8. Morinelli EN, Najac RD, Speaker MG, Tello C, Liebermann JM, Ritch 12. Lee DA, Wilson MR, Yoshizumi MO, Hall M. The ocular effects of
R. Repair of Descemet's membrane detachment with the assistance gases when injected into the anterior chamber of rabbit eyes. Arch
of intraoperative ultrasound biomicroscopy. Am J Ophthalmol. Ophthalmol 1991; 109: 571-575.
1996;121(6):718-720
13. Shah M, Bathia J, Kothari K. Repair of late Descemet's membrane
9. Radhakrishnan S, Goldsmith J, Huang D; et al. Comparison of detachment with perfluoropropane gas. J Cataract Refract
optical coherence tomography and ultrasound biomicroscopy for Surg.2003;29(6):1242-1244.
detection of narrow anterior chamber angles. Arch Ophthalmol.
2005;123(8):1053-1059. 14. Jeng BH, Meisler DM. A combined technique for surgicalrepair
of Descemet´s membrane detachments. Ophthalmic surge Lasers
10. V Menezo, Y F Choong , N R Hawksworth.Reattachment of extensive Imaging2006;37: 291-297.
Descemet’s membrane detachment following uneventful phaco-
emulsification surgeryEye (2002) 16, 786–788.
11. Sevillano C, Viso E, Millán-Rodríguez AC.Descemet's membrane
detachment as a complication of cataract surgery]. Arch Soc Esp
Oftalmol. 2008 Sep;83(9):549-51
First Author
Manisha Acharya MS, DNB
www.dosonline.org 63
Macular Hole Retina
2Priyank Garg MS, FNB, 1Arindam Chakravarti, 1,3Sundaram Natarajan
The term Macular Hole implies that a part of macula is missing. • It represents an excavation of the inner layers of retina
These are an important cause of vision loss in elderly. characterized by recognizable retinal tissue at its base.
These can be: -
• Partial-Thickness. Causes: -
• Full-Thickness. • Chronic CME.
Partial-Thickness Macular Hole • Radiation retinopathy.
• Idiopathic perifoveal telangiectasia.
Two types of partial-thickness holes occur: - Clinical Features: -
• Outer lamellar hole (OLH). • Visual acuity ranges from 20/20 (6/6) to 20/80 (6/24).
• Inner lamellar hole (ILH). • Distortion may be noted without scotoma on Amsler grid
Outer Lamellar Hole(OLH): - testing.
• Borders may not appear as sharp as in FTMHs because of
Causes: -
• Collapse of outer wall of large cyst. sloping margins & thin, irregular edges.
• Trauma- there is a breakdown outer blood-retinal barrier at • There is usually no cuff of surrounding subretinal fluid & no
the RPE. RPE alteration.
• Optic pits associated with macular schisis. • Can be differentiated from FTMH by “slit-beam test”.
• Solar retinopathy. • F/A – Either no transmitted fluorescence or minimal window
Clinical Features: - defect if the ILH is nearly a FTMH.
• Vision varies from 20/20 (6/6) to 20/400 (3/60), depending • Progression to a FTMH with subsequent fall in vision is
on the size & degree of photoreceptor destruction of the & possible, but rare, if the ILH has been present for many
on the cause (e.g., traumatic, solar). months.
• On biomicroscopic examination, a slightly irregular deep, • There is no known treatment.
round, or oval excavation is seen with intact inner retinal Full-Thickness Macular Hole
tissue. An FTMH is a round break that involves all the layers of the retina,
• F/A- demonstrates a variable degree of “window defect” from the internal limiting membrane through the outer segments
resulting from the RPE atrophy & may fortuitously show dye of photoreceptor layer.
in a retinal capillary direct overlying part of OLH. Etiology
• OLHs may increase in size over time, with subsequent • Most Macular Holes occur in the absence of antecedent injury
decrease in vision. & are referred to as idiopathic.
• They may also transform into FTMH if the intact inner retina • Trauma (4-5%).
atrophies or is avulsed by vitreal traction. • Pathological Myopia.
• There is no known treatment. • Laser.
• Electric Current.
Inner Lamellar Hole(ILH): - • Misc. causes
• An ILH is much more common than an OLH & may be an Idiopathic Macular Hole
intermediate stage in the development of some FTMHs.
1.Aditya Jyot Eye Hospital Pvt. Ltd., Introduction: (ICD-9 #362.54)
Mumbai, Maharashtra, India. • The term Macular Hole implies that a part of macula is
2. Dept. of Ophthalmology, missing.
LLRM Medical College, Meerut, UP.
3. TNMGR University,
Chennai,Tamilnadu, India.
www.dosonline.org 65
• This is an important cause of vision loss in elderly. • Hypertension.
Epidemiology • Diabetes mellitus.
• Prevalence rate of macular hole in India is a reported 0.17%, • Coronary artery disease.
• Previous cerebrovascular accident.
with a mean age of 67 years.1 • Elevated plasma fibrinogen levels.
• Idiopathic macular holes develop predominantly in older Pathogenesis
Vitreous traction, anteroposterior as well as tangential, plays an
patients at an incidence ranging from 0.03% to 0.05%.2 important role in the pathogenesis of macular holes. Posterior
• The prevalence is three times greater among women than vitreous detachment decreases the risk for future macular hole
formation. Fellow eyes with vitreomacular separation have less
men.2 than a 5% risk for macular hole18,19,20 versus as high as a 29% risk
• Macular Holes are bilateral in upto 29% of patients.3 for macular hole in eyes with no posterior vitreous detachment20.
• Peak incidence is seen in seventh decade of life. As described above, tangential traction caused by the condensed
• In a case-control study, 72% of the idiopathic macular holes perifoveal cortical vitreous was supposed to be the main factor
in the initiation and progression of macular hole formation17.
occurred in women and more than 50% of the macular holes Evaluation of the early stages of hole formation with OCT by
occurred in patients 65 to 74 years old. Only 3% were found Gaudric et al21 led to the postulation of a new mechanism for
to occur in patients under age 55 years.4 macular hole formation, which is based on anterior-posterior
Risk Factors tractional forces. These investigators have documented that
• Largely unknown. posterior hyaloid detachment begins in the posterior pole around
• A few epidemiologic risk factors of uncertain importance the macula and gradually spreads with focal attachment to the
have been reported:
Historical Timeline of Macular Hole Theories
Year Author Description
1869 Knapp First case description of macular hole (traumatic)5
1871 Noyes First detailed clinical description of macular hole (traumatic)6
1900 Ogilvie Published case series & proposed terminology including macular hole7
1900 Kuhnt Atraumatic theories of cystic retinal degeneration leading to macular hole8
1901 Fuchs Early histopathologic descriptions of macular hole including cystic retinal
changes9,10
1907 Coats
1912 Zeeman Histopathologic recognition of premacular vitreous condensation219
1924 Lister Vitreous forces and “vitreous traction bands” (anteroposterior) may cause
macular holes11
1967 Reese et al Vitreous separation critical to macular hole formation12
1982 McDonnell et al Possible female hormonal influence on vitreous separation and macular hole
formation2
1983 Avila et al Vitreous separation not necessary in formation of a macular hole13
1986 Morgan & Schatz Involutional macular thinning is a premacular hole condition14
1988 Gass & Johnson Tangential vitreous traction and Gass biomicroscopic classification of Johnson
premacular hole and macular hole lesions15,16
1995 Gass Centrifugal displacement of retinal receptors with umbo dehiscence
Reappraisal of biomicroscopic classification of premacular hole and macular
hole lesions17
66 DOS Times - Vol. 16, No. 10,April, 2011
foveal center. This focal attachment creates retinal convexity • May be associated with recent mild decrease in visual
consistent with anterior-posterior vitreoretinal traction. acuity or metamorphosia.
More recently, Gass has emphasised the importance of the foveal
Muller cell “cone”,22 originally described by Yamada23 and Hogan • F/A: -Faint hyperfluorescence or no abnormalities.
et al24 in histological studies of the normal human foveola. These • Visual acuity may be only mildly reduced & Amsler grid
studies showed the foveola to be composed of an inverted cone
of Muller glia with a truncated apex up to the external limiting abnormalities are detected only 50% or more of the time.
membrane (ELM). Between the apex and the ELM were radially • About 50% of holes resolve following spontaneous vitero-
oriented inner cone segments radiating towards the beginning
of the outer nuclear layer of cone nuclei. The base of the cone foveolar separation.
formed the umbo and extended into the clivus in the perifoveolar
region. The internal limiting membrane (ILM) lining the base Stage 2 (Early FTMH): -
of the cone was extremely thin (10–20 nm) compared with the • Small full thickness (less than 300 microns in diameter) retinal
peripheral fovea. The sides of the cone were apposed to radiating
inner segments centrally and cone nuclei in the outer nuclear layer defect in an eye with a stage 1 macular hole
more peripherally towards the perifoveolar region. • Epiretinal membranes are uncommon
Staging & Clinical features: - • Visual symptoms include metamorphopsia and decreased
Based on clinical observations, Gass in 1988 proposed a four-stage
classification for macular holes15,16 & modified it in 199517. vision
• Visual acuity 20/25 to 20/80
Stage 1: • At this stage, the posterior cortical vitreous is still attached at
Further sub-divided into 2 stages: - the fovea and, in many cases, radial tractional striae may be
• Stage 1a (Impending Macular Hole): visible around the edges of the hole at the level of the inner
• Rarely seen clinically. retina and internal limiting membrane.
• Usually detected in a patient with a full thickness macular • In addition, intraretinal cystoid spaces appear around the
edges of the hole.
hole in other eye. • Two configurations may occur at stage 2:
• Loss of the foveal depression and a yellowish foveal spot • Centric: The full thickness tear begins at the centre of the
(100 to 200 microns in diameter) fovea (umbo dehiscence) and expands in a symmetric
• Localized shallow detachment of the perifoveal vitreous fashion.
• Pericentric: A full thickness tear arises at an eccentric
cortex with persistent adherence to the foveola initially position in the fovea and extends in a “can opener”
• Vitreofoveolar traction may cause a split of the retina at fashion to form a crescentic hole progressing to a
“horseshoe” shaped hole and eventually, when the can
the fovea (“pseudocyst”) that corresponds to the yellow opener is complete, to a round hole with a fully detached
spot operculum of tissue suspended on the posterior vitreous
• Epiretinal membranes are uncommon cortex in the prefoveal plane. This configuration is typical
• Visual acuity 20/25 to 20/80 in the majority of stage 2 FTMH (80–90%).
• Stage 1b (Occult Macular Hole):
• Yellow ring 200 to 350 microns in diameter Stage 3 (Established FTMH): -
• Posterior extension of the “pseudocyst” with disruption • Full thickness hole 300 to 400 microns in diameter
of the outer retinal layer • Posterior hyaloid is completely separated over the macula but
• Roof remains intact with persistent adherence of the
posterior hyaloid to the retina may be attached to the optic disc and more peripherally
• Epiretinal membranes are uncommon • Operculum or a flap on the posterior hyaloid over the hole
• Visual acuity 20/25 to 20/80
• Results from centrifugal displacement of the foveolar usually evident on optical coherence tomography (Figure 4)
retina & xanthophyll. and may be apparent clinically
• Characterized by a yellow ring with bridging interface • Cuff of subretinal fluid, intraretinal edema, and cysts
of vitreous cortex. • Drusen-like deposits (may represent macrophages at the level
of the retinal pigment epithelium and may indicate chronicity
of disease) often in the base of the hole.
• Rim of retinal pigment epithelium hyper/hypopigmentation
often present at the junction between edematous or detached
retina and normal-appearing, attached retina in long-
standing cases.
www.dosonline.org 67
Figure 1: Colour Photo of Full Thickness Figure 2: Red Free Photo of Full Thickness
Macular Hole Macular Hole
Figure 3: SD-OCT of Full Thickness Figure 4: SD-OCT of Full Thickness Macular
Macular Hole Hole with operculum
• Epiretinal membranes may be present • Some patients achieve better visual acuity by employing
• Visual acuity 20/100 to 20/400. eccentric fixation.
• Characterized by a round retinal defect greater than 400 µ
Diagnostic Tests
with an attached posterior vitreous face with or without an
overlying pseudo-operculum. Watzke-Allen Test: -
• No Weiss’ ring present. • Performed by projecting a narrow slit beam over the centre
• Rim of elevated retina with or without prefoveolar opacity.
of the hole both vertically & horizontally with a 90D or 78D
Stage 4: - lens.
• Characterized by enlargement of the round defect which is • Pt. With macular hole will report that the beam is broken or
thinned.
now surrounded by cuff of sub-retinal fluid & exhibits tiny
yellowish deposits at the base of the crater (Figure 1,2 & 3). Laser aiming beam test: -
• The posterior vitreous is completely detached, as evidenced • Performed by projecting a 50 µ spot of a laser aiming beam
by a Weiss ring.
• Visual acuity tends to deteriorate progressively, stabilizing at (e.g. He-Ne) at the centre of the hole.
6/60 or worse as the hole reaches its maximum diameter. • A patient with macular hole will report that the spot has
disappeared.
68 DOS Times - Vol. 16, No. 10,April, 2011
Figure 6: SD-OCT of Full Thickness Macular
Hole with Retinal Detachment
Figure 5: Full Thickness Macular Hole
with Retinal Detachment
Fluorescein Angiography:-
• Shows a corresponding area of hyperfluorescence.
• This result from unmasking of background choroidal
fluorescence caused by a window defect in xanthophyll d/t
centrifugal displacement.
Optical coherence tomography:- Figure 7: SD-OCT showing Type 1 closure of
• Provides high resolution optical sections of the retina & Macular Hole
affords measurement of retinal thickness.
• It’s useful in diagnosis & staging of macular holes.
• It also measures the volume of full-thickness macular hole.
Scanning Laser ophthalmoscopy:-
• It is used to evaluate the characteristics of macular holes &
outcomes of surgery.
Retinal Thickness Analyzer: -
• This has shown promise in detecting & accurately measuring
macular holes.
Fundus Autofluorescence:-
• Has been used as indication of the level of lipofuscin in the Figure 8: SD-OCT showing Type 2 Closure
retinal pigment epithelium. of Macular Hole
• Normally, autofluorescence of the retinal pigment epithelium
underlying the fovea is decreased because the overlying
macular yellow pigments absorb the exciting light.
• Stage 1 macular holes without a PVD were found to progress
to an FTMH in 33% of patients but no stage 1 lesions with a
• Without the overlying absorptive pigments, a macular hole PVD progressed to an FTMH.
creates a window defect so that autofluorescence is increased.
• Thus, this change in visible autofluorescence can be used as • Most stage 2 FTMHs progress to stage 3 or 4 (especially
an indication of a full-thickness macular hole or of failure of centric stage 2 holes with “pericentral hyperfluorescence” &
surgical repair. eccentric stage 2 holes).
Natural History: - • Stage 2 FTMHs that are 400 microns or smaller without a
PVD may have a greater risk of enlarging with a larger rim
• The natural outcomes of stages 1, 2, 3 & 4 FTMHs is different. of sub-retinal fluid & decreased visual acuity.
www.dosonline.org 69
Stage Management Follow up
1A Observation • Prompt return if new symptoms.
1B • Every 4 to 6 months in the absence of
2 PPV + BBG assisted ILM peeling + C3F8 + symptoms.
Prone position for 2 weeks • 1 to 2 days postop, then 1 to 2 weeks
3 • If no surgery, every 4 to 8 months
4 • 1 to 2 days postop, then 1 to 2 weeks
Hole form factor (HFF) = c + d/a • Stage 2 holes progressed 84% of the time, stage 3 holes
a = base diameter progressed 55% of the time & stage 4 holes enlarged 16%.
b = minimum diameter • Visual acuity decreased two or more lines in the majority
c = left arm length of stage 2 holes (68%) & less significantly for the other
d = right arm length stages (stage 1 - 30%; stage 3 - 29%; stage 4 – 13%).
• In another study –
• 96% of stage 2 holes progressed to stage 3 or 4, with 71%
having a two or more line reduction in visual acuity.
• The authors concluded that even though vitreomacular
separation may improve the prognosis of a macular hole,
stage 2 lesions usually will develop an enlarged hole and
decreased visual acuity.
• The incidence of disappearance of idiopathic FTMHs is low.
Differential Diagnosis: -
Macular Hole Index (MHI) = b/a Pseudoholes: -
• Most pseudoholes are often undiagnosed & are the result
of a dehiscence of a portion of gliotic preretinal membrane
overlying the macula, producing a lesion with surprisingly
sharp but often irregular borders.
• Seen most often in association with: -
• Idiopathic epiretinal membrane formation
• Vitreomacular traction syndromes
• Proliferative diabetic retinopathy
• Rhegmatogenous retinal detachment
• Intraocular inflammation
• Venous occlusive disease
• Trauma.
• White dot fovea
• The vitrectomy for Prevention of Macular Hole Study Group Visual acuity: -
found that:-
• May be normal or slightly reduced.
• the risk of progression to an FTMH was much higher in • Contraction of associated fibrous proliferation may produce
eyes with stage 1 macular hole who had best-corrected macular pucker, which may effect vision by virtue of distortion
visual acuity 20/50 or worse. more than acuity decline, since the retina underneath is intact.
70 DOS Times - Vol. 16, No. 10,April, 2011
• A circular dehiscence in a prefoveal membrane may allow for • Retinal vascular occlusive disease.
surprisingly good visual acuity. • Trauma.
• Ocular inflammation.
• Extensive preretinal membranes may be associated with • Exudative macular degeneration.
perifoveal axoplasmic debris accumulation, which may • Diabetes mellitus.
influence the visual status. • Macular pucker.
• Retinitis pigmentosa.
Fluorescein angiography: - • Macular telangiectasias.
• No abnormal fluorescence except for traction-induced retinal
Visual acuity : -
vascular leakage. • Usually ranges from 20/20 to 20/100.
• However, faint central fluorescence coincident with choroidal
Fluorescein Angiography:-
filling that later fades occurs in pseudoholes with epiretinal • Reveals pooling of the dye in the cystoid spaces in the late
membranes.
• Red-free photography is helpful in outlining the extent of the venous phase.
preretinal membrane bordering the defect. • An RPE detachment can be distinguished by slow & complete
Prognosis: - subpigment epithelial leakage & neurosensory detachment
• Usually good but depends on the underlying cause of the will be associated with a focal RPE leak.
• Traction neurosensory retinal detachment will show no
preretinal membrane. abnormal fluorescence.
• Progressive contraction may increase perifoveal intraretinal
Diagnosis: -
vascular leakage(macular edema). • Watzke-Allen test differentiates a hole from a cyst.
• If a complete interruption or an interruption greater than one
Treatment: -
• There is no evidence that laser treatment, even in eyes with half the width of the slit then FTMH.
• No interruption or slight narrowing or distortion in the slit
associated angiographic leakage, is of value.
• Indeed, photocoagulation may worsen contraction of the correlates – pseudohole, cyst or lamellar hole.
• The Amsler grid although sensitive is not specific.
membrane on the surface of retina because of thermal energy
absorption. Prognosis:-
• Surgery is successful in vast majority of cases. • Depends on the underlying cause.
• If the vision is 20/80 or less & the patient’s vision is disturbed • The size & chronicity of the cystoid edema, associated vitreal
by distortion then vitrectomy surgery to peel the epiretinal
membrane is justified, this relieves surface traction. traction & disruption in the anatomic architecture of the
• This management has yet to be evaluated since the return perifoveal tissue may lead to inner lameller or FTMH.
of vision is usually incomplete & the risks of vitrectomy &
progression of nuclear sclerosis always exist. Treatment : -
• No treatment is indicated except in patients with partial PVD
Macular Cysts: -
• It has an intact inner & outer retinal layer with fluid present with ongoing traction to a cystic macula, esp. in a patient with
poor vision in the fellow eye.
intraretinally. • Pars plana vitrectomy is used to separate partially detached
• Cystic macular degeneration involves extensive inner retinal posterior hyaloid face from underlying cystic retina.
ischemic atrophy with loss of nerve fiber layer, ganglion cells, Treatment of FTMH: -
inner plexiform & inner aspects of inner nuclear layers.
• Cystoid spaces in the macula develop from degeneration of Indications of Surgery: -
muller cells & eventually progress to irreversible liquefaction • Stage 2 MH with VA < 6/12
necrosis of these cells & neuronal degeneration. • Stage 3 or 4 MH
• Collapse of smaller cystic cavities, creating a large confluent
cyst, in chronic or severe CME creates a lesion that may Case Selection: -
appear similar to macular hole on direct ophthalmoscopy. • Careful patient selection is critical to a successful outcome.
• CME may be associated with : -
• Use of intraocular gas.
• Choroidal tumors.
www.dosonline.org 71
• Ideal candidate would be a patient with bilateral holes of Chemical vitrectomy/ Enzymatic Vitrectomy: -
recent onset, with vision in his better eye inferior or equal to • An in office procedure
6/36. • Enzymatic manipulation of posterior hyaloids & vitreous
• Patients with symptomatic unilateral holes with recently cortex is carried out using 0.4 IU autologous plasmin & the
reduced vision to 6/24 or worse are also good candidates. solution is lavaged followed by 14% C3F8.
• Since stage 1 macular holes have a high rate of spontaneous Adjunctive Agents: -
resolution & reported studies have failed to demonstrate any
benefit from vitrectomy, surgery is not usually recommended Thrombin:-
for this early stage. • A known stimulator of RPE & glial cells.
• Failed to show marked increase in the success rate of macular
Prognostic Factors
i) Stage of hole – earlier the better hole closure.
ii) Pre-op VA – the good the better • Increased post-op inflammation.
iii) Pre-op Lens Status – the clearer the better
iv) Duration of hole – longer the duration, grim surgical results. Gelatin plugs: -
v) Hole Form Factor (HFF) – indirect indicator of the size of • Preliminary results of vitrectomy followed by placement of
hole. The higher the value of HFF (>0.9) the better are the an absorbable cross-linked gelatin plug in stages 3 & 4 have
results. Calculated as follows: - been encouraging.
• Recommended use in high myopes with posterior staphyloma
vi) Macular hole Index (MHI)– is basically the ratio of hole height or recurrent macular hole.
with base diameter. Higher MHI (≥0.5) correlates with better
visual outcomes. TGF ß-2: -
• It appears to promote wound healing by stimulating collagen
vii) No. of surgeries - Patients who have had two failed surgeries
for a macular hole generally derive little or no visual benefit fibril growth, glycoproteins & proteoglycans.
even if a third surgery closes the hole. • Studies have suggested a potential benefit using human
viii) Scanning Laser Microperimetry – maximum para hole recombinant TGF ß-2 for persistent FTMHs following failed
sensitivity showed a positive correlation with post-op VA. primary surgery & for traumatic holes.
Stimuli are positioned on the retina around the macular hole.
The first stimuli are presented at 15–20 dB. If the patient Autologous platelet concentrate: -
identified all stimuli around the hole or if none of the stimuli • It induces a localized fibrocellular response that seals the
are seen, the intensity was adjusted until some stimuli are
seen. The intensity is then decreased gradually until the retinectomy edge, involving a mixed population of glial, RPE
patient did not see any stimuli around the hole, which is & fibroblastic cells.
defined as the “maximum para hole sensitivity”. • It has a beneficial effect in primary FTMH surgery & also
increased the surgical success rate in reoperations combined
ix) Shorter axial length with rigorous epiretinal membranectomy.
Results: - References
Two types of hole closure has been defined: - 1. Sen P, Bhargava A, Vijaya L, George R. Prevalence of idiopathic
• Type 1 closure indicates that the macular hole is closed macular hole in adult rural and urban south Indian population.
Clin Experiment Ophthalmol 2008; 36: 257–60.
without foveal defect of the neurosensory retina (Figure 7). 2. McDonnell PJ, Fine SL, Hillis AI: Clinical features of idiopathic
• Type 2 closure indicates that a foveal defect of the macular cysts and holes. Am J Ophthalmol 93:777–786, 1982
3. Ezra E, Wells JA, Gray RH, et al. Incidence of idiopathic full-
neurosensory retina persists postoperatively although the thickness macular holes in fellow eyes: a 5-year prospective natural
whole rim of the macular hole is attached to the underlying history study. Ophthalmology 1998;105:353– 359.
RPE with flattening of the cuff (Figure 8). 4. The Eye Disease Case-Control Study Group. Risk factors for
• Visual improvement is achieved in 55% to 85% of eyes with idiopathic macular holes. Am J Ophthalmol 1994;118:754-61.
a final visual acuity of 6/12 or better in upto 65%. 5. Knapp H: Ueber isolerte zerreissungen der aderhaut in folge von
• Stage 2 holes randomized to surgery had a significantly lower traumen auf dem augapfel. Arch Augenklinik 1:6–29, 1869
incidence of hole enlargement. 6. Noyes HD: Detachment of the retina, with laceration at the macula
• Bilateral visual function improves after successful FTMH lutea. Trans Am Ophthalmol Soc 1:128–129, 1871
surgery, especially in patients with subnormal (<20/40) visual 7. Ogilvie FM: On one of the results of concussion injuries of the eye
acuity in fellow eye. (“holes” at the macula). Trans Ophthalmol Soc UK 20:202–229, 1900
72 DOS Times - Vol. 16, No. 10,April, 2011
8. Kuhnt H: Uber eine eigenthumliche veranderung der netzhaut ad 17. Gass JD: Reappraisal of biomicroscopic classification of stages of
maculam (retinitis atrophicans sive rareficans centralis). Ztschr development of a macular hole. Am J Ophthalmol 119:752–759,
Augenheilk 3:105–112, 1900 1995
9. Coats G: The pathology of macular holes. Roy London Hosp Rep 18. Fisher YL, Slakter JS, Yannuzzi LA, et al. A prospective natural
17:69–96, 1907 history study and kinetic Ultrasound evaluation of idiopathic
macular holes. Ophthalmology 1994;101:5 –11.
10. Fuchs E: Zur veranderung der macula lutea nach contusion. Ztschr
Augenheilk 6:181–186, 1901 19. Lewis ML, Cohen SM, Smiddy WE. Bilaterality of idiopathic macular
holes. Graefes Arch Clin Exp Ophthalmol 1996; 234:241–5.
11. Lister W: Holes in the retina and their clinical significance. Br J
Ophthalmol 8:1–20, 1924 20. Trempe CL, Weiter JJ, Furukawa H. Fellow eyes in cases of macular
hole: biomicroscopic study of the vitreous. Arch Ophthalmol 1986;
12. Reese AB, Jones IS, Cooper WC: Macular changes secondary to 104:93–5.
vitreous traction. Am J Ophthalmol 64:544–549, 1967
21. Gaudric A, Haouchine B, Massin P et al. Macular hole formation:
13. Avila MP, Jalkh AE, Murakami K: Biomicroscopic study of the new data provide by optic coherence tomography. Arch Ophthalmol
vitreous in macular breaks. Ophthalmology 90: 1277–1283, 1983 1999; 117:744– 51.
14. Morgan CM, Schatz H: Involutional macular thinning: A premacular 22. Gass JDM. Muller cell cone, an overlooked part of the anatomy of the
hole condition. Ophthalmology 93: 153–161, 1986 fovea centralis. Hypotheses concerning its role in the pathogenesis
of macular hole and foveomacular retinoschisis. Arch Ophthalmol
15. Gass JD: Idiopathic senile macular hole: Its early stages and 1999; 117: 821–3.
pathogenesis. Arch Ophthalmol 106:629–639, 1988
23. Yamada E. Some structural features of the fovea centralis in the
16. Johnson RN, Gass JD: Idiopathic macular holes: Observations, human retina. Arch Ophthalmol 1969; 82: 152–9.
stages of formation, and implications for surgical intervention.
Ophthalmology 95:917–924, 1988 24. Hogan MJ, Alvarado JA, Weddell JE. Histology of the human eye.
An atlas and textbook. Philadelphia: WB Saunders, 1971:492–7.
First Author
Priyank Garg MS, FNB
New Members List (Contd....) from page 53
V-4460 DR. V. PANIMALAR A. VEERAMANI V-4281 DR. GHARAT MIHIR VINAY WD-1472 DR. BATRITI SHYMPLIANG WALLANG
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www.dosonline.org 73
Post Traumatic Glaucoma Glaucoma
Manav Sachdev MBBS, Usha Yadava
Glaucoma is a well known complication in various forms of • Men
eye trauma. It is the major cause of unilateral blindness world • Age less than 30
wide. Proper management of glaucoma requires careful history • Professional athletes particularly Boxing And Ball games
taking and examination in every case of eye trauma so as to detect
Glaucoma early and to manage it effectively. Such As volley ball, toy gun pellet, badminton shuttle, cricket,
Classification Glaucoma after trauma can be categorized by tennis
• Type of injury • assault
• Onset of glaucoma • Child abuse
According to Onset of Glaucoma causes can be Immediate and • African-american race
Delayed Onset. • Sickle cell disease
Immediate Contusion Injury
• Contusion In this there active inflammation of the trabecular meshwork
• Trabecular disruption soon after the injury, leading to transient decrease in outflow
• Hyphema facility from the TM. There is no evidence of angle recession,
• Massive choroidal haemorrhage angle disruption or Hyphema, angles are typically open.. It is a self
• Chemical injury limiting condition. Sometimes topical and hyperosmolar agents
Delayed may be required to control the IOP.
• Angle recession Trabecular Disruption
• Peripheral anterior synechiae If gonioscopy is done within 48 hours of the injury damage to the
• Lens induced angle structures can be identified. There might be haemorrhage in
• Subluxation to the schlemm’s canal or damage to trabecular meshwork which
• phacomorphic might be restricted to outer sheets or there might be full thickness
• phacolytic injury to the TM. A flap of injured TM is created just below the
• lens particle sight of rupture which hinges at the scleral spur.
• Ghost cell Glaucoma Hyphema
• Closure of cyclodialysis cleftAccording to Type of injury Blood in AC can be either due to Blunt or Penetrating injury, in
blunt trauma there is antero-posterior compression and equatorial
responsible for causing glaucoma expansion leading to damage to ciliary body and TM. There are
• Fibrous epithelial downgrowthBlunt trauma shearing forces acting on the angle structures and the ciliary body
• Retained Intra ocular foreign Penetrating trauma leading to damage to the anterior face of ciliary body and damage
• BodyChemical injury to major arterial circle acusin the hyphema,
• Rhegmatogenous RDRadiation injury Penetrating injury leads to hyphema by damaging the blood
• Surgery vessels and due to hypotony. Certain conditions lead to
Blunt trauma is the most common cause of glaucoma throughout HYPHEMA even in MINOR TRAUMA – Rubeosis iridis, juvenile
the world. High risk groups include . xanthogranuloma, iris melanoma, iris leiomyosarcoma, myotonic
dystrophy , vascular iris tufts blood dyscrasias.
Guru Nanak Eye Centre Hyphema resorption occurs by anterior surface of the iris and TM.
Maharaja Ranjit Singh Marg, New Delhi Uncomplicated hyphemas are cleared with in 1 week.
Grading
• grade 1: < 1/3th of AC
• grade 2: 1/3oth -1/2 of AC
• grade 3 > ½ of AC
• grade 4: total or eight ball hyphema.
www.dosonline.org 75
Complications of Hyphema Angle recession occurs in 20-94% cases of eye trauma. Studies
• Increased IOP: various causes of high iop in hyphema are: indicate that incidence of glaucoma in angle recession ranges
• occlusion of trabecular meshwork by clot, inflammatory from 7-9%.
Pathologically angle recession is a separation between the circular
cells, erythrocytic debris. and the longitudinal fibers of the ciliary body, longitudinal muscles
• papillary block due collar button shaped clot. remain attached to the scleral spur. There might be associated
• Peripharal anterior synechiae: PAS are formed if hyphema cyclodialysis, iridodialysis, damage to the lens manifested as
cataract, subluxation ,dislocation , hyphema. Later the inner later
pesists for more than a week . of ciliary body atrophies leading to broadand fusiform ciliary band
• Optic atrophy : optic atrophy in hyphema can occur because appearance on gonioscopy.
Grading is done according to Howard’s Classification as Grade I
of high IOP , contusion to the optic nerve, secondary to (shallow), grade II (moderate), grade III (deep)
damage to short posterior ciliary arteries. Risk of optic Gonioscopic findings:
atrophy increases when th IOP is > 50 mmHg for 5 days or • deepening of angle
35 mmHg or more for 7 days. Patients with sickle cell disease
have optic atrophy even at normal or slightly raised IOP.
• Corneal blood staining:. Factors which influence corneal • widening of exposed face of ciliary body
blood staining include: rebleeding, prolongd clot duration, • posterior displacement of iris root
sustained increase in IOP and corneal endothelial dysfunction. • disruption of uveal processes
• abnormal whitening of scleral spur
Two main risk factors of corneal blood staining include
IOP>25mmHg and >6 days duration.
Earliest sign of corneal blood staining is a straw coloured • grey white membrane over the TM
discoloration of deep stroma, presence of tiny yellow granules in Bilateral simultaneous gonioscopy is a very effective way detecting
posterior 1/3rd of the cornea. even the subtle changes in the angle.
In sunlight the haemoglobin gets converted in to porphyrins, Mechanism of elevated IOP is damage to the TM instead of the
which toxic to the corneal endothelium therefore patching might actual angle recession. Angle recession indicates the extrent and
have a role in management of hyphema. severity of the injury. It is advised to do gonioscopy within 48
Corneal blood staining can cause decreased visual acquity and hours of trauma to detect trauma to the TM.
depriviation amblyopia in children. Peripheral Anterior Synechiae
• Secondary haemorrhage: rebleed occurs because of clot PAS can form due to various reasons as there is inflammation,
apposition of iris to the cornea, there might be hyphema leading
retraction on and after day 4. signs of rebleed incude increase to organization of blood. Penetrating trauma can lead to PAS
in size of hyphema, layer of freas RBCs over previous clot, formation by chronic shallowing of AC, endothelialization of
change of colour from dark red to bright red. angle. Epithelial or fibrous downgrowth in to the AC.
Chances of rebleed are more with black race and children
• Accomodative impairment Ghost Cell Glaucoma
Massive Choroidal Haemorrhage Campbell described a condition in cases of blunt trauma with
It is rare cause of pressure elevation in trauma signs include vitreous haemorrhage and hyphema. Hyphema cleared with in 2
shallow AC, poor red reflex, choroidal elevation in IO. Indications weeks but RBCs in vitreous lost their HB and degenerated it to
of surgical intervention include persistent elevation of IOP, lens gost cell in 2 weeks. Due to the associated break in the anterior
cornea apposition, kissing choroidals hyloid phase these cell come in to the AC and being less pliable
Chemical Injury they block the TM leading to elevation of IOP which usually
Alkali burns are the main cause of glaucoma amonst chemical occurs 2 weeks – 3 months aafter the injury.thease cells have a
injuries. Mechanism is by shrinkage of the outer coats of the eye, characteristic ochre color can form a layer of cells in AC leading
release of prostaglandins, and blockage of TM by inflammatory to a psuedohypopyon and may give rise to Candy-Stripe Sign
cells formation o PAS Lens Induced Glaucoma
Late Onset Glaucoma after Trauma This group has lens as a common pathogenic cause, the angle
Angle Recession might be open or closed. Various causes are
COLLINS was the first person to describe angle recession due to • Lens swelling: trauma can lead to swelling of the lens and
blunt trauma in 1892. Wolf and Zimmerman in 1962 linked angle
recession to development of Glaucoma. cataract. Swollen lens pushes the iris len diaphragm forwards
and causes papillary block leading to HIGH IOP
• Lens dislocation/subluxation: lens may be dislocated in to
the AC leading to papillary block mechnically or it may be
76 DOS Times - Vol. 16, No. 10,April, 2011
dislocated posteriorly leading to vitreous coming in to the incidence of secondary haemorrhage.predinislone in dase of
AC and causing papillary block 40mg/day or 0.6 mg/kg in children is effective in reducing
• Phacolytic glaucoma. An open angle glaucoma occurs due to the incidence of rebleed statistical analysis indicates that
release of lens proteins through an intact lens capsule. coticosteroids decreased the incidence of rebleeding without
• Lens particle glaucoma: due to frankly disrupted lens capsule having any effect on the longterm visual outcome.
frgaments of lens and protein block the TM. • Studies advocate use of mydriatics as they relieve ciliary spasm
Delated Closure of Cyclodialysis Cleft and prenents formation pf PAS. Aspirin should not be given
Formation of a cyclodialysis cleft leads to hypotony due to in cases of hyphema
decreased production of aqueous, which leads to decreased flow • Outpatient management : can be considered in following
across the TM resulting in reduced permeability of the TM. When Cases (Walton et al):
closure of the cleft occurs, IOP increases acutely leading to pain, • no associated injury
corneal edema, DOV, open angles. • hyphema< ½ of AC volume
Retained Intraocular Foreign Body • satisfactory IOP
iron foreign body might lead to siderotic glaucoma which is • no blood dyscrasia
associated with heterochromia, mydriasis, rust like discoloration • safe home environment
anterior subcapsular ares of lens and the posterior surface of • good patient compliance
cornea. • good follow up (no time delay at presentation)
Retinal Detachment • Indications for surgical management (irrigation, vitrectomy,
Glaucoma can be attributed to trabecular inflammation leading to trabeculectomy)-walton et al:
decreased outflow, blockage of TM by pigment or photoreceptors. • microscopic corneal blood staining
Repairing the RD cases permanent decrease in IOP provided there • Risc of optic atrophy/ CRAO (sickle cell disease/tait,
is no other abnormality in TM.
Management of Post Traumatic Glaucoma IOP avg >25 mmHg> 24 hours or spikes repeatedly >
In acutely elevated IOP is managed by giving topical antiglaucoma 30mmHg, IOP >60mmHg for 2 days OR 50mmHg for
agents as well as systemic carbonic anhydrase inhibitors, >4 days, presence of pre-existing glaucomatous optic
hyperosmolar agents until the trabecular inflammation subsides. atrophy and “unacceptable” IOP.
However certain cases needs specific interventions which are • Risc of corneal blood staining( e.g 4 days fter the onset
mentioned here of glaucoma, > ½ - total hyphema with IOP > 25mmHg
> 6 days
Hyphema: Medical Management: • Risc of synechiae formation ( e.g > 50% hyphema for >
• Anti fibrinolytic agents: epsilon amina caproic acid( EACA) 8 days.
Alkali Injury
and Tranexamic acid are used to prevent rebleed in cases of Topical antiglaucoma agents which reduce the formation of
hyphema aqueous production can be used to lower the IOP. If IOP is very
EACA( amicar ) binds to lysine molecules in the clot via high systemic drugs can be used. Corticosteroids can used in
lysine binding site and inhibits fibrin clot digestion. Its dose the first week after injury which decreases inflammation and
is 100mg/kg every 4 hours to a maximum dose of 30g/day prevents fibrosis. Steroids should not be used after first week due
by mouth for 5 days. to risc of corneal melting. Since prostaglandins are responsible
Side effects include nausea, vomiting, diarrhea, postural for inflammation and high IOP, indomethacin and other agents
hypotention, pruritis, muscle cramps, rash, nasal stuffiness, which decrease their production can be used.
arrhythmia, confusional state. Rhabdomyolysis and Angle Recession
myoglobinuria are rare.. Contraindications include drug Management consists of medical therapy followed by ndYAG laser
allergy, active intravascular clotting, history of thrombosis trabeculoplasty. Filteration surgery can be done if conjuntiva is
hematuria, renal failure and hemophilia. not injured by primary injury
Tranexamic acid also has similar mechanism. Side effects are PAS
lesser as compared to amicar Iridogonioplasty with Argon laser can be used to pull the iris away
The results of various studies indicate that both amicar and from the angle, failing which surgical goniosynechiolysis may be
tranexamic acid have beneficial effect on rate of secondary effective in reopening the angle.
haemorrhage but none of them had improved the final visual
outcome.
• Corticosteroids: by stabilizing the blood-ocular barrier and
by directly inhibiting fibrinolysis corticosteroids decrease th
www.dosonline.org 77
Ghost Cell Glaucoma by intrcapslar approach with anterior vitrectomy or pars plana
Treatment involves conventional medical therapy followed by lensectomy with vitrectomy can be done.
surgical treatment if it doe not respond. According to Campbell Lens swelling: cataract extraction along with iridectomy or
only less than half of thesecases respond on medical therapy alone. trabeculectomy is the treatment of choice. Treatment of PAS as
Surgical intervention in form of AC irrigation along with pars mentioned above can be required.
plana vitrectomy to clear blood components trapped in vitreous Phacolytic and lens particle glaucoma are managed by conventional
if required. medical and surgical methods.
Lens Induced Glaucoma Retained Intraocular Foreign Body
Dislocation: treatment of papillary block by LASER or surgical Foreign body removal has to be done as soon as possible along with
Iridectomy. Lensectomy may be done if pupillary block recurs vitrectomy to prevent further damage and irreversible vision loss.
or visual rehabilitation is not possible. Lensectomy can be don
First Author
Manav Sachdev MBBS
78 DOS Times - Vol. 16, No. 10,April, 2011
Myopia: An Overview Miscellaneous
Kapil Khurana DOMS, S.P. Chaudhary MS,FMRF, Manisha Agarwal MS, DNB, FMRF
Refractive error, predominantly myopia (short sightedness), been put forward to explain how myopia develops in premature
is the most common eye disease and thus the major cause of babies. These include bone deficiency, temperature, light, visual
reduced vision worldwide.1 Myopia is a condition in which parallel deprivation and retinal dysfunction.
rays of light are brought to a focus in front of the retina, which Three types of myopia are associated with premature birth: (1)
leads to blurred distance vision. This leads to loss of productivity physiological and temporary myopia (2) myopia without ROP
and co-morbidity due to vision impairment, as well as the direct (MOP) and (3) myopia induced by severe ROP disease.
costs of correction through glasses, contact lenses, and surgical Physiological and temporary myopia
treatment.2 The major structural correlate of myopia is an increase Myopia is probably the normal refractive state in infants before
in the axial length of an eye. full term with the eye becoming more hypermetropic in early
Epidemiology infancy. Compared with the eye of the full term baby the features
Mild or moderate myopia currently affects at least 25% of the of this myopia are shorter axial length, flatter anterior chamber,
populations in Europe and North America, approximately 5% in and more spherical lens.
Africa, and up to 80% in East Asia.4-9 In contrast, “pathological
myopia” (very severe) affects less than 3% of most of the
populations. Myopia in several Indian age groups increases from
16.1% in the late teens to 20-50% in the 70s.3 Women are affected
twice as commonly as men.
Pathogenesis
The pathogenesis of myopia in general, and progressive myopia
in particular, is unclear, but both heredity and environment play
a role. The mode of inheritance may be autosomal recessive or
dominant, but it also can appear sporadically. The most widely
accepted environmental influence is excessive near work.
Sustained accommodation and intraocular pressure (IOP), both
basal and phasic, are suspected to influence axial elongation in
eyes that have decreased scleral resistance.4
Genetic Factors: The most widely accepted theory of the cause of
myopia is that it is mainly hereditary. Measures of the heritability
of myopia have yielded figures as high as 89%, and recent research
has identified genes that may be responsible: defective versions
of the PAX6 gene seem to be associated with myopia. According
to this theory the eye is slightly elongated front to back during
development, causing images to be focused in front of the retina
rather than directly on it.
Environmental Factors: Another theory is that myopia is caused
by weakening of the ciliary muscle which control the eye's lens.
The weak muscle is unable to adjust the lens enough to see far
distances, causing far-off things to be blurred. This theory states
that the muscle's weakness is usually caused by doing lots of "near
work", like reading books or using a computer screen. Since the
eye rarely has to focus on far distances, the muscle is rarely used
and, as a result, becomes weak.
Other factors: Myopia is seen commonly in individuals of
hyperinsulinemia and also commonly in prematurity with or
without ROP (Myopia of Prematurity-MOP).5 Many theories have
Dr. Shroff ’s Charity Eye Hospital, Figure 1: Color fundus photograph of both eyes
Darya Ganj, New Delhi showing Optic Disc crescent
www.dosonline.org 81
Myopia without ROP (myopia of prematurity-MOP) Figure 2: Color fundus photograph of the left eye
This type of myopia has an early onset and compared with full- showing Foster Fuchs’ Spot
term and juvenile onset myopes the MOP eye exhibits a relatively
highly curved cornea, shallow anterior chamber and thick lens. Systemic associations of Myopia
Axial lengths are shorter than expected for the dioptric value. • Albinism
The hallmark of MOP is arrested development of ocular anterior • Congenital rubella Gyrate atrophy—hyperornithinemia
segment. • Laurence–Moon–Bardet–Biedl syndrome
Myopia induced by severe ROP disease • Marfan’s syndrome
The prevalence of myopia increases with the presence and severity • Pierre Robin’s syndrome
of ROP. There is a dramatic jump in the prevalence of myopia • Stickler’s syndrome
when stage 3 ROP is reached.6 ROP induced myopia cannot be • de Lange’s syndrome
fully explained by increased axial length as it is also associated • Down’s syndrome
with evidence of arrested development of the anterior segment: • Ehlers–Dahlos syndrome
microcornea, steep corneal curvature and thickened lens. This Among all these Marfan’s syndrome, Stickler syndrome and
could be due to a mechanical restriction of ocular growth. albinism are commonly associated with myopia.
Classification of myopia Fundus changes in high myopia
• Donder’s classification (1864)- based on the rate of Excessive axial elongation of the globe in high myopia can cause
mechanical stretching and thinning of the choroid and retinal
progression pigment epithelium (RPE) layers, resulting in various retinal
• Stationary degenerative changes. High myopics have an increased risk of
• Temporarily progressive myopia retinal complications such as peripheral retinal degenerations,
• Permanently progressive myopia retinal tears, retinal detachment, posterior staphyloma,
• Duke Elder’s classification (1949) chorioretinal atrophy, retinal pigment epithelial atrophy, lacquer
• Simple myopia (generally less than -6 D) - occurring as cracks, choroidal neovascularization (CNV) and macular
haemorrhage.
a result of normal biological variation. Optic disc crescent
• Degenerative myopia (more than -6 D) This is an early change in the myopic fundus and is due to a
• Grosvenor’s (1987) classification- based on the age of onset pulling away of the choroid and RPE usually from the temporal
• Congenital myopia (present at birth and persisting edge of the nerve to expose the sclera .The incidence of crescent
formation is significantly associated with increasing axial length
through infancy) in high myopics.
• Youth-onset myopia (<20 years of age)
• Early adult-onset myopia (20-40 years of age)
• Late adult-onset myopia (>40 years of age)
• According to degree of myopia
• Low (≤ -3D)
• Medium (-3D to -6D)
• High (≥ - 6D)
Ocular associations of Myopia
The various ocular associations are:-
• Premature nuclear sclerosis
• Posterior subcapsular opacities (less common)
• Glaucoma where the prevalence of glaucoma is related to the
degree of myopia. All myopic discs should be evaluated with
high suspicion of glaucoma
• Strabismus especially exophoria and exotropia
82 DOS Times - Vol. 16, No. 10,April, 2011
Figure 3: Fundus fluorescein angiography of the left eye showing early
hyperfluorescence with late leakage in the macula suggestive of classic myopic CNV
Posterior staphyloma (PPV) surgery with gas or silicone oil tamponade is performed
under local or general anesthesia.
A posterior staphyloma is a backward ectasia of the fundus, Myopic foveoschisis and macular hole
the hallmark being tessellation and pallor of the area involved Recent advancement in retinal imaging technology using optical
(Figure3). Posterior staphyloma can be of five types7:- coherence tomography (OCT) has demonstrated that high myopic
Type 1- The area of tessellation and pallor includes the region of patients with posterior staphylomas are predisposed to develop
the optic disc and macula. It is the most common type macular pathologies such as myopic foveoschisis and macular
Type 2- includes the region of the macula hole.
Type 3- involves the peri-papillary region Myopic foveoschisis is the splitting of the retinal layers in the
Type 4- extends nasally from the disc macula and can result in metamorphopsia and blurring of vision.
Type 5- most rare and involves the fundus inferior to the optic disc In more advanced stage, myopic macular hole can develop which
Steidl and Pruett et al8. suggested that eyes with the shallow may be associated with retinal detachment and patients will suffer
staphylomas showed larger drop in visual acuity and a greater from severe visual loss with reduced visual acuity. PPV with
occurrence of CNV and macular hemorrhage. The possible reason peeling of the internal limiting membrane and gas or silicone
for this could be the better preserved choriocapillaris underneath oil tamponade followed by post operative prone positioning is
the shallow staphylomas. performed for treating macular holes.
Peripheral retinal degenerations and rhegmatogenous Lacquer cracks
retinal detachment Lacquer cracks are formed by spontaneous ruptures in the Bruch's
membrane and small hemorrhages may develop within the
Lattice degeneration is the most important peripheral retinal lacquer cracks. Lacquer cracks may cause sudden loss of vision
degeneration which can predispose to rhegmatogenous retinal secondary to the development of a CNV in close proximity to
detachment (RRD). This is because retinal tears can develop the lacquer cracks.
secondary to posterior vitreous detachment (PVD), at the Foster Fuchs’ Spot
posterior and lateral margins of the lattice degeneration where Foster Fuchs’ spots appear as round or elliptical lesions that are
strong vitreoretinal adhesions exist. Symptoms of PVD and retinal predominantly dark but can have a gray, yellow, red, or green
break formation include sudden or gradual increase in the number coloration. They arise due to proliferaration of RPE associated
of floaters and/or flashes of light. with choroidal hemorrhage.9
Dilated fundus examination should be carried out in patients with Choroidal neovascularisation in high Myopia
these symptoms as soon as possible to detect early development Myopic CNV is one of the most vision threatening complications
of retinal break or retinal detachment. of high myopia (Figure 2). Myopic CNVM develops in around 5
Laser photocoagulation is used for the treatment of eyes which to 10% of the eyes with high myopia and is the commonest cause
have developed retinal hole or break. of CNV in young individuals.
In eyes with retinal detachment either pneumatic retinopexy,
scleral buckling (SB) with cryopexy or pars plana vitrectomy
www.dosonline.org 83
The incidence of myopic CNV in the second eye in patients with 2. Javitt J, Chiang YP. The socioeconomic aspects of laser refractive
pre-existing myopic CNV in the fellow eye is as high as 30% within surgery. Arch Ophthalmol 1994;112:1526 –30
eight years after the first eye.10
Therefore Amsler grid monitoring of the second eye is very 3. Lopes MC, Andrew T, Carbonaro F, et al. Estimating heritability and
important for early detection of the CNV in the second eye. Poor shared environment effects for refractive error in twin and family
prognostic factors for patients with myopic CNV include age of studies. Invest Ophthalmol Vis Sci 2009;50:126–31
greater than 40 years, larger CNV, and worse initial visual acuity.11
Currently myopic CNV are treated with anti-vascular endothelial 4. Vitale S, Ellwein LB, Cotch MF, et al. Prevalence of refractive error
growth factor (anti-VEGF) agents such as Ranibizumab (Lucentis), in the United States, 1999-2004. Arch Ophthalmol 2008; 126:1111–9.
Bevacizumab (Avastin) and pegaptanib sodium (Macugen) given
as an intravitreal injection under topical anesthesia and aseptic 5. Ling CS, Fleck BW, Wright E, Anderson C, Laing I. Diode laser
precautions. treatment for retinopathy of prematurity: structural and functional
Conclusions outcome. Br J Ophthalmol 1995;79:637–41.
Individuals with high myopia are subject to various retinal
pathologies including peripheral retinal degenerations, retinal 6. Scharf I, Zonis S, Zeltzer M. Refraction in premature babies. Metab
detachment, and posterior pole pathologies such as CNV, lacquer Ophthalmol 1978;2:395–6.
cracks and macular haemorrhages. These retinal pathologies may
cause serious sight-threatening complications. Therefore patients 7. Hoffman DJ, Heath DA. (1987) Staphyloma and other risk factors
with high myopia should be educated about the symptoms of in axial myopia.J. Am. Optom. Assoc. 58: 907-913
posterior vitreous detachment such as flashes and floaters, falling
of a black curtain in-front of the eye or development of a central 8. Steidl SM, Pruet RC. (1997) Macular complications associated with
scotoma secondary to a myopic CNV. Patients should be advised posterior staphyloma. Am. J. Ophthalmol. 123: 181-187
to seek prompt medical care should such symptoms arise. Prompt
diagnosis and treatment may greatly help in preventing severe 9. Klein RM, Curtin BJ. (1975) Lacquer crack lesions in pathologic
visual loss secondary to retinal complications arising in high myopia. Am. J. Ophthalmol. 79: 386-392
myopic patients.
References 10. Curtin BJ, Karlin DB. (1971) Axial length measurements and fundus
1. Thylefors B. A global initiative for the elimination of avoidable changes of the myopic eye. Am. J. Ophthalmol. 71: 42-53
blindness. Am J Ophthalmol 1998;125:90 –3. 11. Morse PH. (1989) Vitreoretinal disease 2nd ed, Year Book Medical
Publishers, Chicago.
First Author
Kapil Khurana DOMS
84 DOS Times - Vol. 16, No. 10,April, 2011
Ocular TB Miscellaneous
Bobby Bhalotra MD, Amit Khosla MD
Tuberculosis [TB] is a serious global public health problem. In TST test has only one per cent probability of having active TB.
a report from a sanatorium in the USA, 1.4 per cent of 10 524 However, recent conversion of a previous non-reactor favors the
patients were treated for ocular TB between 1940 and 1966. The diagnosis of TB.
incidence of TB uveitis in India has varied from two to thirty per Use of systemic corticosteroids for severe ocular inflammation can
cent. The large variation in the incidence rates in different reports interfere with the TST results. Therefore, though a routine TST
possibly stems from differences in the diagnostic criteria used in has been advocated in patients with uveitis, it is rarely diagnostic.
the studies reporting higher incidence rates; the diagnosis of TB In countries where TB is highly endemic, a caution is advocated
uveitis was often based on a positive tuberculin skin test [TST]. before interpreting a positive TST result in isolation. A positive
Ocular manifestations of TB are protean. While TB can affect TST can be considered to be supporting evidence in a patient
all areas of the visual system, the choroid is probably the most with a clinical picture highly suggestive of TB such as choroidal
commonly affected intraocular structure. Choroidal tubercles tubercles or tuberculoma or when other investigations such as a
constitute the most common intraocular manifestation of TB. chest radiograph also have findings compatible with TB. On the
Woods estimated that-the choroid is involved in about one other hand, a negative TST is considered by some as being more
per cent of patients with pulmonary TB. Primary TB of the relevant as it rules out TB if the patient is immunocompetent.
eyelid, conjunctival sac and optic nerve is rare. Rarely, serious This, however, is also not always true as there are several causes
manifestations, such as panophthalmitis or endophthahnitis can of anergy.
also occur. Certain ocular manifestations, such as vasculitis due In patients with ocular TB, it is seldom possible to procure
to TB [e.g., Eale’s disease] are presumably due to hypersensitivity adequate tissue for diagnosis and the number of organisms present
to a sequestered antigen rather than TB disease per se. may be too small to be detected by conventional methods. The
Primary and Secondary Ocular Tuberculosis utility of serological tests in the diagnosis of ocular TB needs
The term “primary ocular TB” has been used when the TB further evaluation in well-designed studies with a large sample
lesions are confined to the eyes and no systemic lesions are size. Polymerase chain reaction appears to be a promising tool
clinically evident. “Secondary” ocular TB has been defined as to establish the definitive diagnosis of ocular TB, if the sample is
ocular infection resulting from congruous spread from adjacent taken from the representative tissue
structures or haematogeneous spread from the lungs. Despite rapid advances in medicine, ocular TB still remains an
Definitive diagnosis of ocular TB can be made only by important diagnostic challenge. The criteria for the diagnosis of
demonstrating Mycobacterium tuberculosis in the ocular tissues. ocular TB differ greatly and very often the diagnosis is based on
However, obtaining ocular tissue for diagnostic purposes is a compatible clinical picture and good therapeutic response to
not only difficult, but is also associated with significant ocular antituberculosis treatment rather than mycobacterial isolation.
morbidity. Hence, the diagnosis of TB can rarely be definitely Earlier, it has been suggested that clinical diagnosis of ocular TB be
confirmed before enucleation. Only 25 per cent of patients with based on the presence of at least three of the following five features
ocular TB give past history of TB and 50 per cent have normal [i] suggestive clinical picture; [ii] exclusion of other aetiology;
chest radiographs. Orbital radiographs may reveal bony erosions. [iii] positive TST; [iv] therapeutic response to antituberculosis
A high degree of clinical suspicion is, therefore, the key to early treatment; and [v] present or past history of TB.
diagnosis. Easily accessible sites, such as eyelid, conjunctiva In patients with a clinical picture suggestive of intraocular TB.
, lacrimal gland and sclera , should preferably be biopsied to The criteria shown below can be helpful.
demonstrate the characteristic findings of caseating granulomas Major criteria
with Langhans’ giant cells and Mycobacterium tuberculosis. Despite Evidence of pulmonary or other systemic pathology consistent
all investigations patients with clinically suspicious lesions should with TB occurring concurrently with the ocular disease. Response
receive empirical standard antituberculosis treatment and should of ocular and systemic disease to antituberculosis treatment [with
be carefully followed-up for therapeutic response. or without steroids]
A positive TST in a patient with granulomatous uveitis was Exclusion of other etiological causes, like sarcoidosis, tumors,
considered to be a positive evidence of ocular TB. A positive secondary metastases
TST is, however, only indicative of infection with Mycobacterium. Minor criteria
tuberculosis and does not necessarily reflect the disease activity. Positive Quatiferon gold essay or TST
‘Wernik calculated that a patient with uveitis and a positive Positive PCR for Mycobacterium tuberculosis in ocular fluids or
biopsy
Department of Chest Medicine
Sir Ganga Ram Hospital,
Rajinder Nagar, New Delhi
www.dosonline.org 87
Suspected case of Tuberculosis • Cell count and differential
Pulmonary Disease is Suspected • Chemistries to include glucose and protein
• AFB smear (typically ergative) and culture (10 ml.
Send
1. Three induced or spontaneous (respiratory isolation) 1 cm. offers required)
• Consider PCR
spectures samples for AFB staining and microscopy: c. Pleural pericardial, or asdisk fluid
• 5 to 10 ml. each, accept in wistery specimens • Cell count and differential
2. One sputum sample for MTb complex PCR: • Chemistries to include glucose and protein
3. Same three sputum samples for culture; • AFB smear and culture (lining biopsies have
4. It effusion is present, consider sending diagnostic
higher yield)
thoracenteds sample for smear, culture, PCR, and adenmine • Consider ADA analysis
deaminase (ADA) testing-pleural biopsy has higher culture • PCR
sensitivity. d. Other theses (bone marrow, skin, liver, spices…
5. Consider early morning gastric aspiration of 50 ml in
children or failed sputum inductions; and, kidney)
6. Consider an IFN based away on sacrum or Tuberculin Skin • AFB smear and culture
Test – negative text does not exclude disease. • Histopathologic analysis, may consider, specialized
Other than pulmonary disease is suspected
AFB staining, and subsequent targeted PCR
Send: • PCR
1. Samples an you would for suspected pulmonary disease; e. Blood
• Culture
and, • PCR
2. Sample from suspected site. For these collection, collect f. Stool, consider, intestinal biopsy
• Culture
both with and without formalies. • PCR
a. Lymph mode g. Urine (first morning mid-void stream collections, three
• Exclusional biopsy preferred
• Fine needle aspiration if unable to obtain daily samples
• Urinalysis and conventional culture
exclusional biopsy, e.g. CT guided biopsy in setting • Culture
of mesenteric adenitis. • PCR
• AFB smear and culture
• Histopathologic analysis
b. CSF
All major criteria fulfilled = highly probable intraocular TB; 2 Anterior segment inflammation should be managed with topical
major and 1 minor criterion fulfilled = probable intraocular TB steroids and cycloplegics. Treatment of TB phlyctenulosis also
When patients with TB elsewhere in the body develop clinical involves topical corticosteroids and cycloplegic agents in addition
features of ocular involvement, thorough ophthalmologic to standard antituberc ulosis treatment. Conjunctival lesions
evaluation is warranted. Similarly when patients are detected to causing only mild symptoms may respond to local astringents.
have ocular involvement, a complete systemic evaluation must be Muco-purulent discharge suggests secondary bacterial infection
done. Treatment of ocular TB is on the same lines as treatment and should be treated accordingly. Conjuctival lesions heal
of TB elsewhere in the body. The disease is said to respond well without scarring, but corneal phlyctenules leave superficial scars
to standard antituberculosis treatment and there is no role for of variable severity.
topical treatment Antituberculosis Treatment Induced Ocular Toxicity
However, as significant damage can occur to ocular tissues from Several antituberculosis drugs can cause ocular adverse effects,
infection as well as inflammation, it is prudent to add systemic which if not recognized early can result in an irreversible loss
corticosteroids as an adjuvant to the standard antituberculosis of vision. Often patients are referred to ophthalmologists for
treatment. This must be done in consultation with a physician evaluation of ocular toxicity following prescription of drugs for
88 DOS Times - Vol. 16, No. 10,April, 2011
TB elsewhere in the body. Sometimes patients themselves notice was 2 in 10. In other studies with culture-proven disease, a single
a diminution in vision while on antituberculosis treatment sputum sample detected disease in one-half to two-thirds of cases,
and get evaluated by an ophthalmologist. Ocular toxicity while three or four specimens detected as many as 9 of every 10
due to ethambutol, isoniazid and streptomycin has been well cases.
documented. Of these, ethambutol has the greatest potential to In most cases bronchoscopy or lavage is required when sputum
cause ocular toxicity. In general, adverse drug reactions occur less smears are negative in the setting of a known radiographic
frequently in patients receiving intermittent regimens as compared lesion allowing focused lavage. Induced sputum collection and
to daily regimens. bronchoalveolar lavage can be used together, detecting 8 of 10
Three types of optic neuritis have been described with ethambutol patients.
These include the axial, the periaxial and the mixed type. Both Auramine staining of sputum is superior. It has greater sensitivity
eyes are usually involved and the visual loss may vary from mild with a requirement for fewer screened microscopic fields as a lower
to severe. Colour vision is also variably affected. In the axial form magnification can be used. Stain superiority in tissue samples is not
of optic neuritis, on visual field recording pericentral or peri clear. Typically, 104 to 106 organisms/ml are required for detection,
pheral scotoma may be evident. Quadrantic field defects have also although concentration techniques can lower this number.
been commonly found. Although mild disc hyperaemia and disc Histopathology: The hallmark finding on histopathology is the
oedema have been reported, fundus examination may be normal necrotizing or caseating granuloma. When found, tuberculosis
in the acute phase of ethamb utol toxicity. Peripapillary splinter should be presumed until disproven.
haemorrhages, macular oedema and focal pigmentary changes Culture
have also been described. Ethambutol related ocular toxicity is Culture remains the gold standard for diagnosis. Egg-based plate
strongly dose related . media such as Löwenstein–Jensen are used, but agar media such
As the incidence of ethambutol toxicity is low with the currently as Selective 7H11 and liquid-based media (Becton–Dickinson
favoured dose of 15 to 20 mg/kg/ day, and also because it is and Co., BACTEC™ and BACTEC™ MGIT™) now are the standard.
reversible in most cases, sophisticated electrophysiological Growth often can be detected within 2 weeks. Typical hold periods
tests like electroretinography and VER are not required in all are for 4 to 6 weeks. Use of these systems also allows expeditious
cases. However, in all patients receiving ethambutol, a baseline drug susceptibility assessment when agents are added into the
best corrected visual acuity and colour vision record should be liquid media.Culture yields in extrapulmonary tuberculosis are
routinely obtained. Thereafter, patients should be questioned significantly lower than from sputum samples.
monthly about any changes in vision. Any significant alteration Improvements in sample processing for use in PCR have increased
in vision needs to be promptly investigated. culture yields, resulting in detection of less than 102 organisms/
The most common adverse effect of rifampicin in the eye is mL. Pleural culture yields range from 23 to 67% from fluid, and
conjunctivitis. It can result in the production of tears that are 90 to 97% from biopsy. Despite high yields, finding providers to
orange coloured and this can stain contact lenses. Rifabutin has perform pleural biopsy is problematic.
been associated with the development of an endophthalmitis-like Molecular Methods: NAA/PCR
response. Clofazimine has been associated with several ocular side NAA assays allow rapid turnaround time (24 to 48 hours) when
effects; these include: a brownish discolouration of the conjunctiva, samples are smear positive and can be done on smear-negative
brown swirls in the corneal and bull’s eye maculopathy resulting specimens, but with less sensitivity and specificity. They are
in visual loss due to macular degeneration. performed directly on specially processed specimens to provide
Laboratory Diagnosis of Tuberculosis in Primary Care simultaneous detection and identification. Culture of the organism
is still necessary to confirm the identification and to perform
Laboratory diagnosis of tuberculosis requires a multimodality drug-sensitivity tests. Molecular targets usually include both an
approach, as well as recognition that empiric therapy often is insertion sequence and a 16S rRNA sequence.
appropriate. Two FDA-approved molecular tests are available for rapid
Diagnosis of tuberculosis is tricky, up to 20% of U.S. tuberculosis diagnosis: a revised Amplified Mycobacterium Tuberculosis
cases are clinically diagnosed. CDC surveillance data from 2004 Direct Test (MTD) by Gen-Probe, and the Mycobacterium
reveals 42% smear-negative and 17% culture-negative rates for Tuberculosis Test (MTT) by Amplicor.
pulmonary tuberculosis. Smear-negative index cases contribute Molecular Methods: Inflammatory Marker Measurements
to as much as 17% of newly transmitted cases. Inflammatory marker measurements exploit differences in
Laboratory features of a tuberculosis are the following: the predominating immune response to different pathogens.
Algorithm for the laboratory diagnosis of tuberculosis. Adenosine deaminase (ADA) and interferon gamma (IFN-ã)
Bacteriology and Microscopy sometimes are used to diagnose tuberculous effusions. Combined
PCR, ADA, and culture techniques have been used.
Tuberculosis is caused by a bacillus of the Mycobacterium Fluid Cell Counts and Chemistries, Nonspecific Changes
tuberculosis complex. Evaluation of sputum smears and tissue Fluid analysis may provide helpful clues in the diagnosis of
samples is accomplished with two main stains: Ziehl–Neelsen tuberculosis. Involved pleural, pericardial, and CSF fluid may
and auramine orange fluorescence.
Auramine orange fluorescence staining of three sputum samples
per patient detected 7 of every 10 cases. The false-positive rate
www.dosonline.org 89
manifest neutrophilia, although a lymphocytosis eventually Calmette-Guérin (BCG)-vaccinated persons, low sensitivity in
predominates. Protein is elevated and glucose levels may be low or people with weakened cellular immunity, and several logistic
low normal. Lactate dehydrogenase usually is elevated as effusions drawbacks.
most often are exudative. Persistent sterile pyuria in an ill patient Recent advances in mycobacterial genomics and human
should raise suspicion for tuberculosis cellular immunology have resulted in two new blood tests that
New technologies such as proteomics and microarrays may soon detect tuberculosis infection by measuring in vitro T-cell
find their place in the evaluation of patients. However, sputum and interferon (IFN)-b release in response to two unique antigens
tissue analysis remain the cornerstone of laboratory diagnosis. that are highly specific for Mycobacterium tuberculosis but
Diagnosing Latent Tuberculosis Infection in the 20th Century absent from bacille Calmette-Guérin (BCG) vaccine and most
nontuberculous mycobacteria. One assay, the enzyme-linked
The biology of latent tuberculosis infection (LTBI) is poorly immunospot (ELISpot) [T-SPOT.TB; Oxford Immunotec;
understood, and the condition has hitherto been defined by a Oxford, UK] enumerates IFN-b–secreting T cells, while the
positive tuberculin skin test (TST) result in an asymptomatic other assay measures IFN-ãconcentration in supernatant by
person exposed to tuberculosis with no clinical or radiographic enzyme-linked immunosorbent assay (ELISA) [QuantiFERON-
signs of active tuberculosis. The clinical relevance of this definition TB Gold; Cellestis; Carnegie, Australia]. A large and growing
is that it carries a small but significant forward risk of progression clinical evidence base indicates that both tests are more specific
to active tuberculosis, which is significantly increased in persons than the skin test because they are not confounded by prior BCG
with suppressed or immature (ie, young children) cellular immune vaccination. In active tuberculosis, ELISA has similar sensitivity
systems. Unfortunately, the TST has poor specificity in bacille to the skin test, while ELISpot is significantly more sensitive.
Author
Bobby Bhalhotra MD
Sah Hospital
(AN ISO 9001:2008 CERTIFIED HOSPITAL)
(Most Advance Centre of Eastern U.P.)
(Recognised Centre for Fellowship by ARC (AIOS)
Required
Ophthalmologist
(Surgeon with Experience in Phaco / Vitreo Retinal Surgery)
Freshers can also Apply
For Modern, Equipped Eye Hospital with Dedicated
• Eye Bank with Specular Microscope and DSAEK & DALK
• Cornea Centre with Confocal Microscope & Cross Linking
• Glaucoma clinic with CO2 Laser, Yag Laser, HFA & HRT
• Cataract with Cold Phaco, IOL Master and Multifocal & Toric IOL’s
• Vitreo Retinal setup with Acurus, FFA, Green Laser & HD OCT
• Carl Zeiss Lumera T Operating Microscope
• Refractive Surgery with Lasik Laser
• Charitable & Free Cases with Mobile Eye Unit
Salary will commensurate with experience
Accommodation will be provided.
Apply with detailed bio-data to
Dr. Sunil Sah, Chairman
Sah Hospital, J.12/9D, Ramkatora, Varanasi
Tel.: 0542-2202263, 64 Email: [email protected]
90 DOS Times - Vol. 16, No. 10,April, 2011
Forthcoming Events: National
April 2011 October 2011
15-17 New Delhi 7-9th Rishikesh, UTTARAKHAND
Annual Conference The VIII annual conference of UKSOS,
Delhi Ophthalmological Society UTTARA EYECON -11
Venue: Hotel Ashok, Chanakya Puri, New Delhi Himalayan Institute of Medical Sciences
Contact Person & Address Swami Ram Nagar, Rishikesh
Dr. Amit Khosla, Secretary DOS Contact Person
Room No. 2225, 2nd Floor, New Building, Dr. Renu Dhasmana,
Sir Ganga Ram Hospital, Uttara eyecon 11
Rajinder Nagar, New Delhi - 110 060 Department of Ophthalmology
Ph.: 011-65705229, E-mail: [email protected], Himalayan Institute of Medical Sciences
Website: www.dosonline.org Swami Ram Nagar, Dehradun
Mobile: 08954785343,
May 2011 Phone: 0135-2471355, 0135-2471440
29th PILIBHIT, UTTAR PRADESH Email: [email protected]
Mid-term Converence of UPSOS
UP State Ophthalmic Society October 2011
Conference Secretariat 9th Sitapur, u.p.
Dr. Vipin Sahni 1st Meeting of “Association of Children Eye Specialists
Kaushalya Devi Eye Institute of India” Regional Institute of Ophthalmology
Near Chhatari Chauraha, Pilibhit, U.P. Contact Person
E-mail: [email protected] Dr. V.B. Pratap
Website: www.practicesolutions.in Sitapur Eye Hospital, Sitaput, U.P.
(M): 91-9897504744 Mobile: 09336838343
E-mail: [email protected]
SITUATION VACANT
For
OPTHALMOLOGIST
For 60 bedded Modren Eye
Hospital[ Estd 1992]
Contact/Send CV to:
GANGA MATA EYE HOSPITAL
Sapat Rishi Link Road
HARIDWAR-249410
Fax: 01334260175
M: 09412931046
[email protected]
www.dosonline.org 93
Delhi Ophthalmological Society
submission online www:dosonline.org
(Life Membership Form)
Name (In Block Letters)________________________________________________________________________________________________
S/D/W/o_____________________________________________________________________________ Date of Birth____________________
Qualifications_________________________________________________________________________ Registration No._________________
Sub Speciality (if any)_________________________________________________________________________________________________
Address
Clinic/Hospital/Practice___________________________________________________________________________________________
______________________________________________________________________________ Phone________________________
Residence_____________________________________________________________________________________________________
______________________________________________________________________________ Phone________________________
Correspondence________________________________________________________________________________________________
______________________________________________________________________________ Phone________________________
Email _____________________________________________________________ Mobile No.______________________________
Proposed by
Dr.________________________________________________ Membership No.___________ Signature__________________________
Seconded by
Dr.________________________________________________ Membership No.___________ Signature__________________________
[Must submit a photocopy of the MBBS/MD/DO & State Medical Council / MCI Certificate for our records.]
I agree to become a life member of the Delhi Ophthalmological Society and shall abide by the Rules and Regula-
tions of the Society.
(Please Note : Life membership fee Rs. 3100/- payable by DD for outstation members. Local Cheques acceptable, payable to Delhi Ophthalmo-
logical Society)
Please find enclosed Rs.___________in words ____________________________________________________ by Cash
Cheque/DD No.____________________ Dated_____________ Drawn on______________________________________
Signature of Applicant Three specimen signatures for I.D. Card.
with Date
For Official Use Only
Dr._______________________________________________________________has been admitted as Life Member of
the Delhi Ophthalmological Society by the General Body in their meeting held on________________________________
His/her membership No. is _______________. Fee received by Cash/Cheque/DD No._______________ dated_________
drawn on __________________________________________________________________. (Secretary DOS)
www.dosonline.org 95
INSTRUCTIONS
1. The Society reserve all rights to accepts or reject the application.
2. No reasons shall be given for any application rejected by the Society.
3. No application for membership will be accepted unless it is complete in all respects and accompanied by a Demand Draft of
Rs. 3100/- in favour of “Delhi Ophthalmological Society” payable at New Delhi.
4. Every new member is entitled to receive Society’s Bulletin (DOS Times) and Annual proceedings of the Society free.
5. Every new member will initially be admitted provisionally and shall be deemed to have become a full member only after formal
ratification by the General Body and issue of Ratification order by the Society. Only then he or she will be eligible to vote, or apply
for any Fellowship/Award, propose or contest for any election of the Society.
6. Application for the membership along with the Bank Draft for the membership fee should be addressed to Dr. Amit Khosla,
Secretary, Delhi Ophthalmological Society, Room No. 2225, 2nd Floor, New Building, Sir Ganga Ram Hospital, Rajinder Nagar,
New Delhi - 110 060
7. Licence Size Coloured Photograph is to be pasted on the form in the space provided and two Stamp/ Licence Size Coloured
photographs are required to be sent along with this form for issue of Laminated Photo Identity Card (to be issued only after the
Membership ratification).
8. Applications for ‘Delhi Life Member’ should either reside or practice in Delhi. The proof of residence may be in the form Passport/
Licence/Voters Identity Card/Ration Card/Electyricity Bill/MTNL (Landline) Telephone Bill.
96 DOS Times - Vol. 16, No. 10,April, 2011
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