Diabetic maculopathy is a form of damage to the eye causing by diabetic macular oedema where fluids build up on the macula. It can be cured by laser surgeries.
2. Pathogenesis of Diabetic Maculopathy
Anatomic Change Pathophysiology
Intraretinal
Macular edema Increased retinal vascular
permeability & retinal vascular
occlusion
Macular hard exudate
Macular ischemia
Preretinal and Vitreoretinal
Thickened posterior hyaloid Proliferation and shrinkage of
fibrous, glial, and fibrovascular
tissue
Thickened preretinal membrane
Macular traction
- Surface wrinkling retinopathy
- TRD of macula
- Macular ectopia
3. Incidence of DME
More common in NIDDM(3/4) than IDDM(1/4)
Occurs in 10% of all patients of DR
Can occur at any stage or DR
- 3% in Mild NPDR
- 38% in Moderate/Severe NPDR
- 71% in PDR
(OCNA 2002)
4. Risk factors for DME
Duration
- 3% in patients with DM<5 years
- 28% in >20 years (WESDR)
Level of Hyperglycemia
- 18.1% when HbA1C 6.8 - 9.7%
- 36.4% when HbA1C 13.2-19.2% - (WESDER)
Hypertension
Hyperlipidemia
Others
Pregnancy, renal disease, PRP & cataract extraction
6. CLINICAL
CSME is a clinical diagnosis
Best done with 78 or 90 D bio microscopy
Stereo fundus photography
Macular oedema-
thickening of the macula with
blurring of the underlying choroidal pattern,
loss of foveolar light reflex when fovea is involved
presence of cystoid spaces in severe cases
7. Clinically Significant Macular Edema
Thickening of the retina located
≤ 500 microns from the center
of the macula
Hard exudates ≤ 500 microns
from the center of the macula
with thickening of the adjacent
retina
A zone of retinal thickening, 1
disc area or larger in size, any
portion of which is ≤ 1 disc
diameter from the center of the
macula.
8. International Clinical Diabetic Macular edema
severity scale
1.Diabetic macular edema: absent
No retinal thickening or hard exudates in posterior pole.
2.Diabetic macular edema :mild
Some retinal thickening or hard exudates in posterior pole
but distant from the center of the macula
9. International Clinical Diabetic Macular edema
severity scale
Diabetic macular edema: moderate
Retinal thickening or hard exudates
approaching the center of the macula
but not involving the center.
Diabetic macular edema: Severe
Retinal thickening or hard exudates
involving the center of the macula.
11. Systemic control of DM
Metabolic control of diabetes( blood sugar and HbA1c)
Endocrinologist
for HbA1c <7%,
HT <130/80 mm Hg
Nephropathy
Fluid retention ,progression of maculopathy and DR
Hyperlipidemia
- Increased exudation
- LDL Lipoproteins are and < 100mg/dl
Anemia
Resolution of micro aneurysms with correction of anemia (BJO Feb 2005)
12. Systemic control
DCCT- To know the effect of intensive blood sugar
control in type 1 DM
Reduction of mean risk of DME by 29%,CSME by 23%
Complications secondary to hypoglycemia noted as well
UKPDS - To know the effect of intensive blood sugar
and HT control in type 2 DM
slowed progression of retinopathy
reduced risk of microvascular complications of DM.
13. Elevation of total and LDL cholesterol is associated with
greater severity of hard exudates in the macular area
(WESDER Report XIII & ETDRS Report 22)
Treatment of hyperlipidemia is associated with decreased
incidence of macular hard exudation
(Amod Gupta et al (AJO 2004)
16. SIGNIFICANCE OF FFA
Distinguishing the type of maculopathy
- Is there a discrete or deep diffuse leakage
- Not absolutely necessary in eyes with localized edema
(especially within discrete circinate rings – ETDRS Report 2)
- Essential to diagnose macular ischemia
Not needed for diagnosis of CSME, guide for treating
CSME
Recommended to identify treatable lesions
19. Often accompanied by diffuse macular oedema
as large amount of extracellular fluid
accumulates in OPL.
petalloid pattern on late phase
Cystoid macular oedema:
20. Ischemic maculopathy
Represents closure / nonperfusion of perifoveal capillaries
and often in type 1 DM
Positive correlation between FAZ size and advancing level
of retinopathy
Multiple dot-blot hemorrhages
Presence of multiple CWS
Visual acuity not corresponding to macular findings
21. Macular ischemia Angiographic
features
Irregularities of the avascular
zone margins
Abnormally tortuous capillaries
budding into the FAZ
Terminal arterioles/venules
directly abutting FAZ margins
Enlargement of intercapillary
spaces
Longest diameter of FAZ more
than 1000 µ
22.
23. ROLE OF OCT IN DME
Can detect subtle edema
Defining the disease pattern
Measure the retinal volume and central foveal thickness
in microns
Defining the treatment and indications for vitrectomy.
Longitudinal tracking of tissue alteration following an
intervention.
OCT categorizes DME - tractional vs. non-tractional
- Tractional macular edema always needs PPV.
- Non-tractional macular edema may require the presence of
cystic spaces, massive retinal thickening
25. Spongy Thickness
Diffuse homogenous intraretinal swelling with reduced
reflectivity.
fluid accumulation throughout the neurosensory retina.
Confined mainly to outer retinal layers
responds well to laser treatment (focal oedema on FA)
26.
27. Cystoid Macular Oedema
• Appear as optically clear cystic spaces with bridging
elements between them.(diffuse oedema on FA)
• Initially may be confined to outer retina mainly
• cysts may fuse to involve almost entire thickness of the
retina.
28. Cystoid Macular Oedema
• Visual loss in CME correlates more with degree of
macular thickening then with leakage seen on FA
• Responds poorly/ may worsen to laser
• Usually warrants periocular or intravitreal steroids
29.
30. Subfoveal serous retinal detachment
An area of hyporeflectivity in the subfoveal region
Usually not appreciated clinically or on FA
31. Tractional retinal detachment
An indication for pars plana vitrectomy to
release the traction.
Laser photocoagulation - may worsen the macular
oedema
32. Taut Posterior Hyaloid Membrane
• may result in recalcitrant macular oedema with foveal
detachment
• usually do not respond to laser treatment
33. Improvement in vision and
macular edema following PPV and
posterior hyaloid removal.
34. What are treatable lesions ?
Focal leaks greater than 500um from
the centre of macula causing retinal
thickening/hard exudates.
Focal leaks within 300um-500um
from the centre of macula thought to
be causing retinal thickening/hard
exudates
Areas of diffuse leakage from
microaneurysms and capillary leak
Avascular zones, other than FAZ, not
previously treated.
35. Laser treatment
works best in eyes with-
Discrete areas of leakage on FA
Mild to moderate thickening on OCT
No vitreo-macular interface abnormalities on OCT
Visual acuity good or with only a mild to moderate
decrease
Ischemic maculopathy does not respond to laser
36. Pharmacotherapy
(Steroids, anti-VEGFs)
Eyes with diffuse leakage on FA with moderate to
severe thickening,
cystoid macular oedema (CME) or
serous macular detachment on OCT,
Moderate to severe decrease in visual acuity
Alternative - laser in combination with these agents
37. Laser treatment consideratons
• Informed Consent
• Goal of treatment is to stabilize the VA
• Risk of moderate vision loss is reduced by > 50%
• Need for periodic follow up, repeated FA/OCT and the
possibility of further t/t
• Eyes with CSME with severe NPDR/PDR
-Treatment for the macular edema first followed by PRP
after 4-6 weeks
38. Direct Focal Laser
Directly over all focal FA leaks
MA, IRMAs, capillary segments
Goal:
Obliteration of leak
Endpoint: Whitening/blanching of MA
Protocol:
Spot size: 50-200micron
Area: 500-3000micron from centre of
macula
Duration: 0.1sec or less
39. Mechanism of Action of Laser
Changes in the metabolic activity of the RPE
Release of signals that reduce vascular leakage
Facilitate fluid absorption
on follow up - If macular edema persists
- focal leaks within 300-500µ treated provided there
is a good perifoveal network
40. Grid treatment
Thickened retina with diffuse leak or capillary drop-out
100-200 microns spot size
0.1 seconds duration
Power adequate to produce faint white burn
1 burn width apart in the areas of thickening
Grid
Not placed within 500µ of the foveal center and margins of the
optic disc
Papillomacular bundle is usually avoided
Could extend upto 2 DD from the center of the macula
41. MODIFIED GRID
• Grid + focal
• Given only to areas of non-
perfusion / thickening
• 100 micron burns near the FAZ
• 200 microns outside these
• Papillomacular bundle spared- C
shape
42. Ischemic maculopathy
Laser - not indicated for eyes with visual loss solely
due to ischemic maculopathy.
If oedema and ischemia co-exist - the oedema may
be treated after explaining the guarded prognosis.
No more than 6 clock hours of juxtafoveal capillary
nonperfusion on FFA
Laser’s in ophthalmic surgery: David b karlin : blackwell 1995 P. 105
43. Re-Treatment
• Re-evaluation at 3 months
• Focal/grid treatment supplemented, if CSME persists
• Temporary increase in the HE following treatment can occur
• Oedema & exudates subside in 4-6 mths, if persist do FFA
• Most patients require more than one treatment session
• Recalcitrant CSME - more than 3 treatment sittings
- requires alternative pharmacological agents
44. Clinical Guidelines
Clinically Significant Macular Edema Treatment
First-line therapy
• Focal or modified ETDRS grid photocoagulation for focal or diffuse CSME
• Intravitreal pharmacotherapies ± photocoagulation for more advanced,
diffuse CSME
For persistent or recurrent CSME (visual acuity <20/40)
• Repeat photocoagulation
• IVTA or IV anti VEGF agent
45. Micropulse Diode Laser
Iris Oculight Micropulse 810 nm diode laser
Spot size : 200 - 500
Micropulse :
On time - 100 - 300 microsec
Off time - 1900-1700microsec
Power initially adjusted till a barely visible burn
is seen
Power then set at half that value and treatment
started
Conventional grid pattern done in areas of
retinal thickening
• Subthreshold micropulse diode laser and conventionalargon laser
treatment showed an equally good effect on visualacuity
• Stabilisingor even improving effect on macular oedema
• combinationof primary diode laser and supplementary argon laser
might beparticularly favourable in reducing diabetic macular oedema
British Journal of Ophthalmology 2004;88:1173-1179
46. PPV
Intravitreal triamcinolone
OCT can help in decision making
Recalcitrant CSME:
• Despite focal laser photocoagulation,
• Diffuse Retinal thickening
• Macular ischemia +
• Taut, Opaque Persistent hyaloid
• CME
Limited treatment options :
48. Triamcinalone
Indications
- Diffuse/ cystoid diabetic macular edema
- Refractory diabetic macular edema
Dose – 4mg / 0.1 ml
Longer retention time
41 days in a non-vitrectomised eye
17 days in vitrectomised eye
49. Mechanism of action
ability to inhibit arachidonic acid pathway
Stabilize retinal vascular endothelial tight junctions,
which decreases permeability
Inhibits inflammatory mediators and VEGF
Transient increase in IOP may favourably alter the
haemodynamics within the eye
Induction of PVD
• Contraindications
- Local infections
- Glaucoma patients
- Steroid responders
- Systemically uncontrolled diabetes
50. Post operative monitoring
Head-end elevation/sitting for 1 day
IOP monitoring
Check for inflammation
Antibiotic eye drops qid x 5 days
• Increase in IOP – 19 to 50%
• Dispersal leading to visual axis blockage
• Endophthalmitis
• RD
• Vitreous haemorrhage
• Cataract
Complications
51. Symptoms & signs of inflammation are
masked
Pseudohypopyon after 2days
White, crystalline corneal endothelial
precipitates after 1day
53. STUDIES
Intravitreal triamcinolone (4 mg in 0.1ml) in refractory
diabetic macular edema.
- Improvement in visual acuity with decrease in central macular thickness
as measured by OCT
- Re-injection was performed after 6 months in 37% because of recurrence
of DME
Martidis et. al -
54. Combined IVTA and PRP for diabetic macular edema and
proliferative diabetic retinopathy.
Provide benefit in patients with diffuse diabetic macular edema who
require urgent PRP for proliferative diabetic retinopathy by preventing
exacerbation of macular edema
Retina. 2005 Feb-Mar;25(2):135-40
Posterior subtenon triamcinolone acetonide for refractory
DME
VA remained stable or improved over a 12-month period There was a
statistically significant improvement in visual acuity at 1 month.
Am J Ophthalmol. 2005 Feb;139(2):290-4
STUDIES
55. FLUCINOLONE ACETONIDE IMPLANT
drug pellet
- (2 x 2 x 6 mm) surgically placed inside the eye
- releases flucinolone at a constant rate over a 3 yr period.
A multi centric, masked randomized controlled trial –
80 patients of DME (BCVA of >20/400 and less than 20/50), with a history of
one episode of laser treatment 3 months back
RESULTS –
- complete resolution of macular edema in 54% of eyes with
implant compared to control group at 24 months
- decrease in retinal thickness in 46% of treatment groups
compared to 15% in control group.
SIDE EFFECTS - increased IOP in 32%
increased incidence of cataract
56. Ozurdex
Dexamethasone biodegradable posterior
seg. Drug delivery system.
It’s use is FDA approved in macular
edema of retinal vein occlusions and post.
Noninfectious uveitis
But ongoing research for use in DME .
0.7mg dexamthasone implant had
significant improvement in v/a and
retinal thickness compared to control
group
phase 2 trial kupperman et
al AAO2003
57. Role of VEGF
Produced by glial cells, RPE.
Is normally present in retina and vitreous in low
levels
Upregulation of VEGF ⇒ by hypoxia
Pro inflammatory effect
Breakdown of blood retinal barrier ⇒
-Increased vascular permeability - edema
Endothelial cell growth & Neovascularisation
58. Angiogenesis Inhibitors
Matrix Metalloproteinase
Inhibitors
a. Marimastat (BB2516)
b. Prinomastat (AG3340)
c. BMS 275291
d. BAY 12-9566
e. Neovastat (AE-941)
Novel Agents Inhibiting
Endothelial Cells
a. Thalidomide
b. Squalamine
c. Celecoxib
d. 2D6126
e. Integrin antagonists
Drugs Blocking
Endothelial Cell Signaling
a. RhuMAb VEGF
b. VEGF receptors Inhibitors
c. SU5416
d. SU6668
e. ZD6474
f. CP-547,632
g. Tyrosine kinase inhibitors
Endogenous inhibitors of
angiogenesis
a. Endostatin
b. Interferons
59. Role in DME
PDR with diabetic macular edema
Persistent NV despite extensive PRP
Used 2-5 days prior to vitrectomy - preparatory
Rubeosis
Action lasts for 2-4 weeks
Retinopathy recurs & at times with a vengeance
Grid laser may be done once edema decreases postGrid laser may be done once edema decreases post
intravitreal injectionintravitreal injection
60. Role in DR
PRP removes the incentive for VEGF formation thus suppressing their
release
Complimentary to each other
IVTA has risk of cataract & secondary glaucoma
Trials have shown good efficacy:
Pegaptanib sodium: Macugen Diabetic Retinopathy Group
Ranibizumab: READ Study by Nguyen et al
63. 55 years male
DM and HTN since 17 years
S/P BEs CE + IOL x 3 years
PRP in 2001
IOP: OS-18
20 OCT 07 OS: AGS at Aravind
Last seen on
22 APR 2008
IOP: OD-20 OS-25
BCVA : OD: 6/36 OS: CF 3 MTR
Case 2(LE)
10 nov 2006
1 mar 2007
23 Apr 2007
30 May 2007
333 microns
326 MICRONS
871 MICRONS
525 MICRONS
CF 3 Meter
6/60
6/24
6/60
6/36
214 MICRONS
4 July 2007
15/12/2006 LE-PRP Aug WITH IVTA
15 mar 2007 LE- IV macugen given(1 st injection)
27/08/07
OS: PRP aug + IV Macugen (2nd injection) + s/t Kenacort given
64. PROTEIN KINASE C-beta Inhibitors
Ruboxistaurin Mesylate (oral selective PKC beta
inhibitor) - delay the progression of diabetic
retinopathy.
PKC-DMES
686 patients with diabetic macular edema,
BCVA 20/25 or better and no prior laser treatment.
At 36 months - excluding the patients with poor glycemic
control showed a reduction in progression of DME
Aiello RC et al, initial results of PKC beta inhibitor diabetic macular edema
study. D iabetologica 2003;46:A42
67. Cataract and DR
DM ↑ incidence of Cataract
C/E cause progression of maculopathy and to some extent
retinopathy
Good peri-operative DM control
Prior laser PC if possible
Intravitreal anti VEGF can be given in suspicious cases
If not ⇒ early post-operative laser
Phacoemulsification
Lesser inflammation
Larger CCC (anterior capsular contraction)
Large diameter non-silicone IOL
Combined with vitrectomy and endolaser
remains a significant cause of central visual loss in patients with dm,
Dme is defined as retinal thickening involving the macular area. Caused primarily by breakdown of the inner brb resulting in leakage of fluid, Plasma contituents from abnormally permeable MA ,irma, and dilated retinal capillaries. The visual loss may also be worsened by capillary closure involving the foveal capillary arcade– ischemic maculopathy
CSME is a clinical diagnosis made with slit-lamp biomicroscopy.
Macular edema is best evaluated by dilated eye examination using slit-lamp biomicroscopy with a 78 or 90 D lens and/or stereo fundus photography
It is convenient to subdivide CSME according to involvement at the center of the macula, because the risk of visual loss and the need for photocoagulation is greater when the center is involved.
Whats common to all treatments is systemic control not only of dm but also associated HT nephropathy, lipid derangements, anaemia
Vn 20/80 28/11/02…..20/40 macch 03.. No laser
Ozurdex With newer options like intravitreal / subtenons steroids and intravitreal anti VEGF agents (Bevacizumab, ranibizumab,
Pegaptanib sodium) now available to us for the treatment of DME,it sometimes becomes difficult to decide between laser and pharmacotherapy. A logical manner in which to tailor a treatment plan takes into account the FA and OCT picture as well as the visual acuity of the patient.
Fluorescein angiography (FA) prior to laser for CSME is helpful for identifying areas of focal and diffuse leakage and for identifying pathologic enlargement of the foveal avascular zone (ischemic maculopathy), which may be useful in planning treatment. It is helpful to have the angiogram printout or digital display in the laser room to better direct therapy.
Pale retinal edema
Presence of white vessels
Provides information about vitreoretinal interface relationships that can help define the treatment
SPONGE LIKE THICKENING
CYSTOID MACULAR EDEMA
SUBFOVEAL SEROUS DETACHMENT
FOVEAL TRD
TAUT POST HYALOID
In the long term
This improvement may be due to reattachment of the macula, as opposed to a decrease in macular edema.
PC
first give an injection to bring down the oedema and then do grid laser
Patients with very good vision - treated if they have CSME
Informed Consent , stressing that the treatment is designed to stabilize or slow the rate of vision loss rather than to improve vision. The risk of moderate visual loss is reduced by more than 50% for patients who undergo
appropriate laser photocoagulation, compared with those who are not treated. Vision improves for a lucky few; for the majority of cases, the goal of treatment is to stabilize the visual acuity. Patients with very good vision (i.e. 6/6 visual acuity) should also be treated if they have CSME. Treatment is unlikely to restore the visual acuity once it goes down, so treatment prior to visual loss is sometimes appropriate.
GOAL OF MACULAR LASER PC is to limit vascular leakage thr focal laser burns of leaking MA or grid laser burns in areas of diffuse breakdown of brb
Laser may induce changes in the metabolic activity of the retinal pigment epithelium and cause the release of signals that reduce vascular leakage and facilitate fluid absorption.
Although spot sizes as small as 50 μm were used in the ETDRS 5, a 50-μm spot increases the power density and may increase the risk of breaks in Bruch’s membrane and secondary choroidal neovascularization.
Objective : Tickle RPE cells & cause rapid absorption All areas of thickened retina within the arcades that show diffuse fluorescein leak or capillary dropout
Any focal leaks within the zone of grid treatment are treated focally.
In cases where the oedema is limited to certain sectors of the macula, it is important that the laser is not done all over the macula but only in the thickened areas showing dye leak Modified grid
fluid is reabsorbed and precipitation of lipid occurs.
Exudates can also persist for many months after absorption of fluid; therefore associated thickening must be present if re-treatment is considered.
(dacryocystitis, blephritis)
Persistent CME despite heavy laser. IVTA cased resolution of cme but progression of laser scarring subfoveally.
IVTA (25 mg in 0.2 ml) - similar results
- Positive effect of triamcinolone reaches its maximum at 1-3 months.
- Repeated IVTA treatment is generally required
Jonas et. Al -
There are various ways to stop VEGF formation, Various case control studies are going on
4- cases of pdr/ refectory dme needing vitrectomy
Reduces intra-op bleeding & allows better dissection & peeling of membranes Reduces rebleed Temporary measures, short term
Pegylated aptamer- a modified oligonucleotide
Selective for VEGF 165 isoforms
Selectively binds to vegf 165 therby inhibiting vegf 165 to its receptors
Nandkishore Soni ,68 Years male, DOV for 6 Months(Bes)
25 sept 2007 Baseline CF and OCT done LE 521 MICRONS (510+/-45), 16 Nov 2007 OS IV macugen Given
MUKESH PATE, L48 YEARS MALE, DOV LE SINCE 1 YEAR, SEEN ON: 17 JAN 2008
S/P LASER 8 MONTHS BACK, DM SINCE 6 YEARS
BCVA: OD-6/12 OS- CF3 METER, DIAGNOSIS: PDR WITH DME, 19 JAN 2008 OS: IVTA GIVEN
25 JAN 2008 BCVA: OD-6/12 OS-6/60 PRP DONE IN JUNE 2008 AT LONDON, 31 JUL 2008 BCVA: OD-6/18 OS-CF 3METER
1 AUG 2008
OD: PRP AUG + IV MACUGEN GIVEN
7 AUG 2008
OCT: Pre injection-261 microns , Post injection- (1 week)312 microns.
14 AUG 2008
BCVA: OD-6/12 OS CF 41/2 METER
IOP: RE-10 LE:11
Name: Dahyabhai T Patel
55 years male
Reg No: 2006/11/4791 First seen On: 10/11/2006
Dov BEs since 2 months
S/P BEs CE + IOL x 3 years
Laser Tt in 2001
DM and HTN since 17 years
BCVA: OD:CF 6 MTR OS:CF 3 MTR
IOP= OU= 14
Diagnosis: OD-NPDR with CSME OS-PDR with CSME
11/11/2006 RE-PRP Aug WITH IVTA
15/12/2006 LE-PRP Aug WITH IVTA
22 JAN 2007 BCVA: OD-6/36 0S-6/60
1 MAR 2007
OCT: PRE IVTA- RE- 679 MICRONS LE- 871 microns
POST IVTA- RE- 501 MICRONS LE- 525 microns
15 mar 2007 LE- IV macugen given(1 st injection)
22 mar 2006 BCVA: OU- 6/36
OCT: Pre Macugen: 541 microns
Post macugen:138 mocrons
4 Apr 2007 RE- IV macugen given(1 st injection)
23 Apr 2007
OCT: RE - 349 microns, CRT-409 microns
LE - 214 microns
30 may 2007
BCVA: OU-6/24
OCT: RE-541 micron
LE-326 micron
16 jun 2007 RE- IV macugen given(2nd injection)
4 JUL 2007
IOP OD= 14 OS= 46
BCVA: OD- 6/24 OS- 6/60
0CT: OD- 533 microns
OS- 154 microns
19 jul 2007 IOP= OD-11 OS-19
27/08/07
OS: PRP aug + IV Macugen (2nd injection) + s/t Kenacort given
17 sep 2007 IOP: OD-16 OS-35
20 OCT 2007 OS: AGS at Aravind
20 NOV 2007: IOP=OD: 21 OS: 38
22 APR 2008
IOP: OD-20 OS-25 BCVA : OD: 6/36 OS: CF 3 MTR
Name: Dahyabhai T Patel
55 years male
Reg No: 2006/11/4791 First seen On: 10/11/2006
Dov BEs since 2 months
S/P BEs CE + IOL x 3 years
Laser Tt in 2001
DM and HTN since 17 years
BCVA: OD:CF 6 MTR OS:CF 3 MTR
IOP= OU= 14
Diagnosis: OD-NPDR with CSME OS-PDR with CSME
11/11/2006 RE-PRP Aug WITH IVTA
15/12/2006 LE-PRP Aug WITH IVTA
22 JAN 2007 BCVA: OD-6/36 0S-6/60
1 MAR 2007
OCT: PRE IVTA- RE- 679 MICRONS LE- 871 microns
POST IVTA- RE- 501 MICRONS LE- 525 microns
15 mar 2007 LE- IV macugen given(1 st injection)
22 mar 2006 BCVA: OU- 6/36
OCT: Pre Macugen: 541 microns
Post macugen:180 mocrons
4 Apr 2007 RE- IV macugen given(1 st injection)
23 Apr 2007
OCT: RE - 349 microns, CRT-409 microns
LE - 214 microns
30 may 2007
BCVA: OU-6/24
OCT: RE-541 micron
LE-326 micron
16 jun 2007 RE- IV macugen given(2nd injection)
4 JUL 2007
IOP OD= 14 OS= 46
BCVA: OD- 6/24 OS- 6/60
0CT: OD- 533 microns
OS- 154 microns
19 jul 2007 IOP= OD-11 OS-19
27/08/07
OS: PRP aug + IV Macugen (2nd injection) + s/t Kenacort given
17 sep 2007 IOP: OD-16 OS-35
20 OCT 2007 OS: AGS at Aravind
20 NOV 2007: IOP=OD: 21 OS: 38
22 APR 2008
IOP: OD-20 OS-25 BCVA : OD: 6/36 OS: CF 3 MTR