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Subspeciality-Retina

Type 2 NVE from the larger vessels. It is the most Type 3 NVE
Type 2 originate from the capillary common subtype.
plexus, and all NVEs are located in the The branches extended in the retina Type 3 originate from the sea-fan-like
CNP; all type 2 NVEs arise from the first and then breach the ILM to form IRMAs, and NVEs are located in the
inner nuclear layer (INL) and extended an neovascular complex (NVC). This CNP or at its margin, arising from the
in all directions. Many branches arise kind of NVC contain a large amount of INL and ganglion cell layer. This type
from the neovascular mass in the CNP dense ‘‘pier-like’’ structures and adhered of NVE is usually located in the CNP
and appear as an octopus. Type 2 NVEs firmly to the retina. [Fig 4] and is primarily located in the retina,
are located more peripherally and away except that some advancing tips which
may breach the ILM to form sea-fan-like
Figure 4: A type 2 neovascularization elsewhere (NVE) (A,B) Patient with PDR, The new NVEs firmly adhere to the retina [Fig 5].
vessel (arrow) is inconspicuous in the photograph and was confirm by FFA. (C) The octopus-
shaped neovascular mass (arrow) is isolated with major retinal vessels. (Flow scan) The Fig 6 schematic drawing demonstrate
initial layer of the new vessel is identified at inner nuclear layer (INL) (arrow). (D) Branches various morphologic features,
extended intraretinally (arrow) and then breach the ILM to form the neovascularization originating from various vessels and
complex extended in various ways in 3 types of
NVE and IRMA.
Type 3 NVEs are located more peripherally from the arcades and spanned the
affiliated major retinal veins. • OCTA feature of neovascularization
of disc (NVD)
Table 1- Classification of Neovascularization Elsewhere.[7]
NVD are defined as neovascular
Type 1 NVE Type 2 NVE Type 3 NVE complexes located in the disc or within
IRMA 1 disc diameter from the margin. NVDs
Origins Venous side Capillary Side GCL originat from the retinal veins, from the
Sea Fan retinal arteries, and from cilioretinal
Initial Layer NFL INL In arteries. Most NVDs arise from the
All Directions bending vessels near the rim of the
Shape Tree Octopus optic disc NVDs. In a similar manner to
the NVE originating from the venous
Location with CNPs At the margin In side, the NVD remains as only a primary
vessel before touching the posterior
Extension direction Towards CNPs All Directions hyaloid surface, and then sprouted
many branches to form NV networks.
[Fig 7]

On OCTA NVD appears as meandering
vessels and hyperreflectivity at vitreo
retinal interface.[8] [Fig 7A]

In conclusion OCTA is an emerging
technology that allows for the detection
of angiographic features of DR and
changes in the macular capillary
network, even before disease onset. It
can show much greater detail compared
with FA. It cannot show leakage but
can better delineate areas of capillary
dropout and detect early retinal
neovascularization. OCTA may be
useful in the near future for the earlier
diagnosis and better management of
DR.

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Figure 5: A type 3 neovascularization elsewhere (NVE) (A,B) Patient with PDR, the new vessel (arrow) is demonstrate in the fundus
photograph and is confirm by FFA. (C) The initial layer of new vessel was confirm as the ganglion cell layer (arrow). (D) The new vessels
are located at the margin of capillary nonperfusion (CNP), and the main parts of the new vessels are intraretinal (arrow), apart from some
advancing tips that may have breach the ILM (arrowhead).

Figure 6: Schematic drawings showing the characteristics of NVE and IRMA. (Top row) Stereo schematic drawings (Center row) En face
schematic drawings and (Bottom row) Layer segmentation schematic drawings of NVE and IRMA

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Figure-7: (A and B) En-face view at vitreoretinal interface on OCTA and structural OCT respectively, showing hyper-reflectivity
corresponding to the main trunk of vessel shown with arrow. (C)Cross-sectional OCTA showing plane of acquisition as the vitreoretinal
interface (arrow) (D) Radial peripapillary frame of OCTA shows meandering vessel shown by blue arrows not visible on the en-face view

References 5. A. Ishibazawa, T. Nagaoka, A. Takahashi neovascularization on optical coherence
et al., “Optical coherence tomography tomography angiography. Graefes Arch
1. Nentwich MM, Ulbing MW: Diabetic angiography in diabetic retinopathy: Clin Exp Ophthalmol 2017;255, 753–
retinopathy – ocular complications a prospective pilot study,” American 759.
of diabetes mellitus. World J Diabetes Journal of Ophthalmology, vol. 160, no.
2015; 6: 489–499. 1, pp. 35–44, 2015, e1. Corresponding Author:

2. Jau JW, Rogers SL, Kawasaki R, et al: 6. A. Couturier, V. Mané, S. Bonnin et al., Dr. Shalin Shah
Global prevalence and major risk factors “Capillary plexus anomalies in diabetic MS, Vitreoretina Services
of diabetic retinopathy. Diabetes Care retinopathy on optical coherence Dr. Shroff’s Charity Eye Hospital,
2012; 35: 556–564. tomography angiography,” Retina, vol. 5027-Kedar Nath Road, Daryaganj,
35, no. 11, pp. 2384–2391, 2015. New Delhi, India-110002.
3. JiaY,TanO,TokayerJ,etal.Split-spectrum
amplitudedecorrelation angiography 7. Pan J,ChenD,YangXetal:Characteristics
with optical coherence tomography. Opt of Neovascularization in Early Stages
Express 2012;20(4):4710–25. of Proliferative Diabetic Retinopathy
by Optical Coherence Tomography
4. Jia Y, Bailey ST, Wilson DJ, et al. Angiography. Am J Ophthalmol. 2018
Quantitative optical coherence Aug;192:146-156
tomography angiography of choroidal
neovascularization in age-related 8. Singh, A., Agarwal, A., Mahajan,
macular degeneration. Ophthalmology S. et al. Morphological differences
2014;121(7):1435–1444. between optic disc collaterals and

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Uveal Effusion Syndrome:
An Ongoing Uncertainty

Preeti Singh, MBBS, MS, Sonal Vyas, MBBS, MS, Ashish Mahobia, MBBS, MS, FNB
Sai Baba Eye Hospital, Raipur, Chhattisgarh

Abstract : Uveal effusion syndrome (UES) is a rare condition characterized by spontaneous serous detachment of the retina
and peripheral choroid. It typically involves middle-aged men and has a relapsing remitting course. UES may be idiopathic,
or associated with hypermetropia, and should be considered a diagnosis of exclusion. There is abnormal deposition of
glycosaminoglycans within the sclera which possibly reflects in increased scleral thickness seen histologically, that along
with disruption of collagen fibers may impair normal trans-scleral flow of fluid and contribute to effusion. An alternative,
and perhaps complementary hypothesis, is that thickened sclera compresses the transscleral vessels with resulting fluid
retention. Secondary changes within the retinal pigment epithelium are also observed. There is shifting of sub retinal fluid that
may involve the macula. Long standing disease may lead to secondary retinal pigment epithelial (leopard spot) changes and
permanently reduced visual acuity. There are various medical and surgical modalities of treatment have been described, but the
most common treatment is full thickness sclerectomies to provide an exit for choroidal fluid. UES is a serious condition that is
difficult to treat and can lead to severe and permanent visual loss.

Introduction and unilateral cases tend to occur in There are several studies by Ward
Uveal effusion syndrome (UES) older males. et al, Forrester et al and Uyama
is a grave condition which is thin et al. which show abnormal scleral
on the ground. It is characterized Etiopathogenesis composition.iv,v,vi Most light and
by transudation of fluid from electron microscopic studies
the choriocapillaris into the There are several suppositions suggest abnormal deposition of a
surrounding potential space, causing regarding the etiology of proteoglycan, with an appearance
engorgement and thickening of the UES. It may be idiopathic, or similar to glycosaminoglycans which
choroid or choroidal detachment associated with hypermetropia is expanding the space between
and may lead to secondary serous and nanophthalmos.iii The scleral collagen fibers. Some authors
(non rhegmatogenous) retinal principal abnormality lies in the have suggested that UES is a form
detachment. The syndrome typically choroid or sclera which includes, of mucopolysaccharidosis, with
occurs spontaneously and incessantly deposition of dermatan sulphate with
reported in healthy middle-aged I. reduced scleral protein some chondroitin sulfate.vii.viiiAnother
men, but it has also been reported permeability, commonly observed hallmark is
in children as young as 11 years old disruption and disorganization of
and females in 50% of cases in some II. reduced scleral hydraulic the collagen fibers and thickening of
series.i, ii UES is often associated with conductivity, the sclera. Many of these histological
severe visual loss due to chronic features are associated with
submacular fluid and secondary RPE III. vortex vein compression, nanophthalmos, where there is a
changes often difficult to diagnose. congenital scleropathy than UES per
Bilateral involvement is common, IV. increased choroidal vessel se, however, they are also observed in
permeability, eyes with idiopathic UES.

V. Chronic choroidal inflammation
and chronic hypotony.

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Vortex vein compression is based on axial length and thickness Intraocular pressure is normal
another possible causative factor in of sclera.xi It includes in patients with uveal effusion
pathogenesis of uveal effusion. It was syndrome.
first suggested by Schaffer in 1975 Type 1 (nanophthalmic eye, axial
in nanophthalmic eyes.ix This leads length <19 mm), Diagnostic Modalities
to relative obstruction of venous
outflow, give rise to congestion of Type 2 (nonnanophthalmic eye with B-scan ultrasound may show smooth,
the choriocapillaris and alter the abnormal thickened sclera dome-shaped membrane with little
transmural hydrostatic pressure documented on MRI), and aftermovement, choroidal thickening
gradient, advocate increased retention and inferior nonrhegmatogenous
of fluid in the suprachoroidal space. Type 3 (nonnanophthalmic eye retinal detachment.xiii A-scan shows a
without scleral abnormality) thick, 100% spike at tissue sensitivity,
which at low sensitivity can often
Ocular hypotony, may also cause Clinical Features be seen to be double-peaked.xiii In
early presentations of uveal effusion
UES as it decreases the driving force UES follows relapsing-remitting syndrome, the only evidence for
clinical course. Patients with ciliochoroidal effusion may be subtle
for transscleral protein flow and UES complain of blurred vision degrees of supraciliary effusion
or metamorphopsia but gradual on high-frequency ultrasound
increases the transmural hydrostatic superior visual field loss is the biomicroscopy. As an approximate
most common initial complaint.ii guide, a posterior scleral thickness of
pressure gradient. Vascular Clinically on fundus examination greater than 2 mm is abnormal, and
there is ciliochoroidal detachment significantly more than the expected
competence maybe compromised by as uniform brownish color, solid normal value of 1 mm.
elevations typically begins in the
inflammation, which then increases periphery with smooth, convex Fluorescein Angiography shows
surfaces.vi The undulation is not leopard-spot appearance of hyper-
capillary protein permeability and appreciable on ocular movements fluorescence and hypofluorescence.
which differ it from rhegmatogenous Indocyanine green angiography
accumulation of protein in the retinal detachments. In early stage, shows diffuse granular choroidal hy-
the ora serrata is visible without perfluorescence in the early phase,
extravascular space. This reduces the the use of scleral depressor. There is indicating marked hyperpermeabil-
marked shifting of sub retinal fluid ity of the choroidal vessels.vi This
colloid osmotic pressure gradient and with changes in head position. This choroidal hyperfluorescence persists
shifting is due to abnormally high into the late-phase angiogram and
the absorption of extravascular fluid concentrations of serum proteins, becomes more diffuse, demonstrating
into the capillaries. primarily albumin in sub retinal fluid. increased accumulation of fluid in
Typically four-lobed configuration is the choroid.
Classifications created from the attachment of the
The two common classifications of choroid to the sclera at the vortex vein Spectral-domain optical coherence
UES are ampullae. Chronic serous effusion and tomography may show focal
1. Classification given by DR ROBERT sub retinal fluid accumulation leads thickening of the retinal pigment
to depigmentation and multifocal epithelium layer corresponding to
J. BROCKHURST.x hyperplasia of the retinal pigment the areas of leopard spots. xiv
epithelium. In literature it is described
Inflam- 1. Trauma, intraocular as leopard skin spots, tessellation, Diagnosis of uveal effusion syndrome
matory surgery and pseudoretinitis pigmentosa.xii On is made clinically and by excluding
gonioscopy dilated episcleral veins other causes of uveal effusion.
2. Uveitis, sympathetic and blood in Schlemm’s canal may The differential diagnosis may be
ophthalmia be seen. Secondary uveal effusion labelled by other factors causing
may be associated with anterior ciliochoroidal effusion.
3. Vogt-Koyanagi-Harada chamber inflammation or hypotony.
Mild vitreous cells may be present.
4. Scleritis, infected buckle

5. Pan retinal
photocoagulation

Hydro- 1. Dural arteriovenous
dynamic fistula

2. Hypotony, wound leak
3. Nan-ophthalmos

Idiopathic

Neoplastic

2. Uyama et al by their studies on 19
eyes grouped UES into three types

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Subspeciality-Retina

Differential Diagnosis of Ciliochoroidal Effusions:

Scleropathies Hydrodynamic factors Inflammatory factors Neoplastic conditions

Congenital Ocular hypotony • After trauma or surgery • Metastatic carcinoma
• Uveal effusion • Wound leak
syndrome • Overfiltration • After photocoagulation or • Malignant melanoma
• Nanophthalmos • Cyclodialysis cryotherapy
• Penetrating ocular trauma • Lymphoproliferative
• Rhegmatogenous retinal detachment • Drug reaction and melanocytic
• Ciliary body dysfunction choroidal infiltration
• Uveitis

• Scleritis

• Orbital cellulitis

• Idiopathic orbital inflammation

Acquired Elevated uveal venous pressure

• Amyloidosis • Arteriovenous fistula

• Mucopolysaccha- • Sturge–Weber syndrome

ridosis • Idiopathic prominent episcleral vessels

• Vortex vein compression

• Valsalva maneuver

Malignant hypertension

Management of sclerectomy. The glaucoma filtration choroid through the sclera. Delayed
The studies on management of UES device (Ex-press shunt) can also be used diagnosis and treatment of these
suggest that it is refractory to medical to makes sclerotomies patent.xix patients may lead to permanent loss
treatment. On other hand some of vision.
reports have mentioned systemic Combined approach of sclerectomies Financial Disclosures- None
steroids and immunomodulating and pars plana vitrectomy for Conflicts of Interest – None
agents as a very good modality for macula-off nonrhegmatogenous Acknowledgements – None
treating UES.xv,xvi Other proposed retinal detachment in uveal effusion
nonsurgical therapies like local steroids, syndrome allows immediate References
laser photocoagulations, prostaglandin approximation of the photoreceptors
analogue and NSAIDs.xvii and the retinal pigment epithelium 1. Casswell AG, Gregor ZJ, Bird AC.
and prevents further photoreceptor The surgical management of uveal
cell death and hence the visual loss. effusion syndrome. Eye.1987;1:115-
It is reported by Gass in 1983 119.
that ciliochoroidal effusion and
nonrhegmatogenous retinal Conclusion 2. Jackson TL, Hussain A, Morley AM et
detachment can be successfully The diagnosis of uveal effusion al. Scleral hydraulic conductivity and
treated in patients with uveal syndrome is based on characteristic macromolecular diffusion in patients
effusion syndrome by quadrantic clinical findings and exclusion of the with uveal effusion syndrome. Invest
partial-thickness sclerectomy.xi In other known causes of ciliochoroidal Ophthalmol Vis Sci. 2008;49:5033-
1980, Brockhurst reported successful effusion and nonrhegmatogenous 5040.
reattachment of the retina and retinal detachment. Imaging
resolution of ciliochoroidal effusion modalities can be useful for making 3. Elagouz M, Stanescu-Segall D, Jackson
in nanophthalmic eyes after surgical diagnosis and for exclusion of TL. Uveal effusion syndrome. Surv
decompression of the vortex veins.xviii other causes of choroidal effusion. Ophthalmol. 2010 Mar 4;55(2):134-
Goal of the surgical intervention is the However some eyes may respond 145.
drainage of sub retinal fluid, reduction well to treatment with oral, topical,
of sclera resistance and deroofing of or periocular corticosteroids, many 4. Forrester JV, Lee WR, Kerr PR, et
vortex veins. Some studies also shown will require surgical intervention to al. The uveal effusion syndrome
the use of mitomycin C for maintenance facilitate the flow of fluid from the and trans-scleral flow. Eye (Lond).
1990;4:354–365.

5. Ward RC, Gragoudas ES, Pon DM, et
al. Abnormal sclera findings in uveal

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Subspeciality-Retina

effusion syndrome. Am J Ophthalmol. Ophthalmology 2000;107:441-9 18. Brockhurst RJ. Vortex vein
1988;106:139–146. [PUBMED] decompression for nanophthalmic
uveal effusion. Arch Ophthalmol.
6. Uyama M, Takahashi K, Kozaki 12. Green RL, Byrne SF. Diagnostic 1980;98:1987–1990.
J, et al. Uveal effusion syndrome: ophthalmic ultrasound. Ryan SJ.
clinical features, surgical treatment, Retina. Mosby: St. Louis; 1989. 19. Yepez JB, Arevalo JF. Ex-Press shunt
histologic examination of the for choroidal fluid drainage in
sclera, and pathophysiology. 13. Olsen TW, Aaberg SY, Geroski uveal effusion syndrome type 2: a
Ophthalmology. 2000;107:441–449. DH, Edelhauser HF. Human sclera: potentially novel technique. JAMA
thickness and surface area Am J Ophthalmol. 2015;133(4):470-471.
7. Ward RC, Gragoudas ES, Pon DM, Ophthalmol. 1998;125:237-241.
Albert DM. Abnormal scleral findings Corresponding Author:
in uveal effusion syndrome. Am J 14. Okuda T, Higashide T, Wakabayashi
Ophthalmol. 1988;106:139-146. Y, et al. Fundus autofluorescence and Dr. Preeti Singh
spectral-domain optical coherence MBBS, MS
8. Forrester JV, Lee WR, Kerr PR, Dua tomography findings of leopard spots Sai Baba Eye Hospital, Raipur,
HS. The uveal effusion syndrome and in nanophthalmic uveal effusion Chhattisgarh
trans-scleral flow. Eye. 1990;4:354- syndrome. Graefes Arch Clin Exp
365. Ophthalmol. 2010;248:1199–1202.

9. Calhoun FP Jr. The management of 15. Johnson MW, Gass JD. Surgical
glaucoma in nanophthalmos. Trans management of the idiopathic uveal
Am Ophthalmol Soc. 1975;73:97–122. effusion syndrome. Ophthalmology.
1990;97(6):778-785.
10. Gass JD. Uveal effusion syndrome:
a new hypothesis concerning 16. Gass JD. Uveal effusion syndrome:
pathogenesis and technique of a new hypothesis concerning
surgical treatment. Transactions of pathogenesis and technique of
the American Ophthalmological surgical treatment. 1983. Retina.
Society. 1983;81:246 2003;23(6 Suppl):159-163.

11. Uyama M, Takahashi K, Kozaki J, 17. Jackson TL, Hussain A, Salisbury J, et
Tagami N, Takada Y, Ohkuma H, al. Transscleral albumin diffusion
et al. Uveal effusion syndrome: and suprachoroidal albumin
Clinical features, surgical concentration in uveal effusion
treatment, histologic examination syndrome. Retina. 2012;32(1):177-
of the sclera, and pathophysiology. 182

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A Classic Case of
Neurocysticercosis with an
Unusual Involvement of Inferior
Rectus Muscle

Nisarga R. Rane, Shwetambari G. Singh, Shivna K. Thaker, Anuja T. Bhatt,
Department of Ophthalmology, NHL Municipal Medical College, Ahmedabad

Introduction medications by a physician. There was Figure 2: A. MRI showing cyst in inferior
Cysticercosis is infestation by no history of fever, headache, vomiting, rectus muscle B. B-scan showing cystic
Cysticercus cellulosae, the larval limb paresis, and mouth deviation or lesion in inferior rectus muscle
form of Taenia solium. Humans get slurring of speech.
infected by ingestion of cysticerci The best-corrected visual acuity in muscle belly of inferior rectus muscle
in undercooked pork or water and both eyes was 6/6. Intraocular pressure of the left eye [Figure 2: A]. MRI brain
food contaminated with its eggs. was within normal range. There was revealed a solitary small cyst and with
Ocular cysticercosis is a preventable no axial proptosis but the left eye was an eccentric focus in the left parietal
and eradicable cause of blindness slightly displaced upwards [Figure 1]. region with associated mild perifocal
endemic in India, commonly among Extraocular movements of the left eye edema.
low socioeconomic groups and areas were restricted in the upward direction. Contact B-scan ultrasonography of
having poor hygiene.(1) The main Slit-lamp examination of anterior left eye showed a well-delineated
sites of cyst lodgement are skeletal and posterior segments, cranial nerve
muscles and subcutaneous tissues. The examination, and the remaining
involvement of eyeball and orbit is extraocular muscle examination were
relatively rare. within normal limits.
This case, reports classic cysticercosis
of the brain with atypical involvement Figure 1: Upward displacement of the left
of inferior rectus muscle in a 16-year- eye
old girl with a review of the literature A provisional diagnosis of inferior
of extraocular muscle form of quadrant orbital tumour was made
cysticercosis. and an MRI brain with orbits (Plain
+ contrast) was advised, which
Case report revealed a well-defined cystic lesion
A 16-year-old female, presented with a (approximately 13*10*6 mm;
complaint of double vision in upgaze hypointense in T1; hyperintense on
in the left eye for three months. There T2) with tiny eccentric hypointense
were no complaints of diminution speck suggestive of scolex in the
of vision, painful eye movements,
retro-orbital pain, or protrusion of
the eyeballs. There was history of two
episodes of seizures a month back for
which she was started on anti-epileptic

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cystic lesion with hyperechoic area visits showed resolution of previously Amongst the orbital tissues, the
suggestive of scolex in left inferior seen cysticercal lesion. At the end extraocular muscles are most
rectus muscle [Figure 2: B]. A diagnosis of six-month follow-up, there was commonly involved. The commonest
of inferior rectus ocular cysticercosis no recurrence of seizures or ocular site for extraocular muscle form
of the left eye along NCC was made. symptoms. remains debatable. Few studies report
A complete systemic examination that superior rectus muscle as the most
included routine blood investigation Discussion common site.(4) While few report
and stool culture, was done. There was The first case of ocular cysticercosis the lateral rectus, medial rectus,
marked eosinophilia and raised ESR. was reported by Sommering in 1830. and superior oblique muscles, to be
The patient underwent complete It can be extraocular (in the affected to a greater extent.(5) Another
neurological evaluation and was subconjunctival or orbital tissues) or case reports the association of multiple
started on oral albendazole (15 mg/ intraocular (in the vitreous, subretinal brain NCC with orbital cysticercosis
kg/day in two divided doses) and oral space, or anterior chamber) infestation. involving levator palpebral superioris
prednisolone (1mg/kg/day), tapered Indian literature, contradictory to and superior rectus muscle.(6) One
over four-sixweeks,andcarbamazepine Western literature reports extraocular study has reported ocular cysticercosis
was started by a neurologist as the form as the most common site of involving the levator palpebrae
diagnosis of secondary epilepsy involvement.(2) superioris and superior rectus muscle
was established. The patient was Recent studies show a switch from the of the right eye.(7) A review of the
observed by both the ophthalmology subconjunctival space to orbit as the literature shows the inferior rectus
and neurology departments. Serial most common site of cyst lodgement.(3) as an unusual site of involvement for
monthly B-scan and MRI on follow-up the extraocular form of cysticercosis.
[Table: 1]

Table 1: Review of literature

Authors/Year Age/Gender Extraocular muscle Associated Treatment/ Final outcome
involved/ Clinical Neurocys-
Mehrotra S K/ 7 years old presentation ticercosis Surgical removal of cyst (involved
1975 part of medial rectus)- Recurrence
Medial rectus/ progressively No of 3 cysts at same site
increasing eyelid swelling Excision biopsy; oral steroids-
Partial resolution of the restricted
Hélio Angotti N 38 years old; Female Superior rectus/ pain, lid No motility
No Albendazole+steroids (oral)-
et al/ 2007 edema, hyperemia, restriction No Spontaneous cyst extrusion
No
of right eye downgaze No Albendazole+steroids (oral)-
Improvement in symptoms
Basu S et al/ 9 years old; Female Superior rectus/ pain, ptosis of
2009 the upper eyelid and restricted Albendazole+steroids (oral)-
ocular motility Improvement in symptoms

Shadangi P et 16 years old; Female Inferior rectus/ unilateral Albendazole+steroids (oral)-
al/ 2010 eccentric proptosis and Improvement in symptoms
restriction of upward gaze

Meenu Babber 19 years old; Female Inferior rectus/ periocular
et al/ 2013 pain, swelling, hyperemia,
restriction of up gaze

Kirti jain et al/ 6 years old; Male Levator Palpebrae
2013 Superioris+Superior Rectus/
increasing swelling, drooping
of eyelid

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Subspeciality-Strabismus

Sanjiv Gohel et 13 years old; Female Inferior rectus/ lower lid No Albendazole+steroids (oral)-
Yes Improvement in symptoms
al/ 2015 swelling, diplopia
No Anti-epileptics; Albendazole+
Akhilesh K S et 30 years old; Female Bilateral extra ocular muscles/ praziquantel+ steroids (oral)-
al/ 2015 headache, generalized tonic- Improvement in symptoms with
clonic seizures; protrusion of NO rcurrence of convulsions
both eyes
Surgical excision of the superior
Ding J et all/ 28 years old; Male Superior oblique/ painless oblique muscle- Persistence of
2015 orbital swelling, diplopia in diplopia, mild restriction in up-
upgaze, high fever gaze

Sujit Das et al/ 10 years old; Female Superior palpebral fissure/ No Albendazole+steroids (oral)-
2017 Improvement in symptoms
bluish-colored swelling bellow
Anti-epileptics; Albendazole+
upper eyelid praziquantel+ steroids (oral)-
Improvement in symptoms with
André 38 years old; Male Lateral rectus/ convulsions; Yes NO rcurrence of convulsions
Rodrigues et al/ conjunctival hyperaemia
2017 Albendazole+steroids (oral)-
Improvement in symptoms
Chowdhury S 10 years old; Male Superior rectus/ protrusion of No
et al/ 2019 eyeball Albendazole+steroids (oral)-
Improvement in symptoms
Nilanjan 20 years old; Female Medial rectus/ esotropia, head No
Kaushik tilting, redness Pterional craniotomy, optic nerve
Thakur et al/ decompression with cyst excision;
2020 Albendazole+steroids (oral)-
Improvement in ptosis with no
Rajnish Kumar 23 years old; Male Superior rectus involvement No visual recovery
P et al/ 2020 at the orbital apex+optic nerve
compression/ ptosis+complete
loss of vision

Extraocular cysticercosis can have study (8), ELISA with larval somatic and the importance of a multidisciplinary
varied clinical presentations like excretory-secretory (ES) antigens was approach in early diagnosis and
proptosis, acquired ptosis, diplopia, positive in few cases. prompt management of such cases
pain, restricted ocular motility, Imaging techniques like orbital for good visual rehabilitation and
strabismus, diminished vision, ultrasound (B-scan), CT scan, or prevention of any serious sequel.
subconjunctival cyst, lid edema, Magnetic Resonance Imaging establish Wide-reaching public health measures
and orbital cellulitis like clinical the diagnosis and help to rule out are required for the eradication of this
impression depending upon the neurocysticercosis. disease.
location of the involvement, number Medical treatment is recommended for
of lesions, and the host immune extraocular cysticercosis. (9,1) Conclusion
response. The current case is an exceptional one This case highlights the importance
The diagnosis is established based on as it reports extraocular cysticercosis of keeping cysticercosis as one of
clinical, serological, and radiological of inferior rectus muscle along with the possible diagnoses especially in
findings. neurocysticercosis. patients coming from endemic areas,
Serological tests may be performed but The authors also intend to focus on along with appropriate diagnostic
their specificity is only 50%. In a recent modalities which are required to

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Subspeciality-Strabismus

establish an accurate diagnosis and Ophthalmology. 2010 Mar; 117(3):600- 9. Extraocular muscle cysticercosis:
initiate treatment to prevent probable 5, 605.e1. clinical presentations and outcome of
visual loss. treatment.
5. Sundaram PM, Jayakumar N,
References Noronha V. Extraocular muscle Mohan K, Saroha V, Sharma A, Pandav
cysticercosis - a clinical challenge to S, Singh U
1. Pushker N, Bajaj MS, Chandra M, Neena. the ophthalmologists. Orbit 2004;
Ocular and orbital cysticercosis. Acta 23(4):255-62. J Pediatr Ophthalmol Strabismus. 2005
Ophthalmol Scand 2001; 79:408-13. Jan-Feb; 42(1):28-33.
6. Verma R., Jaiswal A. Multiple brain
parenchymal neurocysticercosis Corresponding Author:
2. Sekhar GC, Lemke BN. Orbital
cysticercosis. Ophthalmology. with extraocular muscle cysticercosis Dr. Nisarga R. Rane
affecting levator palpebral superioris Department of Ophthalmology,
1997;104:1599–1602. and superior rectus complex: an NHL Municipal Medical College, Ahmedabad
27/C Nandigram Society-2 Sindhwai Mata Road
3. Orbital cysticercosis: clinical unusual association. BMJ Case Rep. Manjalpur, Vadodara, 390004
manifestations, diagnosis,
2013;25
management, and outcome. Rath
S, Honavar SG, Naik M, Anand R, 7. Agrawal S., Somesh Ranjan, Mishra A.
Ocular myocysticercosis: an unusual
Agarwal B, Krishnaiah S, Sekhar GC case of ptosis. Nepal J Ophthalmol.
Ophthalmology. 2010 Mar; 117(3):600- 2013;5:279–281.
5, 605.e1.
8. Sahu PS, Sahu PK, Parija SC. Diagnosis
4. Orbital cysticercosis: clinical of cysticercosis in eye and treatment
manifestations, diagnosis, follow-up of extra ocular forms by
management, and outcome. Rath serum IgG ELISA. Int J Ophthalmic
S, Honavar SG, Naik M, Anand R, Pathol. 2015;4:1.
Agarwal B, Krishnaiah S, Sekhar GC

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Systemic Disease and Eye

An Unusual Presentation of
Miliary Tuberculosis : An Eye
Opener for us!

Rutva Shah, Devendra Saxena
Shri Krishna Hospital , Karamsad, Anand, Gujarat.

Case
A 43 year old male presented to the
eye out patient department with chief
complaint of sudden, painful, loss of
vision and redness in his left eye since
20 days.The patient was a known case
of sputum positive miliary tuberculosis
with severe anaemia and alcoholic liver
disease and was on CAT I AKT since 4
months. The patient was seronegative
for HIV, HCV, HBsAG and RPR.
On ocular examination , the findings
were as under: [table 1][figure 1]

Figure 1: photo of left eye showing pre-operative temporal sectoral congestion

Table 1 - Showing pre operative ocular ON FUNDUS EXAMINATION: retinal detachment.[figure 3]
examination findings RE Fundus findings were: Media: clear, B-SCAN ultrasonography findings were
Disc :normal, but choroidal tubercle as follows : [figure 4]
was found at the supero-temporal y Fairly defined, large round to oval
arcade.[figure 2]
shaped hypo-echoic area measuring
LE fundus findings were : Media: clear, 2.0x1.7x1.5 cm was noted in left
Disc :normal, Cells present in vitreous, temporal aspect of choroid region
choroidal abscess involving macula was which is bulging over the vitreous
found; leading to infero-nasal exudative cavity and showing minimal

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Systemic Disease and Eye

Figure 2: Fundus photograph of right eye showing choroidal tubercle at supero-temporal peripheral vascularity- suggestive
arcade of choroidal abscess with minimal
liquefaction.
y Retinal detachment noted over
infero-nasal aspect.
y Axial length of left eye measures:
2.17cm.
y Optic disc appears normal.
Provisional diagnosis: Based on the
above findings a presumptive Diagnosis
of Left eye exudative retinal detachment
secondary to choroidal abscess was
made.

Plan of management
Systemic Steroids were given
concomitantly with AKT for 2
weeks in tapering doses along with
topical steroids in order to reduce
inflammation and tissue damage from

Figure 3: Colour fundus photograph of left eye showing choroidal abscess involving
macula

Figure 4: b-scan findings of left eye. Figure 5: Intra-operative photograph
showing external drainage of choroidal
www.dosonline.org/dos-times abscess with AC maintainer in place.

DOS Times - Volume 26, Number 5, March-April 2021 63

Systemic Disease and Eye

delayed hypersensitivity. But there of post-operative necrosis on fundus y Ocular TB is a rare finding. In INDIA
was no improvement in patient’s examination, but there was a retinal tear incidence of ocular TB ranges from
ocular condition with conservative infero-temporally at drainage site. On 0.5 to 9.8%. In cases with ophthalmic
management; rather the ocular follow up after 10 days, the visual acuity involvement, any part of the eye
condition deteriorated and the of left eye was PL+, PR FAULTY (nasally) or the orbit can be affected. Three
congestion and the infero-temporal HM +, COUNTING FINGERS CLOSE classic forms of ocular tuberculosis
bulge on the sclera increased .The TO FACE TEMPORALLY and fundus have been described. Direct ocular
patient was on AKT since 4 months examination showed diffuse vitreous infection from an exogenous
and yet the abscess did not resolve. The haemorrhage [figure 6]. However no source may involve ocular adnexa,
patient was explained about no visual retinal detachment was found. The conjunctiva, sclera, or cornea.
prognosis. The abscess was drained vitreous haemorrhage resolved within The second form results from a
under local anaesthesia. The sclerotomy one month and there was secondary hypersensitivity reaction to distant
site was posterior to ora serrata and scar formation at the site of drainage. foci of infection causing episcleritis,
anterior to the equator; and anterior phlyctenulosis, and occlusive retinal
chamber maintainer was used [figure Discussion vasculitis of the type observed in
5]. Approximately 10 cc of abscess y Tuberculosis (TB) is an airborne Eales disease. The third form relates
along with the irrigating solution was to the hematogenous spread of M.
drained and sample was sent for CB- communicable disease that mostly tuberculosis from pulmonary or
NAAT (cartridge based –nucleic acid commonly involves lungs. Nearly extrapulmonary sites.[2] The clinical
amplification test) report(to test the one third of the world’s population manifestations of ocular tuberculosis
sensitivity to anti-tubercular drugs) and is latently infected with TB, and are : [table 2]
rifampicin sensitivity was confirmed. more than 9 million new cases
are diagnosed each year, 95% in y Most common presentation of ocular
Post operative findings developing countries. Ocular TB tuberculosis is posterior uveitis. It can
Patient was relieved of his ocular may not be associated with clinical be seen both in immunocompetent
symptoms ; Visual acuity of the evidence of pulmonary TB; up to 60% and immunocompromised patients.
patient on the next post operative day of patients with evidence of extra
in left eye was PL+,PR FULL, HM +, pulmonary TB may not not have y Choroidal tuberculosis has not
COUNTING FINGERS CLOSE TO FACE diagnosed pulmonary TB. Ocular been so commonly reported.
TEMPORALLY. There were no signs TB may be initial presentation of It is possible that many case of
extra-pulmonary dissemination of choroidal tuberculosis remain
infection.[1] asymptomatic and probably regress
with the anti-tubercular treatment
Figure 6: Post operative fundus photograph of left eye showing resolving vitreous for extra- ocular tuberculosis.
haemorrhage. Choroidal involvements include
multifocal choroiditis, tubercles and
tuberculomas. It usually presents
as multifocal choroiditis. Choroidal
granuloma (tubercle) is focal
elevated dome shaped yellowish
lesion with discrete borders that
maybe unilateral or bilateral and
solitary or multiple usually found at
posterior pole. A very large abscess
like tubercle is called tuberculoma.
Large tuberculomas may undergo
liquefactive necrosis and form
yellowish sub-retinal abscess with
little vitreous inflammation. It may be
associated with an exudative retinal
detachment with variable vitreous
inflammation[3]. Rarely, subretinal
abscess can rupture into vitreous
cavity leading to endophthalmitis or
panophthalmitis . Vascular occlusion
with extensive ischaemia and pre-

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Systemic Disease and Eye

retinal or disc neovascularization points anterior to the equator. The 4. Yanoff, M., Duker, J.S., Augsburguer,
can occur. Macular complications liquefaction of choroid tubercle can be J.J. and Al, E. (2014). Ophthalmology.
include cystoid macular edema and diagnosed by B-scan ultrasonography Philadelphia: Elsevier Saunders, page
epiretinal membrane formation. and the drainage incision is put along 718.
the maximum distance of abscess from
Conclusion retina to prevent perforation. Corresponding Author:

A case of choroidal abscess is usually References Dr. Rutva Shah
MS Ophthalmology, MBBS
drained internally by performing 1. American Academy of Ophthalmology. 20, Ashoknagar Society, Meghani Marg,
internal retinotomy / PPV + INTRA- (2020). Ocular Tuberculosis (TB) - Asia Near Swastik Chowk, Behind Ajramar Flats,
VITREAL GAS/SILICON OIL Pacific. [online] Available at: https:// Surendranagar, 36300,1Gujarat, India.
INJECTION WITH/WITHOUT www.aao.org/topic-detail/ocular-
RETINAL LASER[4]. But the patient tuberculosis-tb--asia-pacific-2
was not willing to undergo extensive
surgery and hence external drainage 2. Schachat AP, Wilkinson CP, Hinton DR,
of the choroidal abscess was done. Sadda SVR, Wiedemann P. Ryans retina,
There was secondary scar formation 6 ed. Philadephia: Elsevier; 2018, page
at the site of drainage and no retinal 1657-1658.
detachment was noted subsequently.
Hence external drainage of choroidal 3. L C DUTTA . modern ophthalmology, 3
abscess is a good option if the abscess ed. new delhi: jaypee brothers medical
publisher (P) Ltd; 2005, page 1135.

www.dosonline.org/dos-times DOS Times - Volume 26, Number 5, March-April 2021 65

PG Corner

Pathological Myopia-
Understanding it’s Classification

Priyangee Sen1, MS, Shrishti Ahuja2, MBBS
1. Associate Professor, Dept of Ophthalmology, F.H. Medical College and Hospital, Etmadpur, Agra
2. Dept of Ophthalmology, F.H. Medical College and Hospital, Etmadpur, Agra
Abstract : Pathological Myopia(PM) is one of the leading cause of vision loss worldwide and a great social and financial burden.
It causes decrease in best corrected visual acuity due to complications specific to PM such as myopic maculopathy and posterior
staphyloma.This article describes the different classification systems used to define the various fundus changes seen in PM.

• What is pathological myopia? 1. Defective Vision track lesions with or without retinal
holes/ tears.
Defined as presence of myopic 2. Muscae volitants i.e., floating black • Total retinal atrophy
maculopathy equal to or more severe opacities in front of eyes. • Posterior Staphyloma
than diffuse chorio-retinal atrophy. • Degenerative changes in vitreous-
3. Night blindness ( in very high Liquefaction, Vitreous opacities,
• How is pathological myopia myopes) PVD.
classified?
• WhataretheSignsofPathological • What are the complications of
META-PM Classification – Divides Myopia? Pathological Myopia?
myopic maculopathy into 5 categories :- • Posterior Staphyloma.
• Prominent eyeballs • Retinal Detachment
Category 0 - No myopic Retinal lesions. • Large Cornea • Complicated Cataract
Category 1 - Tesselated fundus only. • Deep Anterior Chamber • Vitreous Haemorrhage
Category 2 - Diffuse chorioretinal • Large & sluggishly reacting pupils • Choriodal Haemorrhage
atrophy. • Strabismus Fixus Convergence.
Category 3 - Patchy chorioretinal On Fundus Examination :- • How do you define and classify
atrophy. Posterior Staphyloma ?
Category 4 - Macular atrophy. • Large & Pale optic disc, myopic • Defined as “an outpouching of
crescent at temporal edge. wall of eye that has radius of
‘PLUS SIGNS’ – Additional features curvature that is less than the
added to these categories :- • Peripapillary crescent encircling the surrounding curvature of wall of
disc may be present. eye”.
• Lacques cracks
Degenerative changes in Retina & Curtin Classification –
• Myopic choroidal Choroid – ( depends on location and extent )
neovascularisation (CNV) • Chorioretinal atrophic patches at • Types 1 to V – Primary staphylomas.
• Types VI to X – Combined
• Fuchs spot. macula
• Foster fuch’s spot at macula (Dark staphylomas.
According to META-PM STUDY
– Pathological Myopia is defined as red circular patch due to sub-
myopic maculopathy category 2 or retinal neovascularisation & retinal
above, or presence of staphyloma. haemorrhage).
• Cystoid degeneration at the
• What are the symptoms of periphery.
Pathological Myopia? • Lattice degeneration &/or snail

66 DOS Times - Volume 26, Number 5, March-April 2021 www.dosonline.org/dos-times

PG Corner

Ohno- Matsui Classification – 2) Patchy Chorioretinal Atrophy – irregular lines deep to retina
On basis of 3D MR I images, eye shapes • Appears as well – defined, configured in radiating fashion
of PM were classified into 4 types :- greyish- white lesions in macular emanating from optic disc.
• Nasally distorted shape area. - Results From breaks in weakened
• Temporally distorted shape
• Cylinder shape & • Characterised by complete loss of Bruch’s membrane.
• Barrel shape. choriocapillaries, & can progress • Choroidal rupture – breaks in
to absence of outer retina & RPE.
Ohno – Matsui Simplified choroid,Bruch’s membrane & RPE
Classification in 6 types :- 3) Lacquer Cracks – Yellowish- linear that results from blunt trauma.
• Wide Macular lesions in macula. (Horizontal or - Curvilinear lines , parallel to
• Narrow Macular vertical cracks)
• Peripapillary optic disc, mostly on temporal
• Nasal • Seen as criss-cross over side.
• Inferior & underlying choriodal vessels
• Others. 4) MYOPIC CNV - Common cause
• Represent mechanical breaks of of loss of central vision in patients
• What are the various Myopic bruch membrane with PM.
Maculopathy lesions?
• On FA –> show hyper –>Typically appears as flat, small,
1) Diffuse Chorioretinal Atrophy – fluorescence grayish subretinal lesion beneath
• Yellowish – White appearance of or near fovea with or without
posterior pole. In Late Phase of ICGA –> show hemorrhage.
• Extent varies from a restricted hypo- fluorescence
area around optic disc & part of –>Minimal subretinal fluid or
macula to entire posterior pole. • How to differentiate between exudative changes associated c -
On OCT –> Choroidal thinning Lacquer cracks, angioid streaks & myopic CNV.
is disproportionately remarkable choroidal rupture?
compared with thinning of retina FA –> shows well- defined hyper
& Sclera. • Lacquer cracks – fluorescence. (In early phase)
Fine,irregular,pale-yellow or white
lines radiating in stellate or reticular –> Classical CNV pattern of leakage.
pattern in posterior pole of highly (in late phase)

myopic eyes. OCT –> CNV appears as subretinal
elevation.
- Represent breaks in Bruch’s
membrane. Serous RD is seen around CNV

- Not associated with any Rx – 1st line – Anti-VEGF therapy
underlying systemic disease. (Intravitreal Bevacizumab,

• Angioid streaks – Bilateral, narrow, Ranibizumab, Verteporfin)

www.dosonline.org/dos-times DOS Times - Volume 26, Number 5, March-April 2021 67

PG Corner

• Choroidal Neovascularisation – distortion of papillary & peripapillary 5. Wong TY, Ferreira A, Hughes R, et
Related Macular Atrophy – regions, structural abnormalities occur. al. Epidemiology and disease burden
of pathologic myopia and myopic
• After regression of myopic CNV • OCT – Pit like clefts at outer border of choroidal neovascularization: an
with or without anti- VEGF therapy, optic disc or within adjacent scleral evidence-based systematic review. Am J
well- defined macular atrophy crescent may be found in highly myopic Ophthalmol. 2014;157:9–25, e12.
gradually develops around scassed eyes.
CNV. 6. Verkicharla PK, Ohno-Matsui K, Saw SM.
• Pits located in optic disc area, in optic Current and predicted demographics
Site where myopic CNV penetrates into disc pits, or in conus area & conus pits, of high myopia and an update of
retina is originally a Bruch’s membrane outside optic disc. its associated pathological changes.
hole. Ophthalmic Physiol Opt. 2015;35:465–
• Dome Shaped Macula 475.
• Other macular lesions of • Characteristic inward bulge inside
Pathological Myopia – Corresponding Author:
chorioretinal posterior concavity of eye
• Myopic Traction Maculopathy – in macular area. Dr. Priyangee Sen
Includes Retinoschisis, foveal RD, MS, Associate Professor, Dept of
Lamellar or full-thickness macular • Associated local thickening of sub- Ophthalmology
hole &/or macular detachment. foveal sclera . F.H.Medical College and Hospital, Etmadpur,
Agra
Shimada et al have classified MTM References
as :-
1. Ohno-Matsui, Kyoko MD, PhD
- S0 – No retinoschisis Pathologic Myopia, Asia-Pacific
- S1 – Extra foreal Journal of Ophthalmology: November
- S2 – Foveal / December 2016- Volume 5 -
- S3 – Both foveal & extra foveal, but Issue 6 - p 415-423 doi: 10.1097/
APO.0000000000000230
not entire macula.
- S4 – Entire macula. 2. Theory and Practice of Optics &
• Myopic Optic Neuropathy Or Refraction by A. K. Khurrana

Glaucoma – 3. Anatomy and Physiology of Eye 3Ed
• Due to marked mechanical stretching & (MSO Series) (HB 2019) (Modern System
of Ophthalmology (MSO)

4. Tokoro T, ed. Atlas of Posterior Fundus
Changes in Pathologic Myopia. Tokyo:
Springer-Verlag; 1998.

68 DOS Times - Volume 26, Number 5, March-April 2021 www.dosonline.org/dos-times

Photoessay

Aurolab Aqueous Drainage Implant
in a Case of Late-presented
Primary Congenital Glaucoma

Vidya Raja, D.O, D. N. B, Srilekha Pallamparthy, M.S,
Sharmila Rajendrababu, D.N.B, Shiva Krishna Manthravadi, M.S
Department of Glaucoma Services, Aravind Eye Hospital, Madurai

A 3-year-old female child was referred due to increased size of both eyes. The Corresponding Author:
intraocular pressure (IOP) was 58 mmHg and 54mmHg in the right and left eye
respectively. The corneal diameter was over 15mm and there was advanced optic Dr. Vidya Raja
disc damage in both the eyes. Combined trabeculectomy-trabeculotomy was done D.O, Senior Consultant,
in the right eye, and trabeculectomy alone was done in the left eye. An Aurolab Department of Glaucoma Services,
aqueous drainage implant (AADI) was placed in the right eye due to the failure Aravind Eye Hospital, Anna Nagar,
of the primary procedure (Fig). At 3 months followup, the IOP was 16mmHg and Madurai, India, 625020
18mmHg in the right and left eye respectively.We preferred a slightly longer tube
end especially in children in view of early retraction while placing it in the anterior
chamber at the iris plane and away from the endothelium.

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Review

Dry Eye Diagnostics: Historical
Perspectives, Current Practices,
and Future Directions

Shilpa Ghosh, MBBS, Jigyasa Sahu, MS, MRCS(Ed), FICO
Guru Nanak Eye Centre, MAMC, New Delhi

Abstract : Over the past few decades, the number of patients with dry eye disease (DED) has increased dramatically. The incidence
of DED is higher in Asia than in Europe and North America, which makes it an important part of our patient population. The
diagnosis of dry eye for many years remained subjective to a large extent. However with the advent of new tests, it is now
possible to diagnose as well as classify dry eye disease. In this article we discuss the spectrum of traditional and emerging tests
for dry eye disease.

Introduction Tear Film and Ocular surface of the tear film is composed of mucin
Dry eye disease (DED) refers to a Tear film is composed of an external secreted by the goblet cells, which are
heterogeneous group of disorders lipid layer, an aqueous layer, a semi- distributed throughout the bulbar and
of the tear film caused by reduced solid conjunctival goblet cell mucus palpebral conjunctiva. The microvilli
tear production or excessive tear layer, and the epithelial mucin layer (the and microplicae present on epithelial
evaporation often associated with glycocalyx) (Figure 1). The lipid layer cells are covered by glycocalyx.The
symptoms of ocular discomfort. The produced by the meibomian glands hydrated gel formed by inner layers of
clinical manifestations of dry eye are works to decrease evaporation of tears, aqueous and mucin with glycocalyx
quite variable and the diagnosis depends provides lubrication, and stabilises the renders wettability to the hydrophobic
on the combination of symptoms, tear film. The aqueous layer, secreted ocular surface by overlying tears and
clinical signs and diagnostic tests.1 primarily by the lacrimal gland, might facilitate tear film stabilization
contains antibacterial substances, by reducing the surface tension of
The prevalence of dry eye has increased vitamin A, electrolytes, oxygen,glucose, tears.5,6
in recent years, owing to the general and growth factors. The inner layer
aging of the population, increased
screen usage as well as the increased use Figure 1: The three-layered structure of the tear film consists of an outer lipid layer at the air
of certain medications.2 A study from surface, an intermediate aqueous layer, and an inner mucus layer on the epithelial surface. (6)
North India reported prevalence of dry
eye disease (DED) as 32%, and based on
symptoms 81% of them had severe dry
eye.3 Another study from south India
reported 1.46% DED incidence.4

The pre-ocular tear film is essential
for maintaining normal ocular
homeostasis. It evens out the
irregularities in the cornea, contributes
to the optical properties of the eye
and also regulates the hydration and
nutrition of the cornea. In conditions
like, where there is decreased aqueous
production, defense mechanisms of
normal ocular surface are compromised,
rendering the external eye prone to
infections.4

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Review

Pathogenesis of Dry Eye Dysfunctional meibomian glands Classification of dry eye:
Changes in quantity and quality of the influence the composition of tear lipids, (Figure 3)
lipid layer and availability of tear fluid and are a possible source of infection In 2020, a new perspective on Dry Eye
plays an etiological role in the dry eye and inflammation. Figure 2 shows classification proposal has been given
disease process. It leads to functional various interlinked causative factors for by the Asia Dry Eye Society.16
and anatomical changes in the dry eye disease.15
epithelium and hence forms the basis of Figure 3: New dry eye disease classification
the symptoms , and a starting point for by the Asia Dry Eye Society.
inflammation.7 Transmembrane and
secretory mucins, which facilitate the
contact between tear fluid and epithelial
cells, are also adversely affected by tear
film instability.8-10

Friction, adverse environmental factors,
ocular surface irritation and/or nerve
impairment can lead to epithelial
malfunction and further injury.11
Innate immune processes initiate the
inflammatory cascade on the ocular
surface involving epithelial response
to external stimuli, mediated by the
activation of toll-like receptors.12-14 Lid
margin thickening or rounding and
presence of eyelid notches can alter the
shape and function of the tear menisci.

Diagnostic Testing

While clinical history and examination
remain the mainstay of DED, diagnostic
testing with newer imaging technology
has added much to our armamentarium.
However, since DED is a heterogeneous
disease, some tests described may be
useful for only specific subtypes of DED,
but not all. Therefore, an important
point to remember is that the results
of each test should be patient specific
and should not be treated as absolute
markers of DED.

MMP: matrix metalloproteinase. LPS: lipopolysaccharide. MGD:meibomian gland
dysfunction
Figure 2: Schematic diagram showing the vicious circle theory for DED pathology, adapted
from Baudouin.15

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Review

Overview of dry eye diagnostics evaporation, drainage and absorption.
Table 1: Various tests for diagnosis of dry eye according to their test objective. It acts as a quantitative measure to
identify dry eye objectively. Higher
Test Objective Traditional Test Emerging Test levels of solute in tear film indicate
Functional Visual Acuity a reduced aqueous component, due
Symptoms/functional Symptom to increased evaporation or reduced
impact Questionnaires Tear meniscus with ASOCT, aqueous secretion. However it only
fluorophotometry tells the severity of dry eye and does
Tear volume Schirmer, phenol red Biomarkers: MMP-9, lysozyme not distinguish the type.20 Also it
thread can be affected by non-ocular factors
like systemic medications and
Composition of Tear Osmolarity environmental conditions, because of
film which two measurements per eye are
recommended.21,22
Tear film stability Invasive TBUT Non-invasive TBUT, Three main methods are used to
interferometry measure the tear osmolarity: freezing
point depression (the gold standard),
Tear clearance Fluorescein staining Fluorescein clearance, TFI, vapor pressure method and electrical
Corneal evaluation fluorophotometry impedance of tear film.23-26 The cut-off
Epithelial thickness, confocal for normal is 308 mOsm/L or less.27
microscopy, thermography The TearLab test (TearLab Inc., San
Diego, CA, US) is easy and readily
Conjunctival Lissamine green, rose Biopsy, impression cytology, available for use in clinic. It measures
evaluation bengal confocal microscopy the number of charged particles in tear
film.28,29 The I-Pen® is a new device
Corneal sensitivity Cotton wisp test, that measures the electrical impedance
Esthesiometry using a flexible sensor touching the
conjunctiva.30
Lid evaluation Lid morphology, Meibography The literature suggests tear film
Sjögren’s testing expression of Sjo® osmolarity measurement test may be
meibomian glands more accurate for dry eye diagnosis
Serological test, than Schirmers, TBUT and corneal/
combination of signs conjunctival staining31-33 although the
and symptoms, biopsy cost factor may restrict its use.
[C] Tear volume: Schirmer test
MMP-9 = matrix metalloproteinase-9; ASOCT = anterior segment optical coherence The Schirmer test is a common, cheap
tomography; TFI = Tear Function Index; TBUT = tear break-up time. and easy clinical test to perform to
indirectly measure tear production.
Traditional tests week regarding ocular symptoms, Schirmer with anaesthetic measures
[A] Symptom questionnaires the severity, how these affect visual the basal aqueous tear production
While evaluating a patient of dry eye, function and the ocular response to and without anaesthetic additionally
considering their subjective symptoms environmental triggers with a score measures reflex tearing. A filter paper
and the impact on their quality of life range from 0–100 , higher score test strip in the inferior temporal
is of utmost importance. The patients’ being worse. conjunctival sac of both eyes is
experience of their condition is the 2. The Standard Patient Evaluation of placed in a dim lit room. The test is
most important measure and will cause Eye Dryness (SPEED) questionnaire interpreted after 5 minutes and the
them to seek treatment. Symptom helps to identify symptoms and length of the wetted strip is measured
questionnaires are a critical part of dry focuses on their severity and in millimeters. A reading of 10 mm
eye clinical research trials particularly frequency. or greater is considered normal value
because of their ability in screening, 3. Dry eye questionnaire for both tests. An abnormal finding is
assessment of treatment efficacy and 4. NEI-VFQ ( National Eye Institute- highly suggestive of aqueous deficient
grading of disease severity.17 Visual Function Questionnaire) dry eye. This test suffers from variable
5. McMonnies dry eye index
Commonly used validated 6. IDEEL (Alcon)
questionnaires are 18-20
[B] Tear Film Osmolarity
1. The Ocular Surface Disease Index
(OSDI)- validated questionnaire Tear film osmolarity reflects the
includes 12 questions related to balance between tear production,
experience during the previous

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Review

repeatability and a wide range of Lissamine green and rose bengal stain and tear duct positioning and patency
sensitivity and specificity values but conjunctival surfaces not properly have an effect on the tear dynamics
the accuracy seems to increase as the covered by mucin. Lissamine green can and corneal wetting. Dysfunction
severity of the disease increases.34 stain lid abnormalities such as Marx’s of meibomian glands is the leading
[D] Phenol red thread test line and lid wiper epitheliopathy. cause of evaporative dry eye, the most
A cotton thread that contains phenol red common type of dry eye. Meiboscopy
dye is placed in the same location as the Common grading systems based on is a procedure performed in clinic by
Schirmer test and no anaesthetic is used. surface staining are Collaborative applying a transilluminator to the
The alkaline pH of the tears causes the Longitudinal Evaluation of cutaneous side of the inverted eyelid
colour change of dye from yellow to red Keratoconus, Oxford ( Figure 4) and van while observing the silhouette of the
and then the length of the tear wetting Bijsterveld. gland. This can give an indication of the
is measured in millimeters. A reading meibomian gland atrophy/dropout. Lid-
of 10 mm or greater is normal. It is less parallel conjunctival folds (LIPCOFs)
irritable as compared to Schirmers but have been seen as a potential screening
its accuracy is controversial. tool and good diagnostic sign for
[E] Tear film stability : Tear break-up DED. They can be easily detected and
time graded by slit-lamp, however recently
With fluorescein instilled, TBUT is optical coherence tomography (OCT)
the time interval after a patient blinks classification has been developed for
to the appearance of first dry spot in it.26
the tear film.35,36–39 No ocular drops,
forced blinking or manipulation of Emerging tests
lids should be done before the test. [A] Non-invasive Tear film instability
An average of three times of the test is tests
taken into account for reliability. Ten
seconds or greater is considered normal. Figure 4: Adapted from the Oxford grading Various modalities have been
If a patient has immediate dark spot(s) scale. Courtesy of Tim Steffens. developed for non invasive tear film
with TBUT testing in the same location, instability testing These include the
consider anterior basement membrane [G] Corneal sensitivity xeroscope, wavefront aberrometer,
dystrophy as the cause.40 Ocular Decreased corneal and conjunctival TearScope (Keeler Windsor, UK), tear
Protection Index can be calculated as sensitivity due to the deficiency/ film stability analysis system (TSAS),
the ratio of TBUT/BI (blink interval, instability of the tear film is another Oculus Keratograph 5M (Oculus
the time between blinks). The lower manifestation in DED. The superficial Arlington, WA, US) and LipiView II
the value, the more unstable. A value of exposed nerve endings are susceptible (TearScience, Morrisville, NC, US). As
<1 is pathological and implies that tear to damage. There are presently three the precorneal tear film reflects images
break-up occurs more rapidly than the methods : classic cotton-wisp method, of projected rings, they are captured and
blink. Cochet-Bonnet esthesiometer and the analysed. The time between the blink
[F] Ocular surface dye staining air jet esthesiometer. All three tests and the appearance of the first sign
The commonly used dyes for corneal must be carried without anaesthetic of ring distortion is calculated as the
or conjunctival surface staining are drops in the eye. The CRCERT-Belmonte non invasive TBUT. In addition, some
fluorescein, Rose Bengal and Lissamine esthesiometer uses a non-contact air jet of these machines can evaluate other
green. The stained cornea is examined and applies mechanical, chemical and dry eye features such as meibomian
under a cobalt blue filter on the slit thermal stimuli. gland distribution and anatomy. The
lamp whereas the conjunctival staining [H] Lid evaluation: LipiView can also measure the lipid
under a yellow (blue-free) filter, such as Eyelid anatomy and meibomian layer thickness.
a Wratten filter. gland function examination is an
The characteristic staining pattern seen indispensable part of examination [B] Inflammatory biomarkers
in dry eye includes superficial punctate of dry eye. Conditions such as
keratitis (spk) concentrated in the lagophthalmos, entropion,ectropion, Biomarkers can detect subclinical
interpalpebral or inferior area initially. blink evaluation,lid notching ocular inflammation. Matrix
keratinisation, telangiectasias, chalazia metalloproteinase (MMP)-9 is a key
inflammatory marker being used in the
diagnosis of dry eye. This endopeptidase
is a part of the extracellular matrix
remodeling that takes place after injury.

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Review

Quantitative assessment of MMP-9 biomarkers for SS like SS-A/Ro, SS-B/ film in relation to the blink cycle. Prog
levels seem to correlate well with DED, La, ANA, and RF and also incorporated Retin Eye Res 2015;45:132–64
however, qualitative measurements other early biomarkers SP1, PSP, and
have shown variable sensitivities and CA6 that have shown better sensitivity 11. Stepp MA , Tadvalkar G , Hakt R , et
specificities.41 and specificity.48,49 al. Corneal epithelial cells function
Lactoferrin is produced by the acinar as surrogate Schwann cells for their
cells of the lacrimal glands and would References sensory nerves. Glia 2017;65:851–63
be abnormally high in those with
aqueous deficient dry eye. The TearScan 1. Pflugfelder SC, Tseng SCG, Sanabria O, et 12. Aragona P , Rania L , Puzzolo D. The
System, which measures lactoferrin, as al.: Evaluation of subjective assessments role of inflammation, inflammatory
well as immunoglobulin E (an allergy and objective diagnostic tests for cytochines, and ocular surface markers
marker).42 diagnosing tear-film disorders known in dry eye disease. In: Benitez Del
[C] ASOCT to cause ocular irritation. Cornea 1998, Castillo JM , Lemp MA , eds. Ocular
It captures and analyzes the tear 17:38–56. surface disorders . London: JP Medical
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meniscus area, depth, and height. It can 2. Schein OD, Munoz B, Tielsch JM, et al.:
also measure epithelial thickness which An epidemiological study of medication 13. Lemp MA, Baudouin C, Baum J. et al.
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Newer AS-OCT technology can acquire Ophthalmol Vis Sci 1997, 38:S213. eye disease: report of the definition
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clearly visible saccular acini in healthy Sharma N. Prevalence and risk factors Surf 2007;5:75–92.
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[D] Infrared thermography Ocular surface disease index-based 14. Musumeci M , Bellin M , Maltese A ,
This test offers a non-invasive, cross-sectional hospital study. Indian J et al. Chitinase levels in the tears of
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temperature of the cornea. Compared 2008;27:168–73
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temperature is shown to be higher in SS, Singh VS, Das VA, Basu S. Incidence, 15. Baudouin C. [A new approach for better
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becomes significantly lower where report I. Ocul Surf. 2019;17:250–6.
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[E] Meibomian gland Imaging Eye Society. Eye Contact Lens. 2020
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assessed by this method correlates well epithelium and tear fluid. Invest dry eye disease: report of the Diagnostic
with signs and symptoms of dry eye Ophthalmol Vis Sci 2000, 41 : 1316–1326 Methodology Subcommittee of the
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www.dosonline.org/dos-times DOS Times - Volume 26, Number 5, March-April 2021 75

DOS Times Quiz

DOS Times Quiz

Prafulla K. Maharana, MD
Associate Professor, Department of Ophthalmology, Dr. Rajendra Prasad Centre for Ophthalmic Sciences,
All India Institute of Medical Sciences, New Delhi-110029, India.

Who is the father of Modern Eye banking?

Corresponding Author:

Prafulla K. Maharana
Associate Professor, Dep. of Ophthalmology,
Dr. Rajendra Prasad Centre for Ophthalmic
Sciences, All India Institute of Medical Sciences,
New Delhi-110029, India.

ANSWER

Answer _______________________________________________________________________________________________________________________________________
Name: ________________________________________________________________________________________________ Degree: _______________________________
Designation:_________________________________________________________________________ Address:_______________________________________________
_______________________________________________________________________ State _______________________________ Pin _______________________________
Mobile No: ________________________________________________________________________________________ DOS Membership no: ___________________
Email ID: _______________________________________________________________________________________Signature: ___________________________________

Email your answer to: [email protected]

76 DOS Times - Volume 26, Number 5, March-April 2021 www.dosonline.org/dos-times

Tearsheet

Anti VEGF at a Glance

Priyadarshi Gupta, MBBS, Ekta Shaw, MBBS
Guru Nanak Eye Centre, Maulana Azad Medical College, New Delhi

Composition PEGATINIB BEVACIZUMAB RANIBIZUMAB AFLIBERCEPT
Molecular wt (KD) (Macugen) (Avastin) (Lucentis) (Eylea) (VEGF trap)
Half-life (days) Aptamer (single Complete Antibody Humanised monoclonal Recombinant protein
Dose stranded DNA/RNA) antibody fragment (no Fc (consists of Ig domain 2
Side effects 149 component) of VEGFR1 and domain
50 5 3 of VEGFR2) combined
Remarks 2 1.25mg/0.05ml 48 with Fc portion of IgG
0.3mg/0.9ml CVA 3 115
Trials CVA Arterial 0.5mg or 0.3mg/0.05ml 7
Bronchitis/pleural thromboembolic CVA 2mg/0.05ml
effusion/Nausea/ events/ Congestive Acute HTN/Myocardial CVA
Vomiting/carotid artery heart failure/ infarction/facial redness/ HTN
occlusion/TIA/Contact Confusion itchy skin rash
dermatitis/anaphylaxis -Originally developed -Approved for use in wet
-1st Anti VEGF approved to target metastatic -developed specifically ARMD and DME.
for ocular treatment. blood vessel growth. for ocular use -maintenance regimen is
-Results similar to PDT. -used for wet ARMD -approved for use in wet 2 monthly
-Use now is extremely and other indications ARMD and DME -forms stable complex
limited because of s/e. are off-label. -does not incite immune with VEGF receptors.
-much cheaper response against -more efficacious than
VISION -comparable safety complement as Fc RANI
VERITAS wrt RANI portion is absent -costly
-higher systemic s/e
than RANI ANCHOR, MARINA, CLEAR IT 2,
-approved for PIER, EXCITE, PrONTO, VIEW 1/2,
metastatic colon SUSTAIN, HARBOR, VIBRANT, COPERNICUS,
cancer HORIZON, FOCUS, GALILEO,
SANA, IVAN, ABC, PROTECT, TORPEDO, VISTA, VIVID
BRAMD, CATT. DENALI, MONT BLANC,
BERVOLT EVEREST, RADICAL,
CABERNET.
BRAVO, CRUISE,
RELATE, BRIGHTER
RISE, RIDE, RESTORE

www.dosonline.org/dos-times DOS Times - Volume 26, Number 5, March-April 2021 77

Tearsheet

Brolucizumab (Humanised single Indications of Anti Vegf
chain Antibody fragment) (Beovu) 1. CNVM- ARMD/RAP/Myopia/Angioid streaks/Best’s disease/multifocal
FDA approved for Wet ARMD
(2019) choroiditis/CSCR.
Trials- HAWK, HARRIER 2. Neovascularisation- PDR/CRVO/BRVO/sickle cell retinopathy/ROP/COAT’s

disease.
3. Macular edema- DR/BRVO/CRVO/Pseudophakic CME/Uveitic CME
4. Neovascular Glaucoma- CRVO/BRVO/DR/Ocular ischaemic syndrome
5. Anterior segment uses- Pterygium/Post PK corneal vascularisation/chemical

burns/Herpetic stromal keratitis
6. As adjunct to Surgery- Phaco in CSME; PPV for PDR, NRVH; Glaucoma

surgery.
7. Miscellaneous use- Radiation retinopathy, Eales disease, choroidal mets.

Corresponding Author:

Dr. Priyadarshi Gupta
MBBS,
Room 512, Old Residents Doctors Hostel,
Maulana Azad Medical College,
New Delhi

78 DOS Times - Volume 26, Number 5, March-April 2021 www.dosonline.org/dos-times

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