Ocular Disease III: Exam 2: Lecture 8: Diabetic Retinopathy 3 Flashcards
After Slide 28, we start talking about Vascular Occlusive Diseases!
Non-Steroidal Treatments Drug Therapies (Oral Agents)
1. PKC-PKC-B inhib Arxxant (
i don’t think he’ll ask a question on this…more FYI…
- goal to normalize Retinal BF abnormalities for Pt with DR. and Decrease Risk of Mod. Vision Loss in those w/DME
Non-Steroidal Treatments Drug Therapies (Oral Agents)
- IVT Anti-VEGF Agents (Lucentis, Ranibizumab, Avastin, Bevacizumab)
a. Advantages over ROIDS?
b. DISADVANTAGE?
- a. Better side effect profile than Steroids
b. TEMPORARY IMPROVEMENT of DME ONLY, Recurrent injections
Non-Steroidal Treatments Drug Therapies (Oral Agents)
- New Anti VEGF Drug is AFLIBERCEPT (VEGF Trap-Eye, Eylea)
a. Approved by FDA for Tx of what?
b. Compared to Lucentis?
- CNV due to AMD! (2011)
b. It’s simply NON-INFERIOR to Ranibizumab. (has Ab based VEGF binding but uses a different BINDING SITE)
Non-Steroidal Treatments Drug Therapies (Oral Agents)
- DA VINCI Study: Phase 2 VEGF Trap-Eye in Pts w/CSME
a. Looked at DM pts with what? - OUTCOME Goal to MEASURE what?
- Results?
- What ABOUT LONG TERM CONSEQUENCES?
- a. with CSME
- to look at VA and CENTRAL THICKNESS at 6 MONTHS
- At 24 wks (6 months): The Acuity looks much significantly Better than laser, as well as reduction in Central Retinal THICKNESS!
- LONG TERM CONSEQUENCES of these ANTI-VEGF THERAPIES FOR DME in DM PATIENTS REMAINS UNDEFINED!
(they can combine this with Focal Laser)
Management
- Mild NPDR w/CSME
a. FA?
b. Ret. Con?
c. FU Months?
d. Focal Tx?
e. PRP Tx? - Mod NPDR w/CSME
a. FA?
b. Ret. Con?
c. FU Months?
d. Focal Tx?
e. PRP Tx? - Sev/V Sev NPDR w/CSME
a. FA?
b. Ret. Con?
c. FU Months?
d. Focal Tx?
e. PRP Tx? - Non-High-Risk PDR w/CSME
a. FA?
b. Ret. Con?
c. FU Months?
d. Focal Tx?
e. PRP Tx? - HR PDR w/CSME
a. FA?
b. Ret. Con?
c. FU Months?
d. Focal Tx?
e. PRP Tx?
- a. Yes
b. 0-3 wks
c. 2-4 months
d. Yes
e. No - a. Yes
b. 0-3 Wks.
c. 2-4 Months
d. Yes
e. NO - a. Yes
b. 0-3 wks
c. 2-3
d. Yes
e. Occ After Focal - a. Yes
b. 0-2 wks
c. 2-3
d. Yes
e. Occ After Focal - a. Yes
b. 24-48 hrs
c. 1-2
d. YES
e. YES
CLINICAL PEARLS
- Proper DIAGNOSIS!
a. MISDIAGNOSIS by 1 LEVEL UNDERESTIMATES RISK for DEVELOPING PDR in 1 YR by AT LEAST what %?
b. Severe NPDR Pt has % risk
c. PDR in 1 Yr
d. Focal Laser for CSME Decreases Risk for what?
e. ETDRS:
- a. At least 50%
b. 52% of development
c. V. Severe NPDR Pt has 75% risk of developing PDR in 1 yr
d. for Mod. VA Loss (doubling Visual Angle) from about 30% to 12%.
e. PRP decreases risk of Sev. VA LOSS (BVA
Clinical Pearls
- Control levels of what in Diabetics?
a. % that’s Adequate?
b. Norm?
c. % of NPDR over 10 years?
d. Increased risk of progression in PDR over 10 years? - For A1c 5-8%
a. Decrease A1c by what 10% DECREASES RISK of DR PROGRESSION by what %? (Meta-Analysis of what study)? - Decrease BP by how much?
a. this decreases progression of DR by what %? (Study) - When VH Obscures Retina or RD Exists: What MAY BE INEFFECTIVE?
a. What should be done at this POINT and according to what STUDY?
- HbA1c
a. 5-7%
b. 4-6%
c. 44%
d. 145% - a. 43% (of DCCT, and UKPDS)
- 10/5 mmHg
a. 34% (UKPDS) - PRP
a. Vitrectomy and RD Repair (DRVS)
Venous Occlusive Disease
- How prevalent is this retinopathy?
- STRONGLY ASSOCIATED with what?
- Very prominent what 2 things?
- Most COMMONLY seen in Pts over what?
- can you laser Exudates?
- 2nd Most Prevalent Retinopathy (Behind DM retinopathy)
- with SYSTEMIC DISEASE
- morbidity and mortality
- > 45 yrs.
- NO! even if you have CSME, they will NOT LASER it, cuz (slide 9) there’s nothing to laser. So they will probably do an INJECTION of Avastin or something like that (they are moving AWAY from Steroids these days) or Lucentis or Eylea
Anatomy
- Central Retinal Vein
a. Single trunk in Nerve, but may Bifurcate w/in what?
b. Constricts w/in LAMINA CRIBROSA in order to enter what?
c. Drains the Retina thru what? - CRA
a. Feeds what part of the Retina
b. Branch of what artery?
c. Parallels what?
- w/in the substance of the nerve to a DUAL TRUNK
b. to enter the Globe
c. Thru 4 Tributaries
- a. Inner 2/3rds of the Retina
b. of Ophthalmic Artery
c. the Venous Arcades
Venous Occlusive Disease
- What 4 did we talk about?
- CRVO
- HRVO (Hemi-Retinal)
- BRVO (Branch Retinal)
- Papillophlebitis
CRVO: Background
- Age of people this is seen in?
- Incidence b/w men and Women?
- Prevalence?
- USUALLY Uni/Bi?
- 3 Risk Factors for CRVO?
- ELDERY (50-70 yrs)
- Same
- 0.1%-0.4%
- UNILATERAL (BUT: Estimated up to 7% of persons may develop CRVO in the other eye w/in 5 YEARS!)
- a. HYPERTENSION (47-57%)
b. Diabetes
c. POAG
CRVO: Pathogenesis
- Physical Blockage
a. Lumina of CRA and CRV are narrower where?
b. Vessels are bound by what?
c. Lamina Limits Expansion and Displacement of what?
- Hemodynamic Factors
a. Results in what?
- a. at the LAMINA CRIBROSA
b. by a Common Sheath
c. of ON and Vessels! - a. Results in an Obstruction to BLOOD FLOW!
CRVO
- THROMBOTIC/ATHEROSCLEROTIC PHENOMENON
- What is the NIDUS for Occlusion?
a. Why? - WHAT External Factors MAY Cause FURTHER COMPRESSION and Contribute to OCCLUSION? (2)
- Some property of the blood and CRV act in Concert to Cause Occlusion.
- The LAMINAR CONSTRICTION SITE!
a. Due to Intraluminal Pressure of the Vein decreases, leading it to being susceptible to Collapse. Compression by an Arteriolosclerotic CRA further Affects Flow and Thrombus Formation - Increased IOP in POAG and Papilledema (causing increased pressure in the optic nerve sheath)
* Other factors that can cause Occlusion: Many: orbital tumor, abscesses, Cavernous Sinus Thrombosis, Retrobulbar Intranerve sheath Injection
CRVO: Symptoms
- What happens to Vision?
- What other two things?
- Asymptomatic. IT’s RARE. What 2 Occlusive diseases ARE MORE LIKELY to be ASYMPTOMATIC?
- What is the KEY SYMPTOM (HALLMARK)?!
- Blurred (unilateral)
- Scotoma, and Photopsia (rare cases)
- in BRVO or HRVO
- SUDDEN (Keyword) PAINLESS LOSS OF VISION!!!!
CRVO: SIGNS
- WHAT WILL YOU SEE in the FUNDUS?
- Veins?
- MAIN CAUSE FOR VISION REDUCTION?
- What White stuff do you see?
- What will you SEE LATER oN?
- BLOOD AND THUNDER!! All 4 Quadrants!
- DILATED, TORTUOUS VEINS!
- MACULA EDEMA!
- COTTON WOOL SPOTS (cuz it’s an INFARCT. Rarely see exudates in CRVO)
- COLLATERAL VESSELS (as body tries to correct itself) and Post and Ant Segment NEO
* Collaterals form b/w CRV and Vortex Vein thru Unopened Telangiectatic Vessels (they’re already there…but open at this point)