ABCs. ABCs of retinal disease !"#$"%!& Disclosures. ABCs three major threats to vision where 1 o care intervention may be helpful!a = AMD !
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1 Disclosures Stockholder: HPO ABCs of retinal disease Honoraria, Consultant or Advisory Board: Alcon, Allergan, B&L, Arctic Dx, Sucampo, Zeiss. Idaho Optometric Physicians 2016 Leo Semes, OD, FAAO ABCs three major threats to vision where 1 o care intervention may be helpful!a = AMD!B = BRVO!C = CSME, CSR ABCs!A = AMD!B = BRVO!C = CSME, CSR 01/16/ /40 20/40 What interventions were available at the time to possibly alter the natural history of this AMD? Current regimen: Centrum Silver + 5 mg Lutein) Continue vitamin supplements RTC X 1 year 01/09/ /60 20/30 Positive Amsler (wavy lines temporal and inferior OD) Continue vitamin supplements RTC X 1 year %&
2 04/14/2009: I woke up in the middle of the night and I couldn t see the middle number on the digital clock with my right eye. 20/60 20/40 Note significant RPE disruption Management & Follow-up!Retinal consult for CNVM!Avastin injection same day!05/ !! VA 20/60, 20/50 stable macula!! Follow X 3 months Fast forward to 3/21/13 20/80 OD, OS S/P numerous IVAvastin injections 3/21/13 3/21/13 Could the conversion to WAMD have been averted? #&
3 Seen most recently April 1, /200 20/200 Note spontaneous release of VMA Ferris FL, et al. Ophthalmology Apr;120(4): Ferris FL, et al. Ophthalmology Apr;120(4): Ferris FL, et al. Ophthalmology Apr;120(4): Ferris FL, et al. Ophthalmology Apr;120(4): Ferris FL, et al. Ophthalmology Apr;120(4): '&
4 Excessive Weight Lack of Physical Activity Smoking 18% Additional Risk Reduction by Adding L/Z and Eliminating Beta-carotene 40% Probability of Progression 30% 20% 10% AREDS with beta-carotene AREDS without beta-carotene with L/Z *AREDS formulations contains 80 mg Zinc **But one randomization arm used only 25 mg HR=0.82 P=.02 0% Years Age-Related Eye Disease Study 2 Research Group. JAMA. 2013;309(19): The influence of genetic profile on supplement outcome Zinc alone or antioxidants alone can be HARMFUL depending on your genetic profile [compared to A + Z] Awh CC, Lane AM, Hawken S, Zanke B, Kim IK. CFH and ARMS2 genetic polymorphisms predict response to antioxidants and zinc in patients with age-related macular degeneration. Ophthalmology Nov;120(11): Epub 2013 Aug 21. Zn++ harmful 2014 Guidance! New Risk Calculations!AREDS 2 formulation for those at greatest risk (&
5 30 31 AMD progression in a low-risk patient! 7X W/F! 20/25 OS! Baseline AMD progression in a low-risk patient! 7X W/F! 20/200 OS! S/P Avastin AMD Pathogenesis Call for Early Diagnosis David Brown, MD, FACS Retina Consultants of Houston Many AMD patients are arriving at our practice with unnecessary vision loss. Ideally these patients would see their primary eye physician and be diagnosed earlier. Drusen Photoreceptors Sclera Curcio CA, Johnson M. Structure, function, and pathology of Bruch s membrane. In: Ryan SJ, et al, eds."retina, Vol 1, Part 2: Basic Science and Translation to Therapy."5th ed. London: Elsevier; 2013: RPE Bruch s Membrane Cholesterol accumulation leads to panmacular deposits (BlinD and BlamD) Peaks in these deposits eventually become clinically visible drusen These extracellular cholesterol deposits affect photoreceptor health, causing inflammation and predisposing to CNV In addition, they impair normal transport, including that of vitamin A, across Bruch s membrane Curcio CA, Johnson M. Structure, function, and pathology of Bruch s membrane. In: Ryan SJ, et al, eds."retina, Vol 1, Part 2: Basic Science and Translation to Therapy."5th ed. London: Elsevier; 2013: RPE Bruch s Membrane In effect, AMD causes a localized deficiency of vitamin A, and dark adaptation is the best test to measure this change AMD Diagnostic Landscape 3-")42.51&!"#$%& '(")*& Dark Adaptation Genetic Tests Amsler Grid Foresee PHP Fundus Camera SD-OCT Macular Pigment Optical Density (MPOD),-./&0"1(2#& +"(*& '(")*& )&
6 Dark Adaptation Dark Adaptation Dark adaptation is the process of adjusting from day vision to night vision Easy-to-measure aspect of night vision Jackson GR, et al. Vision Res. 1999;39(23): Leibrock CS, et al. Eye (Lond). 1998;12(pt 3b): AMD Causes Major Impairment of Dark Adaptation Rapid Test: #6.5 minutes AMD Normal Extended Test: #20 minutes First dark adaptometer for rapid, routine clinical use Simple, objective tool to measure dark adaptation as earliest functional correlate of macular dystrophies Two clinical protocols! #6.5-minute rapid test (for quick assessment)! #20-minute extended test (for benchmarking) How AdaptDx Works fixation light forehead rest chin rest stimulus light trial lens holder Simple, noninvasive test performed in-office by ophthalmic technician While continuously focusing on fixation light, patient is exposed to a mild bleaching flash and asked to indicate when a progressively dimmer stimulus light appears (randomly timed) ALSTAR Study Prospective Study of Subclinical AMD Sample consisted of 325 adults without clinically detectable AMD. At baseline, 24% of the subjects exhibited impaired dark adaptation. AMD status determined at 3-year follow-up visit. Owsley, C, McGwin G, Clark M, et al. Delayed rod-mediated dark adaptation is a functional biomarker for incident early age-related macular degeneration. Ophthalmology. 2016; 123: !&
7 ALSTAR Study Results! Impaired dark adaptation identifies subclinical AMD at least three years before it can be seen with other methods.! Subjects with impaired dark adaptation were two times as likely to develop clinically evident AMD and eight times as likely to advance beyond the earliest stage of AMD. ABCs!A = AMD!B = BRVO +,&-&#.&/012345&!C = CSME, CSR Owsley, C, McGwin G, Clark M, et al. Delayed rod-mediated dark adaptation is a functional biomarker for incident early age-related macular degeneration. Ophthalmology. 2016; 123: F! VA = 20/20! Normal history! Baseline photo 2000! Predisposing conditions to retinal vein obstruction? 52 W F!! Sudden onset of reduced VA (X 7 $ yrs)!! 20/80 w/central disturbance!! What are you going to do? *&
8 *Most prevalent coagulation and anticoagulation disorders in BRVO 52 W F 9/ 4/ 2008 Rehak J, Rehak M. Branch retinal vein occlusion: pathogenesis, visual prognosis, and treatment modalities. Curr Eye Res. 2008;33: Involvement confined to the inner retina 52 W F 9/ 9/ 2008 Cystoid macular edema; Started on Xibrom (bromfenac) qid) 52 W F 9/ 22/ 2008 VA 20/200; distinct macular involvement; Now what? 52 W F 1/ 14/ 2009 Continued on Xibrom qid Some resolution 52 W F 1/ 19/ 2009 Continued on Xibrom qid 6&
9 52 W F 2/ 17/ 2009 Continued on Xibrom qid 52 W F 2/ 16/ 2009 Recommend anti-vegf intravitreal injection *Treatments for ME following RVO 2/ 24/2009 And an Avastin injection VA = 20/25!!! Restoration of normal anatomy SCORE 5! CRVO standard care = observation! Neither 1 mg nor 4 mg IVTA offered better outcome SCORE SRG Arch Ophthalmol 2009; 127; SCORE 6! BRVO standard care = grid photocoagulation! Both 1 mg and 4 mg IVTA showed 15-letter gains in! 25% of 12 mo.! Fewer IOP elevations and cataract in the lower dose *But wait! There s still more!!! CRUISE! CRVO intervention for CME trial 0.3 or 0.5 mg intravitreal ranimizubab (Lucentis)! 46.2 and 47.7 % of eyes gained >/= 15 6 mo. (1.1 in the sham group) Retina Congress September 2009 NYC BRAVO! BRVO intervention for CME (same dosing as CRUISE)! 55.2 and 61.1% of eyes demonstrated >/= 15 6 mo. (1.9 in the sham group) FDA-approved June 27, 2010 For the treatment of CME secondary to BRVO/CRVO 59 $&
10 BRVO consequences! Identify macular edema! Prompt treatment with anti-vegf agent ABCs!A = AMD!B = BRVO!C = CSME, CSR born: 7 April 1957 (S.T.)!First seen 19 April 2012!DIABETIC (insulin) / HTN X 20 yrs (2 meds)!bs: ; A1C is unknown 19 April 2012 VA 20/25 OD = OS Note cotton wool spots Esp. Note: macula is definable Left eye has CWS as well Right eye Normal macular contour No thickening centrally %.&
11 Left eye Normal macular contour OD Note mild retinal thickening outside the macula but absence of fluid No fluid or thickening OS Note mild retinal thickening (consistent w/cws) surrounding macula but absence of fluid at the macula High-definition images Mild retinal thickening without fluid accumulation Each macula shows mild thickening Note RNFL profile comparing OD and OS to normal Overly thick RNFL = CWS areas %%&
12 Subsequent Visits 17 July 2012 VA = 20/20 20/25 [diffuse DME] ST RNFL defect! VA (1 June 2012) No OCT or photos!! 20/20-20/40! VA (21 June 2012) No OCT or photos!! 20/25 20/25 Recommend retina specialist consult; Treatment recommended; Pt. refuses treatment 2 October 2012 CSME 20/50 (reduced from 20/25 in April 2012) RNFL defect following CWS in hypertension RNFL defect (not glaucoma) And muddy macula Before After Note distinctive RNFL thinning on OCT Zhang L, Xu L, Zhang JS, Zhang YQ, Yang H, Jonas J Cotton-wool spot and optical coherence tomography of a retinal nerve fiber layer defect. Arch Ophthalmol Jul 1;130(7):913. Left eye appears less involved 20/30 Note NV and Pre-retinal heme Nasal to ONH Except nasally... %#&
13 Note fluid IT to macula = CSME Macular thickening Similar pattern but not as severe fluid accumulation OS Macular thickening corresponds to CWS & fluid High definition images show CWS and macular fluid / thickening consistent with CSME (OD, 20/50). Note thickening of RNFL on OCT corresponding to CWS and thinning corresponding to RNFL defect [OD] High definition images show CWS and macular fluid / thickening consistent with CSME (OD, 20/50). High definition images show CWS and macular fluid / thickening consistent with CSME (OS 20/30). %'&
14 CSME! The leading cause of vision loss due to diabetic retinopathy; often asymmetrical! These patients deserve consultation to consider surgical intervention ABCs!A = AMD!B = BRVO!C = CSME, CSR 46 Asian Male! blurry vision 11/20/2012!! X 3 mo OS; began only last night OD! Began new BP med last week! Has never had eye exam! Central blur in OS has improved somewhat! + floaters X 1 yr! - flashes, discharge, pain 46 Asian Male! Previous ocular history is negative for refractive correction, injury, glaucoma, cataract, strabismus, amblyopia, etc.! Family medical / ocular histories negative! No known allergies! Began lisinopril qd X 1 wk. [ACE inhibitor]! BP 150/ Asian Male 11/20/12! VA 20/40-20/400 (PHNI)! -RAPD! IOP: 14/14! No EOM restrictions! Confrontation FTFC OD, OS! / X 070 VA NI! Anterior segment unremarkable OD, OS %(&
15 Note! vitreous traction!!!! inverted foveal contour mild inner thickening significant SRF RPE intact Note serous sub-retinal fluid and cystic macula Note RPE intact and serous sub-retinal fluid Note disc margin elevation Note serous sub-retinal fluid RPE appears intact And CWS %)&
16 And RNFL defect (OS) 46 A M with CSR, HR! Initiated Nevanac bid (11/20/12)! RTC X 1 wk! Correspond with 1- wk F/U (11/27/12)! BP = 138/92! VA 20/25, 20/40!!!!! (-1.00 / X 070)! Continue Nevanac bid 46 A M with CSR, HR 12/11/12! Initiated Nevanac bid 2- wk F/U (12/4/12)! BP = 140/92! VA 20/20-, 20/20-!!!!! (refraction unchanged)! Continue Nevanac bid! RTC X 1 Wk D/C Nevanac 12/11/12 12/11/12 D/C Nevanac %!&
17 12/11/12 12/11/12 Restoration of macular thickness Contour & VA 20/20- - OD, OS %*&
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