Diabetic Retinopathy Flashcards
(30 cards)
NPDR definition
intraretinal vascular changes, no development of extraretinal fibrovascular tissue. Used to be known as NPDR
PDR
presence of retinal neovascularization from diabetes induced ischemia. Characterized as early PDR or PDR with high risk characteristics (HRC)
DME
caused by abnormal vascular permeability
Factors that lead to diabetic damage
- endothelial damage
- pericyte loss
this happens from exposure to hyperglycemia leads to:
-increased inflammatory oxidative stress
-advanced glycation end products, and protein kinase c pathways
BM thickening and pericyte loss lead to:
Capillary occlusion and retinal nonperfusion
Consequences of endothelial barrier decompensation
retinal edema (serum leakage)
Recommended Diabetes follow up
Type 1 DM: 5 years after dx
Type 2 DM: immediately upon diagnosis
Pregnant with either DM: soon after conception and early in first trimester. FU every 1-3 months if severe NPDR or worse
What did the Diabetes control and complications trial (DCCT) and UK prospective diabetes study (UKPDS) show?
Intensive glycemic control was associated with:
- reduced risk of new onset retinopathy
- reduced progression of existing retinopathy
DCCT looked at type 1, UKPDS looked at type 2
What is metabolic memory
in the DCCT, patients who had intensive glycemic control in the beginning had decreased onset, progression, and need for surgery even 20 years after the study ended and the HbA1c levels converged.
What A1c is recommended based on DCCT and UKPDS?
less than 7
What did the ACCORD and ACCORDION study show?
A1c levels less than 6 slowed DR progresison even more in T2DM, but increased mortality
What other factors are associated with DR
- HTN
- severe carotid artery occlusive disease (part of ocular ischemic syndrome)
- Advanced diabetic nephropathy
- Anemia
- cholesterolemia
How does DR lead to vision loss?
capillary leakage (DME)
- capillary occlusion (macular ischemia)
- sequelae from retinal ischemia (neo, vit heme, TRD, NVG)
What to do in DM patients who need CE/IOL
If DME, give anti-vegf
If severe NPDR or PDR, consider scatter PRP before cat removal.
NPDR damage
Dmg stays within ILM:
- MAs
- intraretinal hemorrhage
- CWS
- venous beading
- IRMA
Criteria for Severe NPDR
4-2-1 rule:
- 4 areas of MAs
- 2 areas of venous beading
- 1 area of IRMA
Severe NPDR vs Very severe NPDR
severe NPDR has 1/3 of 4-2-1 rule. Severe npdr has a 15% risk of progression to PDR in 1 year and 60% in 3 years.
Very severe has 2-3/3. Has a 45% risk of progression in 1 year
Signs of macular ischemia
FAZ appears irregular on FA or OCTA and enlarges as the innermost capillaries become nonperfused
Treatment of NPDR
There is no clear treatment mandate for eyes with NPDR wo DME (besides control of glucose, lipids, and HTN)
Anti-vegf, lasers, and steroids have shown NPDR levels
PVDs have been hypothesized to improve outcomes in diabetic eyes bc it takes away the scaffolding for NV
Extraretinal fibrovascular proliferation progression
- New vessels with minimal fibrous tissue cross and extend beyond ILM
- New vessels get larger and become more fibrous
- vessels regress, leaving residual fibrovascular tissue that may be tethered in posterior hyaloid
high risk PDR
- NVE w heme
- NVD w heme
- NVD that is 1/4-1/3 in size
Possible draw back of treatment of PDR
treatment with PRP or anti vegfs may lead to contraction of fibrovascular tissue, and treatment may be followed by increased VR traction, vit heme, TRD, or combined TRD RRD
DRCR.net protocol S
Showed that ranibizumab and prp had EQUAL VISUAL OUTCOMES
Rani had benefits of:
- better average vision
- reduction in peripheral visual field loss
- reduced rates of sx
- less DME
Anti vegf in PDR
Given before vitrectomy, can help treat NVG
Steroids in PDR
reduce PDR related outcomes in DR.
Rates of vit heme, need for prp, rates of NV are reduced when steroids are used for non PDR indications like DME
