular accident. Thus it is prudent to evaluate the source of all asymptomatic plaque(s)…” Optic nerve head swelling is a Suspicious Optic Nerves common, but nonspecific, neuro- ophthalmic sign Pseudoedema vs. True Optic Nerve Edema It may present as either as true edema vs. pseudoedema What goes into your decision making process when you decide if this patient has true disc True edema may arise from a variety causes edema vs. anomalous nerve?
True Disc Edema vs. The Typical Scenario… PseudoEdema True Disc Edema PseudoEdema Disc elevation….looks like disc elevation Absent SVP SVP Present Blurring of the disc margins Absent in 20% of normals No optic nerve dysfunction Anomalous branching Often bilateral…but could be unilateral pattern of the retinal vessels Yellow hazy appearance in deep peripapillary tissue How do you differentiate? Obscuring border b/w disc and retina
What goes into your decision making True Disc Edema vs. process when you decide if this patient has true disc edema vs. anomalous nerve? PseudoEdema True Disc Edema PseudoEdema Hyperemia of the nerve Absent hyperemia – heightened reddish Absent dilation of hugh microvasculature on 2° congestion of the the surface of the micro-vasculature nerve Dilation/telangiectasis of the microvasculature and surface capillaries True Disc Edema vs. Buried Disc Drusen PseudoEdema True Disc Edema PseudoEdema Scalloped appearance to the disc margin Blurred disc margins Blurring disc margins Occurs at the level of result from changes Disc is not hyperemic RNFL occurring at the RPE No microvascular
Obscuring retinal vessels Thus retinal vessels are blood vessel and junction b/w clearly seen as they abnormalities on the mylinated and cross the disc margin surface of the nerve nonmylinated RNFL
Papilledema Buried Disc Drusen
Intracranial mass Anomalous branching Hydrocephalus retinal vessels Loops, trifurcations and Idiopathic intracranial hypertension increased branching Meningitis or encephalitis Gray/black change deep CNS granulomatous or malignant around the nerve transformation
Optic Disc Edema with Optic Hemorrhage or Subretinal Nerve Dysfunction Hemorrhage in the Macula? AION What are the Optic neuritis implications? Leber’s hereditary optic neuropathy Intraorbital optic nerve compression What clinical Infiltrative optic neuropathy decisions to you Toxic optic neuropathy make with regards to etiology? 72 y/o White Male Blurred VA with Glasses R > L The Questions RE: 20/30, LE 20/25 If you can confidently answer No to these questions…and you have explained their acuity (20/30) your job is done If the answer is Yes to any of these questions, then you need to conduct a work up
FA and OCT
72 y/o White Male Age-related Macular Blurred VA with Glasses R > L RE: 20/30, LE 20/25 Degeneration (AMD) Diagnosis Degenerative disorder that affects the macula Age-Related Macular Degeneration Leading cause of legal blindness in people > 65 yo What are the questions that you ask yourself 90% of vision loss is 2° to when you examine the macula of a patient CNV like this?
The Questions Dry ARMD
Is there fluid in Earliest clinically the macula? detectable feature Lie between BM of RPE Do you see subretinal and Bruch’s hemorrhage or Hard drusen: smaller, exudate? calcified or ossified Is the macula flat Soft drusen: ill-defined, or is there any larger, coalesce, resemble elevation? small serous detachments Unexplained Vision Loss Unexplained Vision Loss Causes Obeying the Fundamentals of the Refractive Complete Eye Exam is Important Functional Lens Opacities Its not always what you see, but Neurologic more what you don’t that makes it Occult Retinal/Macular Disease difficult….
When do you refer? Retinal Imaging and OCT has really helped us figure out many of these When should you refer? cases of unexplained vision loss
Optical Coherence Tomography (OCT)
Non-contact, non-invasive imaging device Unexplained Vision Loss Produces high-resolution images of the posterior segment
What are your obligations in Optical biopsy figuring out why? Images are objective and quantifiable Advantages of OCT
Quick – takes less than five minutes to obtain images of both eyes Non-invasive and well tolerated by patients No injection No biohazard or blood-related risk No medication reactions More readily interpreted and understood by patients
Main Clinical Utilities of OCT
High resolution evaluation of retinal anatomy Diagnosis of macular conditions difficult to establish with biomicroscopy Quantitative assessment of retinal anatomic alterations Quantitative assessment of vitreoretinal interface Objective means for monitoring disease progression and/or therapeutic response