WHAT ABOUT DME? José Juan Escobar Barranco, Begoña ...José Juan Escobar Barranco, Begoña Pina...
Transcript of WHAT ABOUT DME? José Juan Escobar Barranco, Begoña ...José Juan Escobar Barranco, Begoña Pina...
We prefer to let the coricosteroids carry out a
reduction of the macular volume in order to
selectively photocogulate the fundus
achieving a more local effect with less energy
diffusion and photoreceptor destruction
Selective multifocal laser
over the exudative spotsguided by OCT and angiography
WHAT ABOUT DME? We choose a different way combined medical approachJosé Juan Escobar Barranco, Begoña Pina Marín, Manel Fernández Bonet
•Conclusions
•Methods
•Purpose
•Results
•Take Home
•The main cause of blindness in type II diabetic patients is
macular edema.•The diabetic macular edema (DME) has a complex
multifactorial pathogenesis involving the alteration of the
blood-retinal barrier, hipoxia which initiates the cascade of
angiogenesis (upregulation of vascular endothelial growth
factor-VEGF-) and inflamation (increase in the leukocytes
density and leukocytes adhered to endothelium)
•Why do we need a combination therapy?
•Only one pathway of the angiogenic cascade or
vasopermeability cascade is blocked by antiVEGF
treatment and other pathways need to be blocked.
• After antiVEGF appears a compensatory upregulation of
VEGF and other growth factors
•We suggest a combined medical approach from the very beginning, which yields a visual acuity (VA) gain
and a stabilization of the symptomatology with a good profile of safety.
•We show 31 eyes from 18 diabetic II patients with very poor metabolic control, all of them with the
diagnosis of diabetic macular edema.
• Therapeutic Guideline
•Follow-up•Monthly:VA (ETDRS),
OCT, biomicroscopy and
funduscopy
•Quarterly:angiography
Day 0
Pathogenesis of de DMEAdvanced glycation end products (AGE), Reactive oxygen species (ROS)
AGE
ROS
Hypoxia
Alteration Blood-retinal Barrier
Increase Vasopermeability
MACULAR EDEMA
Breakdown cell junction
Thickening of basement membrane
Pericytes loss
Upregulation VEGF
Inflamation(leukostasis)
DIABETES
After 1 month
•A total of 31 eyes from 18 diabetic with the diagnosis of DME have been follow-up.
•The mean follow-up period is 18.7 months.
•After the initial approach a cease of exudation at an agiographical level is found, as well as a
reestablishment of the foveal profile (mean diminishment of 280 microns) along with an improvement of
VA of 12/14 ETDRS letters (mean).
•After a mean of 5.5 months an increase of OCT thickness is found in 17/31 cases with a mild worsening
of VA. We reached stabilization and improvement of VA after a retreatment with ranibizumab and
triamcinolone intravitreously.
•The combined treatment from the beginning seems to improve the VA prognosis in multifocal DME.
0.5mg ranibizumab + 2mg triamcinolone
control the VEGF, responsible of
the breakdown in the blood retinal
barrier and neovascularization
to modify the misbalance of
inflammatory factors and
diminish macular thickness
644µmBaseline: 67years ♀. VA: 35 letters (20/200)
644 µm
Month 1 (before laser): VA: 74 letters (20/32)
240 µm
470µm
Month 5: VA: 61 letters (20/63)
•Combination therapy offer a sinergetic effect of multiple targets involved in the process of DME.
•Laser still remains to be the gold standard treatment in stabilization of DME.
•In cases with better initial VA our medical approach seems to improve the VA prognosis.
•Combination therapies offer a reduced risk associated with fewer injections.
283µm
Month 18 : VA: 70 letters (20/40)
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