Event Printable Handouts 1 - University of Houston | Optometry ...

PROGRAM LOCATION 

Four Seasons Hotel 

1300 Lamar Street 

Houston, TX 77010 

JUNE 2 - 3, 2012 

H 

A 

N 

D 

O 

U 

T 

S

presents: 

Everything Retina: Contemporary Optometric Management of Retinal Disease 

Location: 

Four Seasons Hotel 

1300 Lamar St. 

Houston, Texas 77010 

SEMINAR AGENDA 

SATURDAY, JUNE 2, 2012 

7:00 ‐ 8:00 am Registration / Sign‐in / Breakfast & Visit Exhibits 

Cases from the Clinic: 

Proliferative Sickle Cell Retinopathy 

Darcy Sczepanik, OD 

8:00 ‐ 8:50 am 

Is My Child Blind? A Case of Retinoblastoma 

Elizabeth Knighton, OD 

Bioptic Telescope Driving Rehabilitation in Adult Onset Cone‐ 

Rod Dystrophy 

Matt Valdes, OD 

8:50 ‐ 9:50 am 

Retinal Findings with Systemic Disease 

Jeffry Gerson, OD, FAAO and Diana Shechtman, OD, FAAO 

9:50 ‐ 10:10 am Break & Visit Exhibits 

Retinal Findings with Systemic Disease 

10:10 ‐ 11:00 am Continued from Break 


11:00 ‐ 11:50 am 

OCT Grand Rounds: The “HD” Experience 


11:50 ‐ 1:00 pm Lunch & Visit Exhibits 

BREAK‐OUT SESSION 

(OPTION I) 

1:00 ‐ 2:40 pm 

Meet the OCT: Maximizing the Benefits of your OCT Testing 

Anastas Pass, OD, JD, Terry Peterson, & the Carl Zeiss 

Meditec Team 

(OPTION II) 

1:00 ‐ 2:40 pm 

AMD and Nutritional Supplements: Counseling Strategies for 

Your Patients – Sorting Fact from Fiction 


2:40 ‐ 3:10 pm Break & Visit Exhibits 

From Print to Practice: Retina Posterior Vitreous Detachment 

3:10 ‐ 4:50 pm and the Common Process with Potential for Ocular Morbidity 


SUNDAY, JUNE 3, 2012 

7:00 ‐ 8:00 am Registration / Sign‐in / Breakfast & Visit Exhibits 

8:00 ‐ 9:50 am 

Recognizing Signs of Retinal Disease 

Carlo Pelino, OD, FAAO and Joseph Pizzimenti, OD, FAAO 

COPE ID # 34609‐PS 

COPE ID # 32069‐SD 

COPE ID # 32069‐SD 


CE credit available 

for TX Licensed OD’s 



COPE ID # 28196‐ 

PS

9:50 ‐ 10:10 am Break & Visit Exhibits 

10:10 ‐ 11:50 am 

Imaging the Posterior Segment 

Carlo Pelino, OD, FAAO and Joseph Pizzimenti, OD, FAAO 

11:50 ‐ 1:00 pm Lunch & Visit Exhibits 

Comanagement of Retinal Disease 

1:00 ‐ 1:50 pm Carlo Pelino, OD, FAAO and 

Joseph Pizzimenti, OD, FAAO 

Retina Grand Rounds 



3:40 ‐ 4:00 pm Break & Visit Exhibits 

Low Vision Rehabilitation 



CE on CD‐ROM 

Professional Responsibility for Texas Optometrists 

Course is 1‐Hour in Duration 

COPE ID # 30995‐ 

PS 

COPE ID # 31444‐ 

PS 

COPE ID # 28790‐ 

PS 

COPE ID # 29560‐LV

Darcy R. Sczepanik, O.D. 

University of Houston College of Optometry 

June 2, 2012 

CASE HISTORY 

40yo AA female referred for evaluation of 

inferior RH with associated local RD OS 

CC: sudden blurred vision OS x 1 week 

preceded by floaters with VA 

improvement x 2 days 

(‐)flashes 

(‐)trauma 

POHX: unremarkable except mild CMA OU 

FOHX: noncontributory 

PMHX: (+) sickle cell disease –HbSC 

(‐) systemic manifestations 

(‐) previous ocular disorders 

FMHX: 

(+) sickle cell trait 

(+) HTN 

(+) DM Type 2 

5/15/2012 

1

Meds: occasional zolpidem (Ambien) 

Allergies: levofloxacin (Levaquin) 

Social Hx: 

(+) social alcohol use 

(‐) smoking 

(‐) illicit drug use 

Business woman often working overseas 

EXAMINATION 1: 

QUESTIONS? 

BCVA: 20/20 OD and 20/25 OS 

Pupils, EOMs, CF unremarkable OU 

IOP: 17 mmHg OD and 16 mmHg OS – 

Tono‐Pen 

BP: 94/60 mmHg 

5/15/2012 

2

EXAMINATION 1 CONTINUED: 

SLE 

unremarkable anterior segment OD 

(+) pigment in anterior vitreous OS 

DFE 

OD 

OS 

unremarkable posterior segment OD 

• (‐) RH/RT/RD/VH 

(+) diffuse VH OS (‐)RH/RT/RD 

(+) salmon patch temporally bordered by 

nonperfused retina 

5/15/2012 

3

OS 

ASSESSMENT & PLAN: 

Proliferative sickle cell retinopathy OS 

Sector photocoagulation with argon laser 

to nonperfused retina 

IVFA next visit (3‐4 weeks) 

No NSAIDs, ASA, strenuous activity until 

further notice 

EXAMINATION 2 …6 weeks later 

CC: increased floaters and (+)temporal 

flashes x 1 week OS 

(‐) blur 

(‐) NSAIDs, ASA, strenuous activity 

BCVA: 20/20 OD and 20/20‐2 OS 

Pupils, EOMs, CF, and IOPs unremarkable 

5/15/2012 

4

EXAMINATION 2 CONTINUED 

DFE OS 

clearing VH 

regression of salmon patch with pigmented 

laser temporally 

(+) mild ERM and intraretinal hemorrhages 

OS 

OS 

5/15/2012 

5

OS –Early phase 

OS –Late phase 

ASSESSMENT & PLAN: 

Proliferative sickle cell retinopathy with 

resolving VH 

Additional areas of nonperfusion temporal 

to salmon patch 

Neovascularization localized temporally via 

DFE and IVFA 

○ PRP OS completed 

○ RTC x 2 mo for reassessment 

5/15/2012 

6

QUESTIONS? 

SICKLE CELL DISEASE 

Autosomal recessive blood disorder affecting 

those of African and Mediterranean descent 

Sickle‐shaped, rigid red blood cells 

○ Occlusions 

Necrosis, retinal disease, organ failure 

○ Hemolysis (SC RBCs live 10‐12 days vs. normal 120 days) 

Anemia 

Various types with different effects 

○ HbSS 

○ HbSC 

○ HbS‐Thal 

TYPES OF SICKLE CELL 

DISEASE 

HbSS 

Homozygous 

Most common 

1/500 AA births 

○ 1/12 AA carry sickle cell trait 

Systemic > ocular effects 

HbSC 

Heterozygous 

Second most common 

1/1200 AA births 

Ocular >>systemic effects 

○ Mechanisms unclear 

HbA HbS 

HbA HbAA HbAS 

HbS HbAS HbSS 

HbA HbC 

HbA HbAA HbAC 

HbS HbAS HbSC 

5/15/2012 

7

NONPROLIFERATIVE SIGNS 

Anterior 

○ Tortuous vessels 

○ Hyphema 

○ Iris atrophy 

***pts asymptomatic 

Nonproliferative 

○ Salmon patch 

hemes 

○ Black sunbursts 

○ Iridescent deposits 

○ ERMs 

○ CRAO 

○ Macular thinning 

○ Angioid streaks 

PROLIFERATIVE SIGNS & SYMPTOMS 

Signs 

Sea fan neovascularization (15% SS v. 40% SC) 

Vitreous hemorrhage (2% SS v. 20% SC) 

Tractional retinal detachments (O% SS v. 10% SC) 

Symptoms 

Blurred vision 

Floaters 

Flashes 

Loss of vision 

Distorted vision 

A 

OCULAR EFFECTS 

A 

B C 

B 

AA 

C 

5/15/2012 

8

OS 

PERIPHERAL VASCULAR STRUCTURE 

A: HbAA – smooth border with progressive capillary thinning and AV 

loops 

B: HbSS – progressive capillary thinning with AV loops into non‐perfusion 

C: HbSC – irregular border with abrupt termination of dense capillary 

bed and capillary stumps 

A B C 

2 

1 

3 

5/15/2012 

9

IVFA 

ANCILLARY TESTING 

Visualize neovascularization process 

Locate ischemia 

B‐scan –if retina obscured 

OCT – macular thinning 2’ non‐perfusion 

Electrophoresis –ID SCD and genotype 

Isoelectric focusing –more specific ID 

TREATMENT 

Controversial due to auto‐involution of 

neovascularization (32% of cases) 

Photocoagulation with argon laser method of 

choice 

Sectorally anterior to ischemia 

Panretinally (360 degree fashion) 

PPV – recalcitrant cases 

Anti‐VEGF? 

DIFFERENTIAL DIAGNOSES 

Proliferative diabetic retinopathy 

Sarcoidosis 

Embolic (talc) retinopathy 

BRVO with NVE 

5/15/2012 

10

REFERENCES 

Aliyu ZY, Tumblin AR, Kato GJ. Current therapy of sickle cell disease. Haematologica. 2006 Jan; 91(1):7-10. 

Fadugbagbe AO, Gurgel RQ, Mendonça CQ, Cipolotti R, dos Santos AM, Cuevas LE. Ocular manifestations of sickle 

cell disease. Ann Trop Paediatr. 2010; 30(1):19-26 

Centers for Disease Control and Prevention. National sickle cell disease fact sheet: data and statistics, 2011. Atlanta, 

GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 2011. 

Elagouz M, Jyothi S, Gupta B, Sivaprasad S. Sickle cell disease and the eye: old and new concepts. Surv Ophthalmol. 

2010 Jul 8; 55(4):359-77. Epub 2010 May 10. 

Osafo-Kwaako A, Kimani K, Ilako D, et al. Ocular manifestations of sickle cell disease at the Korle-bu Hospital, Accra, 

Ghana. Eur J Ophthalmol. 2010 Nov 4. 

Chow CC, Genead MA, Anastasakis A, Chau FY, Fishman GA, Lim JI. Structural and Functional Correlation in Sickle 

Cell Retinopathy Using Spectral-Domain Optical Coherence Tomography and Scanning Laser Ophthalmoscope 

Microperimetry. Am J Ophthalmol. 2011 Jul 2. 

Liem RI, Calamaras DM, Chhabra MS, Files B, Minniti CP, Thompson AA. Sudden-onset blindness in sickle cell 

disease due to retinal artery occlusion. Pediatr Blood Cancer. 2008 Mar; 50(3):624-7. 

Driss A, Asare KO, Hibbert JM, Gee BE, Adamkiewicz TV, Stiles JK. Sickle Cell Disease in the Post Genomic Era: A 

Monogenic Disease with a Polygenic Phenotype. Genomics Insights. 2009 Jul 30; 2009(2):23-48. 

Diallo JW, Sanfo O, Blot I, et al. Epidemiology and prognostic factors for sickle cell retinopathy in Ouagadougou 

(Burkina Faso). J Fr Ophtalmol. 2009 Sep; 32(7):496-500. Epub 2009 Jun 10. 

Koduri PR, Agbemadzo B, Nathan S. Hemoglobin S-C disease revisited: clinical study of 106 adults. Am J Hematol. 

2001 Dec; 68(4):298-300. 

Gill HS, Lam WC. A screening strategy for the detection of sickle cell retinopathy in pediatric patients. Can J 

Ophthalmol. 2008 Apr;43(2):188-91. 

Dalibalta S, Ellory JC, Browning JA, Wilkins RJ, Rees DC, Gibson JS. Novel permeability characteristics of red 

blood cells from sickle cell patients heterozygous for HbS and HbC (HbSC genotype). Blood Cells Mol Dis. 2010 

Jun 15; 45(1):46-52. Epub 2010 Mar 15. 

Goldberg MF: Classification and pathogenesis of proliferative sickle retinopathy. Am J Ophthalmol 1971; 71:649. 

Penman AD, Talbot JF, Chuang EL, Thomas P, Serjeant GR, Bird AC. New classification of peripheral retinal 

vascular changes in sickle cell disease. Br J Ophthalmol. 1994 Sep; 78(9):681-9. 

Downes SM, Hambleton IR, Chuang EL, Lois N, Serjeant GR, Bird AC. Incidence and natural history of 

proliferative sickle cell retinopathy: observations from a cohort study. Ophthalmology. 2005 Nov; 112(11):1869-75. 

Epub 2005 Sep 19. 

Sayag D, Binaghi M, Souied EH, et al. Retinal photocoagulation for proliferative sickle cell retinopathy: a 

prospective clinical trial with new sea fan classification. Eur J Ophthalmol. 2008 Mar-Apr; 18(2):248-54. 

Farber MD, Jampol LM, Fox P, et al. A randomized clinical trial of scatter photocoagulation of proliferative sickle 

cell retinopathy. Arch Ophthalmol. 1991 Mar; 109(3):363-7. 

Williamson TH, Rajput R, Laidlaw DA, Mokete B. Vitreoretinal management of the complications of sickle cell 

retinopathy by observation or pars plana vitrectomy. Eye (Lond). 2009 Jun; 23(6):1314-20. Epub 2008 Oct 3. 

Mohan JS, Lip PL, Blann AD, Bareford D, Lip GY. The angiopoietin/Tie-2 system in proliferative sickle 

retinopathy: relation to vascular endothelial growth factor, its soluble receptor Flt-1 and von Willebrand factor, and 

to the effects of laser treatment. Br J Ophthalmol. 2005 Jul; 89(7):815-9. 

Cao J, Mathews MK, McLeod DS, Merges C, Hjelmeland LM, Lutty GA. Angiogenic factors in human proliferative 

sickle cell retinopathy. Br J Ophthalmol. 1999 Jul; 83(7):838-46. 

Solovey A, Gui L, Ramakrishnan S, Steinberg MH, Hebbel RP. Sickle cell anemia as a possible state of 

enhanced anti-apoptotic tone: survival effect of vascular endothelial growth factor on circulating and unanchored 

endothelial cells. Blood. 1999 Jun 1; 93(11):3824-30. 

QUESTIONS? 

5/15/2012 

11

19 month old CF 

Is My Child Blind?: 

A Case of Bilateral 

Retinoblastoma 

POHx 

• Retinoblastoma OU 

– Dx at 9 months old 

– Systemic, periocular and 

intraarterial chemotherapy 

• Left esotropia 

• Retinal detachment OU 

– Laser surgery OU 

Elizabeth Knighton, OD 

Pediatric Optometry Resident 

Grand Rounds, Spring 2012 

Patient History 

Examination 

Spectacle Rx: VA: Cardiff Cards 

• OD: +5.25 sph 20/100 

• OS: +2.00 sph UTT, strong RTO OD 

• OU: 20/100 

Hirschberg/Krimsky 

• 16Δ LET 

EOM: FROM 

Pupils: PERRL ‐APD 

Confrontation VF 

• Full to the left OU 

• 30‐40 degrees in all right fields OU 

PMHx 

• Eczema 

• Medications: none 

• Allergies: NKDA 

FOHx 

• Color vision anomaly, 

father 

FMHx 

• DM, pgf 

Social Hx 

• ECI meeting Dec 2011/Jan 

2012 

1

Examination 

Pease‐Allen Color Test: Passed both plates OU 

Dry Retinoscopy 

• +4.00 ‐2.75 x030 

• +2.25 sph 

Cycloplegic Retinoscopy 

• +6.00 ‐1.50 x010 

• +3.50 ‐0.50 x170 

• Anterior Segment: WNL 

• IOP: soft, equal OD OS 

Examination 

• Denver II: 

– passed in all categories 

• Personal/Social 

• Fine Motor/Adaptive 

• Language 

• Gross Motor 

2

Examination 

Posterior Segment: 

• Cup/Disc: 0.3 OD; UTV OS 

• Disc: well perfused, distinct OD; UTV OS 

• Macula: flat, intact OD; UTV OS 

• Vessels: 2/3 OD, OS 

• Post Pole: 

– OD: Calcified retinoblastoma inferior/temporal to 

posterior pole 

– OS: Calcified retinoblastoma central to macula 

• Periphery: no abnormalities in glimpses of 

midperiphery 360 

Treatment & Management 

• New spectacle RX given 

– Includes astigmatism correction 

– No cut back on plus power for magnification 

• Return to clinic in 2‐3 months 

– Check visual acuity, alignment, fields, contrast 

3

Follow Up Examination 

Patient age: 22 months 

Spectacle Rx: VA: Cardiff Cards 

• OD: +6.00 ‐1.50 x010 20/63 (Card I, 50 cm) 

• OS: +3.50 ‐0.50 x170 UTT, strong RTO OD 

• OU: 20/80 (Card H, 50 cm) 

Hirschberg/Krimsky: 30‐35Δ CLET 

EOM: FROM 

Pupils: PERRL ‐APD 

Confrontation VF: Poor patient cooperation 

OD 

OS 

4

OS 


• Mutation of RB1 gene at 13q14 

• Unilateral sporadic form 

– Diagnosed 18‐24 months on average 

• Bilateral germline form 

– Diagnosed by 12 months on average 

• Retinoblastoma survivor has 50% chance of 

giving RB1 mutation to child 

• Unilateral retinoblastoma survivors have a 7% 

risk of having an affected child 


• Endophytic: tumor grows in vitreous cavity 

• Exophytic: tumor grows in subretinal space 

5

Diagnosis of Retinoblastoma 

• Common presentation: 

– Leukocoria 

– Strabismus 

• HPI, FOHx, FMHx, PMHx 

• DFE (patient, parents, siblings) 

• Ultrasound 

• Exam under anesthesia 

Referrals for potential retinoblastoma 


68% 

Other 

32% 

PFV 

10% 

Coats' 

9% 

Other 

13% 

Differential Diagnosis 

Vitroretinopathy 

• Coats’ disease 

• Persistent fetal vasculature 

• Retinopathy of prematurity 

• Familial exudative 

vitreoretinopathy 

• X‐linked retinoschisis 

• Norrie’s Disease 

• Incontinentia pigmenti 

Congenital 

• Cataract 

• Coloboma 

• Morning Glory Disc 

Tumors 

• Meduloepithelioma 

• Astrocytic hamartoma 

• Diffuse choroidal 

hemangioma 

• Juvenile xanthogranuloma 

Infections 

• Toxocariasis 

• Toxoplasmosis 

• Endogenous endophthalmitis 

6

Group Sub‐ 

group 

Quick 

Reference 

Specific Features 

A A Small tumor RB ≤ 3 mm in size 

B B Larger tumor 

• Macula 

• Juxtapapillary 

• Subretinal Fluid 

C 

D 

C1 

C2 

C3 

D1 

D2 

D3 

RB > 3 mm in size OR 

• Macular RB (≤ 3 mm to foveola) 

• Juxtapapillary RB (≤ 1.5 mm to disc) 

• Clear subretinal fluid ≤ 3 mm from margin 

Focal seeds RB with: 

Subretinal seeds ≤ 3 mm from RB 

Vitreous seeds ≤ 3 mm from RB 

Both subretinal & vitreous seeds ≤ 3mm from RB 

Diffuse seeds RB with: 

Subretinal seeds > 3mm from RB 

Vitreous seeds > 3 mm from RB 

Both subretinal and vitreous seeds > 3mm from RB 

E E Extensive RB Extensive RB occupying >50% of globe OR 

• Neovascular glaucoma 

• Opaque media from hemorrhage in anterior 

chamber, vitreous or subretinal space 

• Invasion of postlaminar optic nerve, choroid 

(>2mm), sclera, orbit or anterior chamber 

Treatment of Retinoblastoma 

Treatment Most Effective on: Method 

Laser Treatment • Smaller tumors 

• Chemoreduced tumors 

Cryotherapy • Larger, peripheral tumors 

• Localized vitreous disease close to 

the retina 

External Beam 

Radiotherapy 

• Diffuse disease in the only 

remaining eye 

• Non‐responsive recurrent disease 

Brachytherapy • Localized vitreous disease 

• Elevated tumors where laser is 

ineffective 

532 nM green or 810 nM 

infrared laser 

Probe applied through sclera 

at ‐60° to ‐80°C; cryonecrosis 

Radiation applied to eye from 

external source 

Radioactive plaque of Iodine 

( 131 I) or Ruthenium ( 106 Ru) 

attached to sclera 

Treatment of Retinoblastoma 

Treatment Most Effective on: Method 

Chemotherapy 

4‐6cycles of Carboplatin, 

Etoposide & Vincristine (CEV) 

at 3 week intervals 

Intra‐arterial 

Chemotherapy 

• Any tumors, including extraocular 

involvement and metastases 

• Vitreous and sub‐retinal disease 

Enucleation • Advanced monocular disease 

• Worse eye of bilateral cases 

Transfemoral artery 

cannulation to direct delivery 

of Melphalan to ophthalmic 

artery 

Eye is removed with a long 

segment of optic nerve 

7

Percent Success 

100 

90 

80 

70 

60 

50 

40 

30 

20 

10 

0 

Prognosis of Retinoblastoma 

100 

Success Rate with Chemoreduction 

93 

A B C D 

ICRB Category 

Intraarterial Chemotherapy 

• Cannulation of the internal carotid artery 

• Melphalan infusion administered to 

ophthalmic artery 97.51% of the time 

Intra‐arterial Chemotherapy Prognosis 

• Of mostly advanced eyes (ICRB D), 70% were 

salvaged at two years 

– 81.7% of those initially treated with chemosurgery 

– 58.4% of those with prior conventional treatment 

90 

47 

8

Before & After 

Before & After 

Supportive Treatment 

• Protective eyewear 

• Low vision rehabilitation 

• Prosthesis fitting for enucleated eyes 

• Long term monitoring for other tumors 

• Psychological support for patient and family 

9

Clinical Pearls 

• Mothers are always right. 

• Co‐management is essential. 

• Stay updated on new technologies. 

References 

1. P. Lin and J. M. O'Brien, "Frontiers in the Management of Retinoblastoma," Am J Ophthalmol, vol. 148, pp. 

192‐198, 2009. 

2. M. W. Wilson, "Pediatric Ocular Tumors and Simulating Lesions," in Pediatric Ophthalmology: Current 

Thought and A Practical Guide, Berlin, Springer, 2009, pp. 403‐418. 

3. Kanski, Ophthalmology, New York: Elsevier, 2011. 

4. M. V. Parulekar, "Retinoblastoma ‐ Current Treatment and Future Direction," Early Human Development, 

vol. 86, pp. 619‐625, 2010. 

5. G. T. Lueder, "The Effect of Initial Recognition of Abnormalities by Physicians on Outcome of 

Retinoblastoma," J AAPOS, vol. 9, pp. 383‐385, 2005. 

6. S. K. Houston, T. G. Murray, S. Q. Wolfe and C. E. Fernandes, "Current Update on Retinoblastoma," 

International Ophthalmology Clinics, vol. 51, no. 1, pp. 77‐91, 2011. 

7. C. L. Shields, A. Mashayekhi, A. K. Au, C. Czyz, A. Leahey, A. T. Meadows and J. A. Shields, "The International 

Classification of Retinoblastoma Predicts Chemoreduction Success," Ophthalmology, vol. 113, pp. 2276‐ 

2280, 2006. 

8. C. L. Shields, S. G. Honavar, A. T. Meadows, J. A. Shields, H. Demirci, A. Singh, D. L. Friedman and T. J. 

Naduvilath, "Chemoreduction Plus Focal Therapy for Retinoblastoma: Factors Predictive of Need for 

Treatment With External Beam Radiotherapy or Enucleation," Am J Ophthalmol, vol. 133, pp. 657‐664, 2002. 

9. D. H. Abramson, "Chemosurgery for Retinoblastoma: What We Know after 5 Years," Arch Ophthalmol, vol. 

129, no. 11, pp. 1492‐1494, 2011. 

References 

10. D. H. Abramson, I. J. Dunkel, S. E. Brodie, J. W. Kim and Y. P. Gobin, "A Phase I/II Study of Direct Intraarterial 

(Ophthalmic Artery) Chemotherapy with Melphan for Intraocular Retinoblastoma," Ophthalmology, vol. 115, 

pp. 1398‐1404, 2008. 

11. C. L. Shields, C. G. Bianciotto, P. Jabbour, A. Ramasubramanian, S. E. Lally, G. C. Griffin, R. Rosenwasser and J. 

A. Shields, "Intra‐Arterial Chemotherapy for Retinoblastoma: Report No. 1, Control of Retinal Tumors, 

Subretinal Seeds, and Vitreous Seeds," Arch Ophthalmol, vol. 129, no. 11, pp. 1399‐1406, 2011. 

12. C. L. Shields, A. Ramasubramanian, R. Rosenwasser and J. A. Shields, "Superselective Catheterization of the 

Ophthalmic Artery for Intraarterial Chemotherapy for Retinoblastoma," Retina, pp. 1207‐1209. 

13. Y. P. Gobin, I. J. Dunkel, B. P. Marr, S. E. Brodie and D. H. Abramson, "Intra‐Arterial Chemotherapy for the 

Management of Retinoblastoma: Four‐Year Experience," Arch Ophthalmol, vol. 129, no. 6, pp. 732‐737, 2011. 

14. C. L. Shields, C. G. Bianciotto, P. Jabbour, G. C. Griffin, A. Ramasubramanian, R. Rosenwasser and J. A. 

Shields, "Intra‐arterial Chemotherapy for Retinoblastoma: Report No. 2, Treatment Complications," Arch 

Ophthalmol, vol. 129, no. 11, pp. 1407‐1415, 2011. 

15. D. H. Abramson, "Retinoblastoma in the 20th Century: Past Success and Future Challenges," Investigative 

Ophthalmology & Visual Science, vol. 46, no. 8, pp. 2684‐2691, August 2005. 

16. A. E. Rizzuti, I. J. Dunkel and D. H. Abramson, "The Adverse Events of Chemotherapy for Retinoblastoma," 

Arch Ophthalmol, vol. 126, no. 6, pp. 862‐865, 2008. 

17. T. Marees, A. C. Moll, S. M. Imhof, M. R. de Boer, P. J. Ringens and F. E. van Leeuwen, "Risk of Second 

Malignancies in Survivors of Retinoblastoma: More than 40 Years of Follow Up," J Natl Cancer Inst, vol. 100, 

pp. 1771‐1779, 2008. 

10

Late Onset Cone-Rod Dystrophy 

Bioptic Telescope Driving Rehabilitation 

Patient PP – 49 yo AF 

Matt Valdes, OD 

Resident, Low Vision Rehabilitation 

CC: Evaluation of bilateral 

central field loss 

HPI: 

LEE: 1 month prior (outside clinic) 

Gradual decline in central vision 

and color discrimination 

Patient History 

POH: 

(+) Macular mottling, OU 

(+) Macular thinning, OU 

PMH: 

Unremarkable 

Meds: 

Vitamin D 

Centrum 

ALL: NKA 

FOHx: 

Unremarkable 

FMHx: 

Unremarkable 

No common ancestry 

SH: 

Sales Associate 

Driving: self-restricted 

5/15/2012 

1

PR 

Previous Care: Photos 

Previous Care: OCT 

Previous Care: OCT 

Abnormal Normal 

RPE 

RPE 

PR 

5/15/2012 

2

Previous Care: Electro-diagnostic testing 

ERG 

VEP: 

Very low amplitudes/ 

implicit times 

Could not be reliably 

determined due to poor 

wave form formation. 

ERG: 

Reduced scotopic and 

photopic B-waves, 

Scotopic greater than 

photopic 

Previous Care: HVF 30-2 SITA STD 

OD: Borderline OS: WNL 

Summary 

Assessment Plan 

Late Onset Cone Rod 

Dystrophy 

Reduce central acuity 

Macular thinning 

Macular mottling 

Reduced VEP/ERG 

Intact peripheral vision 

Refer to Center for Sight 

Enhancement for LV 

evaluation 

5/15/2012 

3

Question? 

Low Vision Goals 

Near: 

Increase independence at 

work and home reading 

small print 

Price tags 

Distance: 

Improve distance vision 

Driving: Renew DL 

Recognizing faces 

Seeing the monitor at Temple 

Low Vision Exam 

Entering VA, sc: 

OD: 10/60 (FB) 

OS: 10/60 (FB) 

OU: 10/60 (FB) 

IOP: 

OD: 14mmHg 

OS: 15mmHg 

Pupils: ERRL, (-)RAPD 

EOMS: Full, OU 

SLE: 

Pinguecula, OD/OS 

BCVA: 

-0.50DS 10/60 

Plano 10/60 

5/15/2012 

4

Low Vision Exam: Devices 

Near Devices: Acuity Performance 

+2.50 OTC readers 0.4/01.6M (CT) 

+5.00 Near 

microscopes 

+9D Schweizer 

Okolux Plus 

Distance Devices 

0.16/0.8M (CT) 

0.16/1.0M (CT) 

2.5x HHTS 10/40 (OS) 

Ancillary Testing 

Binocular Esterman Field 

Screener 

Summary Exam #1 

• Unable to read 

small print (1.0M) 

• Good response to 

magnification 

• Adequate working 

distance 

• Resistance to 

device 

(-) alignment 

(-) focusing 

(-) spotting 

Assessment Plan 


Dystrophy 

Goal: Reading 

Goal: Distance Spotting 

Goal: Driving 

Full fields 

Points Seen: 120/120 

Continue care with referring 

doctor 

Released Rx for +5.00D near 

readers 

RTC for additional training 

prior to prescribing any devices 

Counseled and educated on 

DPS guidelines 

Recommendation: D/C driving 

until completion of BTS training 

5/15/2012 

5

Follow up: 9 mos later 

Exam Findings: 

Entering VA, sc: 

OD: 10/80+ (FB) 

OS: 10/60-2 (FB) 

OU: 10/60 (FB) 

Pupils: ERRL, (-)RAPD 

EOMS: Full, OU 

CC: Central vision loss 

secondary to late onset conerod 

dystrophy 

Goals: 

Driving rehabilitation 

Evaluate current low vision 

devices 

+5.00 SV readers 

Low Vision Exam: Near 

BCVA: 

+0.25-0.75x100 10/80+ 

+0.50-0.75x094 10/60- 

Device Acuity Performance 

+5.00 SV Readers: 0.16/0.8M (CT) • Overall good 

Eschenbach 16D 

(4x) Easy Pocket 

IHHM: 

0.5-0.8M (SL) 

Internals: undilated 78D 

ONH: Flat/distinct margins, OU 

C/D: 0.35R, OD/OS 

Macula: (+) macular mottling, OU 

Retina: (-) breaks, OU 

• Trouble with 

working distance 


magnification 

5/15/2012 

6

Low Vision Exam: Distance 

Device Acuity Performance 

2.2x FD WATS: trial 

frame 

10/40 -2 (OD) 

4x Ocutech Sport: 10/20 (OD) 

Ancillary Testing 

Dynavision: Full/Mode A 

Trial 1: 47, 1.25 hits/sec 



Binocular Esterman: 

Full fields (>140 degrees) 

Summary Exam #2 

Assessment 


Dystrophy 

Goal: Reading 

4x Easy Pocket: 0.5-0.8M 

Goal: Driving 

4x BTS: 20/40 

Fields: >140 degrees 

Dynavision: 52 hits/min 


magnification 

• Good spotting 

•Trouble with 

focusing/alignment 


magnification 

Plan 

Continue care with 

referring doctor 

Ordered 4x Easy pocket 

for quick spotting 

OT training recommended 

C+E on BTS driving 

rehabilitation 

RTC for OT training 

Metro-lift application 

5/15/2012 

7

OT Training Summary w/ Danny (4 visits) 

4x Easy Pocket 

IHHM 

Goal: 

1. Quick spotting 

2. Working distance 

1. Price tags 

2. Bills 

3. Magazine print 

Completed 

Questions? 

4x Ocutech BTS 

Goal: 

1. Device efficiency 

2. Distance spotting 

1. Static target/patient 

2. Static pt/kinetic targets 

3. Kinetic target/pt 

Completed 

Dynavision 

Goal: 

1. Safe driver category 

2. Visual scanning 

1. Full/Mode A/1min 

2. Full/Mode A/Distractor 

3. Full/Mode A/4min 

Maintained 

What is Bioptic Telescope Driving? 

Passenger Driving 

Route 

Goal: 

95-100% accurate 

identification 

1. Street signs 

2. Pedestrians 

3. Obstacles 

Pending 

5/15/2012 

8

Bioptic Telescope Driving 

Spectacle mounted 

telescope 

See objects from a further 

distance 

Majority of viewing through 

carrier lens. 

Intermittent use while 

driving (quick spotting) 

DPS regulated 

Bioptic Telescope 

Texas DPS Regulations 

Department of Public Safety 

Unrestricted: 

20/40 (uncorrected) 

Restricted: 

20/50-20/70 (best corrected) 

BTS Driving: 

20/80 – 20/160 (carrier) 

At least 20/40 through telescope 

>140 degs (horizontal field) 

Restrictions: 

Day time only 

Less than 45mph 

No highway driving 

Familiar areas 

With corrective lenses 

DL-63 

DPS office (OT) 

5/15/2012 

9

Center For Sight Enhancement 

What makes a good candidate? 

Motivation 

Confidence 

Stability of ocular 

condition 

* We do not address behind the wheel driving ability 

Cognitive ability 

Mini Mental State 

Examination (MMSE) 

Short Portable Mental 

Status Questionnaire 

(SPMSQ) 

How to predict on-road performance with 

off-road assessment? 

Cognitive Drivers Behavioral 

Inventory (CDBI) 

27 tests of driving related 

visual skills 

Study: 66-95.5% who 

passed CDBI passed onroad 

assessment 

Limitations: 

Cost 

Time Consuming 

Why? 

Independence 

Social 

Economical 

Quality of life 

Depression 

Social Isolation 

Standard of Care 

Don’t get sued! 

Dynavision 

Active visual scanning 

exercise 

Peripheral vision awareness 

Visual attentions 

Visual motor function 

Study: 66-75% who passed 

dynavision passed on-road 

assessment 

5/15/2012 

10

Insights gained 

Don’t let perception 

displace reality 

Premium services in high 

demand are well 

compensated 

There’s no I in TEAM 

Unless you spell it in 

Spanish 

Culture/Family Dynamics 

Codes & Fees 

Visit # Code Description Fee 

1 99204 Initial LV Evaluation 176.00 

LV1 Refraction 60.00 

2 99214 Former LV Evaluation 115.00 

LV2 Refraction 35.00 

92082 Binocular Esterman 75.00 

V2600 Eschenbach 4x Easy Pocket 79.95 

V2600 4x Ocutech Sport BTS 1637.80 

OT #1 97003 Initial OT Evaluation 90.00 

OT #2 97530 OT training session 36.00x2 units 

OT #3 97535 OT training session 36.00x 2 units 

OT #4 97535 OT training session 36.00x 2 units 

Total 2484.75 

Special Thanks 

Dr. Woo 

Dr. Perez 

Dr. Modi 

Dr. Hooper 

Dr. O'Hara 

Danny Zander 

Dr. Desai 

Dr. Frogozo 

Dr. Knighton 

Dr. V 

Dr. Villafane 

Dr. Yousefi 

5/15/2012 

11

Question/Comments 

Strowmatt Driving Rehabilitation 

Defensive Driving Habits 

Keep your eyes moving and be 

alert 

See the whole picture and 

anticipate what they other 

driver will do in advance 

Be sure you are seen 

Follow at a safe distance (four 

second rule) 

Be sure you have an escape 

route as a last resort 

Be prepared by knowing where 

you are going in advance 

Use other aids as necessary 

(hats, visors, tinted lenses, 

magnifiers etc.) 

Driver Skills 

Vehicle speed control, shifting 

and braking 

Depth and spatial perception 

Steering 

Use of Mirrors 

Backing up and parking 

Knowledge of rules of the road 

and courtesy 

Compensation for low vision 

(practice announcing what you 

must react to) 

5/15/2012 

12

Characteristic lacunae 

 

RPE aden adenocarcinoma 

nocar ocar ocarcino cino i ma 

Take NOTE of intra-lesion NODULES 

Shields JA. Adenocarcinoma arising from congenital hypertrophy of the retinal pigment 

epithelium. Arch Ophthalmol . 2001 

Disclosure 

We have in some capacity worked for/ 

with and/or received honoraria from the 

following companies over the course of 

the last year: 

Alcon, Allergan, Carl Zeiss Meditec, 

Optos, Optovue, Reichert, Zeavision, 

Arctic Dx & Annidis 

 

Variability presentations 

Large 

Red-free 

1

• 

 

 

 

 

• 

 

 

 

 

 

 

 

 

 

 

 

 

 

DOES THE SIZE OF THE LESION MATTER? 

Which one are you more concerned about? 

>7DD = 10.5mm 

Slightly bigger than 1DD = ~1.5mm 

2

To Find Small Ocular Melanoma 

5 feature that help identify small choroidal melanoma (Shield Ophth 1995) 

Thickness >2mm 

Orange pigment 

> 3 features = >50% chance of growth in 5 yrs 

Shield Arch Ophththalmol 2000 

FAF 

Symptomatic 

Fluid (subretinal) 

margins near ON 

(W/I 3mm) 

 

 

 

 

Why is Dx a small melanoma so critical? 

Diener-West M, et al. Arch Ophthalmol, 1992;110:245-250. 

Did you know 

Ocular melanocytosis (congenital hyperpigmentation of 

peri-ocular skin, episclera, uvea, etc) may increase the 

chance of concomitant choroidal 

melanoma in WHITE pts 

Ocular melanocytosis affects .04% of WHITE 

1 in 400 WHITE pts w ocular melanocytosis 

develop uveal melanoma during their 

LIFETIME 

Follow up q6M w DFE 

Shield Ophthalmology 2011 n=89 

To Find Small Ocular Melanoma 

using helpful hints daily 

Shield Arch Ophthal 2009 (N= ~2,500 cases) 

UBM's Hollow ll 

Halo/Drusen absence 

Follow-up depends on 

# of features noted 

No signs: annual exam 

(rate of conversion is /= 3 signs: consultation 

This is likely a small melanoma 

3 sings: 

Lipofuscin 

Thicken 

Fluid 

Clinical Pearl: 

This is NOT melanocytosis 

Thin sclera =Sign of age of autoimmune disease 

3

COMS Results 

(Collaboration Ocular Melanoma Study) 

HOW WE DX MELANOMA 

Biopsy is not a necessity SINCE FA, UBM, 

photos & clinic assessment are 99% accurate 

in correct Dx 

Intrinsic vasculature 

Histopath Characterist. COMS Report #6 AJO June 1998 

COMS Results 


Paradigm shift in how we tx melanomas 

In regards to Larger size tumor, when enuclation 

is a necessity, the procedure did not require 

concomitant radiation to decrease the likelihood of 

dissemination 

Question 

Which of the following depicts a retina 

undergoing hydroxychloroquine 

toxicity? 

 

COMS Results 


Paradigm shift in how we tx melanomas 

Plaque (I125 Brachytherapy) was as successful as 

enucleation for medium size melanoma, having 

equivalent survival rate up to 12yrs s/p treatment 

Most widely used tx for md size tumors is plaque 

plaque is generally left in place for 3-7 days. Radiation emitted 

from the plaque kills the cancer cells 

There are complications 

Laser photocoagulation and thermotherapy are re typically typ tyyp y ica i lly ll lly l y 

reserved for small tumors 

Small choroidal have a low 5 yr mortality rate 

COMS report no. 4. The Collaborative Ocular Melanoma Study Group. Arch Ophthalmol. 1997 Jul;115(7): 

886-93. 

Arch of Ophthalmol July 2001 119(7):969-982 

What is the most common location of 

primary uveal melanoma to metastases: 

most common site for reoccurrence? 

Liver 93% according to COMS 

Brain 

Lungs 

Heart 

Breast 

Ocular melanoma has a high recurrence rate of 

> 50% within 15 years of primary treatment. 

Arch of Ophthalmol May 2001 119(5):670 

 

4

www.alberta-retina.com 

 

 

 

 

 

 

 

 

 

 

 

 

BASELINE EXAMINATION 

 

 

 

MONITORIN determine if si/s maculopathy have occurred 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

GOAL OF SCREENING 

 

 

 

 

 

 

Protocol change in 2011 

 

Factors Increasing Risk of Retinopathy 

(HR) 

Duration of use/daily dosage > 5 years or > 400 mg/day 

Cumulative Dose > 1000 g (total) = 400x365X7 yr 

High BMI Waist circumference >30 “ 

Age Elderly 

Systemic Disease Kidney or liver dysfunction 

Ocular Disease Retinal disease or maculopathy 

 

5

TDOCT 

SDOCT 

 

 

AT BASELINE 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

6

SD OCT defect may be very subtle at 1st 

Normal 

Patient 

Further damage leads to Plaquenil Plaqu laq absence aaqu 

aquenil enil en enil en l of PIL 

Patient Patie Pat Pa Pat a ent nt 

Saucer Sauc Sau Sauc Sau Sauc Sau Sa Sauc Sa 

auc a uc ucer 

er e ra a 

a 

a 

appearance ppea ppe ppea ppe ppea ppe ppea pp ppe ppea pp ppea pp ppea pppea p pea pe e a ranc ran ranc r ranc ran ranc rranc anc a anc an a nc c e 

Courtesy Courte Co Courte Court Cou CCourte Courte ou ourte urte u rte rt te e sy y yDr y yD yDr y D 

Dr D 

D Dr. Dr Dr. 

Dr. Dr Dr. Dr Dr. Dr Dr. Dr Dr. Dr Dr. Dr Dr. J JShe J JJShe 

J JShe J J She Sh She Sh S She S She Sherman he h e eerma 

rman rm rma rm rman rm rman rm rman rma rman rm rma rman rma rman rm rman rma 

man mman 

m an a 

 

 

 

 

 

 

 

 

 

7

OUR pt: thinning parafoveally likely represents early damage 

TEST should be repeated & check reliability 

 

 

 

 

 

 

 

 

Supinferior Supinferior 

USE as many tests as possible to evaluate overall true toxicity 

8

9

Retinal Artery ery yOcc Occlusion 

us o 

TYPICALLY 

observed > 60yo 

Painless VL 

CF to HM acuity for r 

CRAO while BRAO O 

may only have VFD D 

or mildly affected VL 

+ APD 

May have had Hx of 

TVL 

Optic atrophy w/ attenuated vessels 

Retinal hypoperfusion with a cherry red spot (in CRAO) 

 

 

 

 

 

 

 

Treatment via unconventional path 

(AH sip thorugh tissue e arou aaround nd uvea) 

a 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

CRAO: Most common etiology 

10

Delayed arterial filling 

BOXCARRING 

(segmentation of the blood columns) 

Cilioretinal AO (branch of the short posterior ciliary) 

CarotidophthalmicShort post ciliary artery 

CRAO 

Good prognosis with most cases having VA better than 20/50 after a few weeks 

Courtesy of Dr. M. Rafieetary 

Initial 

Representation of an OLD CRAO 

Follow-up 

What does the retina look immediately following the event? 

Retinal physician 

11

1-24 hrs window of opportunity 

Primates studies show retinal tissue w/o O2 doesn’t survive >90min 

Within a day worth a TRY: 

In office options: 

Digital massage: increase artery pressuredilate artery 

Hyperventilation in a brown paper bag: retinal autoregulation 

Ophthalmology referral 

A/C Paracentesis 

Diamox to lower IOP quickly 

Injection to dissolve fibrin or blood clots (thrombolytic) 

CONTROVERSIAL 

Although carotid doppler is very helpful in systemic 

Dx…a younger pt needs extensive work-up 

Associated complications 

Stroke 

Myocardial infarction 

Very common complication 

Main cause of death 

mortality rate of 54% was shown within 7 yrs 

Remember, fellow eye involvement if GCA is cause in 

OLDER pts! 

Carotid artery disease eval 

Atherosclerosis or dissection 

GCA evaluation 

Infectious etiologies 

Bacterial Endocarditis 

Syphillis/ Lyme/HIV 

Cardiac evaluation 

Hyperviscosity syndromes 

Leukemia 

Lymphoma 

SC in blacks 

Clotting factor abnormalities 

homocysteinemia 

Anti-phospholipid syndrome 

Cardiac valvular disease 

Vasospam 

Atrial fibrillation 

Cocaine use 

CVD & HTN/DM/chol (as risk factors) 

Causes such as smoking, migraine & birth control pill are Dx exclusion 

Attenuation of artery due to GCA 

12

Common clinical picture 

Headache 

AION 

Retinal artery occlusion 

diplopia 

history of AF/TIA 

Have you had a sudden TEMPORAL headache? 

Any associated scalp tenderness? 

Is it painful to chew? 

Swollen/thicken temporal artery 

May be tender and pulseness 

Jaw claudication 2° to insufficient blood supply to jaw 

GRADUAL Unilateral VL 

Associated with “aching” orbital pain 

AF & TIA 

The 1/3 rule VL 

OIS = CAD + ocular manifestations 

(55-80 yo) males 

Have you felt unwell lately? 

Lost of appetite or unintentional weight loss 

Malaise (general uneasiness) 

Night sweats/fever 

Do you experience aching of neck, upper arms, shoulders? 

Polymyalgia rheumatica 

muscle aches (deep) 

Neck manipulation 

What are you hearing? 

100% occlusion 

OIS: 

Ocular ischemic syndrome 

13

Most common retinal findings (>20% of case) 

Hypoperfusion (Venous Stasis) Retinopathy 

Anterior 

IOP typically low 

Idiopathic uveitis 

Cataract 

Corneal edema 

Dilated episcleral 

vessels 

Neovascularization 

(in absence of DR) 

Posterior 

Hemorrhages & CWS 

Dilated veins 

Macular edema 

Asymmetrical DR 

____ 

AION 

Artery occlusion 

Retinal emboli 

Different color threads woven together to make 

the diagnostic fabric 

OIS 

Mid-peripheral 

Dilated NON-tortuous veins 

Scares dot blot hemorrhages 

Associated anterior segment 

CRVO 

Posterior pole 

Carotid problem, which needs 

treatments leads to: 

Strokes 

Common cause of strokes are due to 

embolism 

Typically associated with TIA/AF 

Cardiac problems 

5 yr mortality rate is 40% in OIS pts 

Dilated tortuous veins 

Confluent superficial and 

intra-retinal hemorrhages 

14

Now What? 

Don’t Substitute a Part 

Of Any Person 

For the Whole Person 

KEY POINT 

Hyperglycemia aggravates all of 

the metabolic abnormalities of DM 

Improving blood glucose control 

improves virtually all metabolic 

abnormalities asociated with DM 

1. Diabetes care 30:713-715, March 2007. 

15

A1C for Diagnosis 

ADA, EASD, IDF expert panel recommends 

HbA1c now be used as front-line test for 

diabetes Dx 

HbA1c > 6.5% diagnostic for DM 

HbA1c of > 5.7% but < 6.5% diagnostic for 

pre-diabetes 

HbA1c is a better predictor of DR than FPG 

Diabetes Care 2009 November;32(11): 2027-32 

 

1. Saudek et al. Panel concensus in J. Clin Endo and Met 7/08. 

2. Pradham et al. Am J Med 2007;120:720-727. 

 

 

DM without 

retinopathy 

Mild -Moderate 

NPDR 

Severe-Very Severe 

NPDR 

12 months 

6-12 months 

2-4 months 

16

Klein, Klein, Moss, et al. Epidemiology of retinal VO: Beaver Dam Eye Study. Trans Am Ophthalmol Soc 2000; 98: 133-41 

How would they manage this? 

BP: 150/98 mmHg 

What do you do next? 

46 BF 

Hx HTN & Overweight 

BP: 160/90 

How would you managed this in 2002 vs 2012? 

IVK(SCORE) 

Off label CRVO 

BP: 150/98 mmHg 

In era of new Tx options how would 

SHE and HE managed VO/ME? 

Steroid implant 

Ozurdex CRVO/BRVO 

FUTURE 

VEGF trap 

Copernicus/Galileo Study 

Anti-VEGF 

BRAVO/CRUISE 

CRVO/BRVO 

Laser for BRVO/ME 

MORE DATA ON Tx OF VO/ME RELEASED IN 2009 

THAN HAVE BEEN IN THE LAST DECADE 

Retinopathy & HIGH BP 

One requires immediate attention while the other 

requires timely/appropriate medical referral 

18

Severe Hypertension + NO End-Organ Damage 

Typically identified during routine evaluation 

Usually represents chronic hypertension, 

especially those that do not adherence to drug 

therapy or inadequate treatment by the PCP. 

Warrant attention but… 

“no evidence to suggest that failure to aggressively lower BP in 

the ER is associated with any increased short-term risk “ 

JNC 7 

 

 

 

 

“Hypertensive emergencies are characterized severe 

elevations in BP (>180/120 mmHg) complicated by 

evidence of impending or progressive target organ 

dysfunction.” (JNC 7 ) 

CNS, cardiovascular or renal…hypertensive encephalopathy, 

intracerebral hemorrhage, acute myocardial infarction, left ventricular 

failure with pulmonary edema… 

Require immediate (but slow) BP reduction (not necessarily 

to normal ranges) to prevent or limit organ damage. 

often admitted through the ER for aggressive treatment. 

Survival rate has changed from 80% (if treated) in 5 yrs 

 

 

 

▪ 

▪ 

 

 

 

 

Urgency but not an emergency 

Advise to PCP this week and RTC 1M 

Lane Am J Hypertension 2009 

19

▪ 

 

CC: Headaches X 2 M 

PMHx: HTN 

Meds: 2 anti-HTN meds 

BCVA: 20/30 OD, OS 

P: (-) APD 

BP: 220/115 mmHg 

She was referred to ER BUT… 

What I learned from this case? 

Directly call & send pictures 

Now it has become an 

emergency! 

Healthy patient??... 

32 yo male healthcare professional in Midwest 

2-3 month history of cough, dyspnea, chills, malaise 

Recently returned from International travel 

No improvement with antibiotics and PO prednisone 

Abnormal chest x-ray 

Good vision 

Referred to Pulmonologist 

20

Calcified Granulomas 

Differentials? 

TB 

Sarcoid 

Histoplasmosis 

Lymphoma 

Chest X-ray 

Systemic Histoplasmosis 

Caused by Histoplasma capsulatum, a dimorphic 

fungus, that turns into a yeast at body temperature 

Endemic to Ohio, Mississippi, and Missouri River 

valleys 

Aerosolized fragments result in alveolar deposition 

Most infected people are asymptomatic 

Can involve CNS, liver, spleen, eyes, rheumatologic 

system, and hematologic system 

Histoplasmosis cont. 

Symptoms can occur 3-14 days after exposure 

Approximately 250,000 infected annually 

Clinical manifestations in less than 5% 

About 90% with acute pulmonary histo are asymptomatic 

Enlarged hilar and mediastinal lymph nodes in 5-10% of 

patients 

Affects males 4:1 

Progressive disseminated histo mostly occurs in 

immunocompromised patients ex: AIDS 

CT ordered with 

contrast 

Labs ordered 

CBC Normal 

Normal Liver function 

ESR 46 mm/hr 

Negative TB skin test 

ACE 44 U/L (7-46) 

Histo Mycelial Ab Normal 

Histo Anti H Ab 1:32 

Case continued 

Ocular Histoplasmosis 

Linked to H. capsulatum (A fungi) 

found in soil with high concentration of fecal material 

(excrements) from chickens, pigeons and bats 

GUANO…OH MY! 

Testing 

Inhale 

spores 

CBC generally normal 

Sputum cultures yield positive results in only 10-15% of acute pulmonary 

histo 

Complement fixing antibodies 

Greater than 1:32 suggests active 

Positive 5-15% of within 3 wks of exposure 

Positive 75-95% at 6wks 

Immunoprecipitating antibodies 

Anti-M detected in 50-80%, and remains elevated for years 

Anti-H detected in 10-20% and becomes undetectable after 6mos. This antibody is 

most specific for active histo 

Imaging studies 

Chest X-ray 

CT scan 

HLA-B7, HLA-DR2 and may be elevated more in people with CNVM 

21

Possible associations 

May develop Flu like symptoms (but not as common) 

scars in lungs 

dense nodules with central calcification 

44WM 

Refer for possible neoplasm nodule in lung 

Note: calcifications 

Peripapillary atrophy 

May represent 

atrophied granulomas 

that formed during 

active infective stage 

of 

Neovascular membranes 

can form here, and 

involve macula 

Courtesy of Dr,. J Sherman 

Treatment 

No treatment needed if asymptomatic 

Treatment if symptomatic, or progressive 

Treatments 

Amphotericin B: drug of choice for overwhelming active 

histo, administered by IV 

Itraconazole: Fungistatic, very active against Histo, minimal 

side affects 

Liver functions must be monitored 

Approximately 86% success when treating > 2mos 

Ketoconazole: Fungistatic, well tolerated, does not cross 

blood/brain barrier 

OHS 

Histo Spots 

Atrophic yellowish white 

scars from previous 

multifocal or disseminated 

choroiditis 

Can form streaks 

22

Treating CNVM from Histo 

MPS 

Submacular Surgery (SST) 

PDT 

Anti-VEGF Therapy 

1. Thomas, Matt at Barnes Retina in St. Louis 3/2008 2. Surg vs observ with POHS 

CNVM. SST group. Arch Ophth 12/08 

23

He said 

She said 

OCT Grand Rounds: The “HD” Experience 

Unprecedented imaging, helping 

differentiate macular abnormalities 

What we may not see w/o an OCT: 

early MH, VMT, small drusen/exudates, subtle edema, early 

ERM, PIL, early CNV… 

and also aids in monitoring pts s/p AVT 

Can you appreciate the differences? 

OS in 2010 

OS in 2011 

 

 

 

 

 

These affiliations will have no affect 

on the content of this lecture 

HOW ABOUT NOW? 

20/50 + 

2011 RT 311 

Case in point 

VMT and early Macular hole may be missed without OCT 

1

24 WM 

CC: Decreased VA longstanding 

since young 

seems to have “gotten” worse 

BCVA: 20/300 OD, OS 

CV: 0/8 plates 

P: (-) APD 

No FR 

Is this another achromotopsia case? 

Solar maculopathy: localized IS/OS disruption w intact RPE 

Laser-like defect with surgical precision… 

Unfortunately there is NO tx (so REFERRAL is NOT a necessity) 

So what is the dx? 

MH 4 

OD 

artifact 

Courtesy Drs. Yu & Paterson 

OS 

Courtesy of Dr. Yu 

OCT OC OCT C he hhelps lps lp lps lp ps p in 

in DD DDx DD DDx 

Described as “punched out” zone with complete absence of PIL 

RASTER image gives us 

higher resolution 

PIL important in visual function… 

2

Advanced RPE Analysis 

Gain new insights on your AMD patients 

• RPE Elevations. If the RPE 

is raised above a baseline 

plane, a new proprietary 

algorithm for Cirrus maps 

and measures the area and 

volume of the elevations. 

• Sub-RPE Illumination. If 

the RPE is absent or has 

lost integrity, the OCT 

beam penetrates into the 

choroid. A new proprietary 

algorithm for Cirrus can 

determine when this occurs 

and then map and measure 

the affected area. 

Carl Zeiss Meditec, Inc Cirrus 6.0 Speaker Slide Set CIR.3992 Rev B 01/2012 

RPE Elevations Sub-RPE Illumination 

 

 

 

 

 

 

 

 

 

 

 

Following change of DRY AMD in the future 

13 

13 

Dr. C Puliafito 

 

This measurements will be important in future research… 

Changing the face of GA: Monitoring GA 

Single snapshot of 

macula encompassing metrics 

Giovanni Gregori, PhD, of BPEI published in retinal physician 2010 

3

Courtesy Drs. Frauens & Besada 

 

 

 

 

 

 

 

 

 

 

OD 

OS 

 

OS foveal 

contour 

Pt did have metamorphopsia (amsler) OS only 

 

 

 

 

 

 

 

 

 

 

 

 

Is this a FULL thickness MH? 

What do you think now? 

4

• 

• 

• 

• 

• 

TDOCT 

SDOCT 

VMT or ERM may or may not be observed 

 

 

FTMH 

Witkin AJO march 2006 

Baseline important 

for documenting 

current function & 

structure 

Protocol change in 2011 

 

 

 

 

 

 

 

 

 

5

RPE en face Slab Analysis OU 

ESTABLISHED maculopathy 

 

 

 

 

33 

SD OCT defect may be very subtle at 1st 

Normal 

Patient 

Further damage leads to absence of PIL Plaquenil Plaqu Plaq Plaquen laq aqu en ennil 

l 

Patient Patie Pat atie a nt t 

Saucer Sauc Sau Sauc Sau Sauc Sa Sauc Sau 

auc a auc a uc ucer 

er ra a aappearance 

a aappea 

a 

ppea ppe ppea ppe ppea pp ppea ppe ppea ppe ppea ppe pp ppea ppe pp ppea pppea p pea pe pea e eea 

a ranc ran ranc rranc ran rranc ra ranc anc an nc e 

Courtesy Courte Cou Courte Cou Courte CCo Courte ourte ou rte rt te t e sy y yD y yDr y yyDr 

y D DDr 

DDr 

D Dr. Dr Dr. 

Dr. Dr Dr. Dr Dr. Dr Dr. Dr Dr. J J JJShe J JShe J She 

Sh S Sh She Sh 

S She S She Sherman he heerm 

rman rma rman rm rma rman rma rman rm rman rm rman rm rman rma rman rm rma man an a 

The thinning parafoveally likely represents early damage 

TEST should be repeated to check reliability 

6

ed 

 

10-2 

 

 

red 

 

10-2 

Case where toxicity may be noted, it may be helpful to use as 

many tests as possible to evaluate overall true toxicity 

7

Previously Dx w ERM…is it? 

Going beyond POAG… 

Vision has worsen over the past yr 

(20/80) 

Reason? 

14D myope 

note 

Courtesy Drs. M. Rafieetary & J. Sherman 

 

Notice the collapse of the retinal layers, creating Mini Bulges. 

 

 

 

TRACTION 

8

50HF 

Asymptomatic 

PMHx: unremarkable 

En face RPE reference 

Note deep elevation…DDx? 

Our pt does NOT have this 

What is it? 

 

 

 

 

 

 

 

 

En n face fac fa fac fa e eR e eR e eR e eR e eR e RPE R RRPE 

PE P reference ref re ref ef efer er ere er ere er ere r nce nc nce ce 

Vitritis view 

 

 

So what is the difference? 

Small melanoma 

9

WHAT A 

OCT 

Courtesy of Dr. J Sherman 

OCT: Retinoschisis vs. Retinal Detachment 

Retinoschisis in a HIGH Myope 

Retinal Detachment 

What are we looking at? 

Is this a BRVO? 

Tri-layer Tri Ti Tri T Tri r ri rii 

-la la layer a yer y er e hemorrhage 

hem he hem he em orr orrhag hag ag age e 

Is this an artery or vein 

10

58 DM pt 

Is this neo of the disc? 

2 presentations in pts w vein occlusions 

Refer either, neither or both? 

FRIEND OR FOE? 

How about this one? 

Small thick bud 

Another peripapillary 

vascular loop 

Courtesy of Dr. J Sherman (Retina Revealed) 

What’s the dx? Referral? 

Nevus with drusen 

or CHRPE with lacunae? 

Project forward 

11

This is a nevus with drusen 

 

 

 

Note 

650um 

Note choriocapillary thinning overlying the nevus 

Shield believes that EDI OCT can give precise measurement of 

tumor thickness with comparatively reduced thickness relative to 

ultrasonography 

Decrease vision since birth 

Another pigmented lesion 

20/200 

But the macula doesn’t seem affected 

You Have Some Nerve 

12

26yo 10D Myope 

Swelling inferior? Dx: Congenital Glial Tissue 

Glial tissue with associated ERM 

traction 

GDx 

Is this peripapillary edema (20/30)? 

What’s going on here? 

Is this related? 

13

vitreoPAPILLARY traction 

Associated with VMT 

Would you refer either, neither or both? 

BOTH have a VFD and BOTH are 20/20 

OU 

OU 

OCT criteria for ON edema: A review 

Elevation of nerve with smooth internal contour 

Increased RNFL thickness 

beyond the Nerve 

Johnson Opt 2009 

2009 

Has traction on the macula 

worsen with time? 

BCVA remains at 20/30 

2010 

Other si/s to look for in papilledema: 

Note the elevation height & smoothness of the internal 

contours (-) SVP, in HA, a papilledema TVOs, diplopia case & tinitis 

Another edema sign 

Lazy V-pattern (Savini) 

14

Simple Modulation 

of ONH drusen 

Other si/s noted in ONH drusen: 

abnormal trifurcation, absence of the cup 

& note the nerve appearance 

Macular RPE 

So which would you hold and which would you 

refer? 

Topographical image of optic pit noted 

using macular cube over ONH 

OCT criteria for ON drusen: A review 

Lumpy bumpy internal contour 

Wester Ophthalmic Surgery, Lasers and Imaging 2010 

Pt refer for glaucoma evaluation 

with possible notch & NFLD? 

Associated complications 

15

Seeing DOUBLE??? 

So would you hold or refer? 

16

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