KERALA JOURNAL OF OPHTHALMOLOGY...President Dr. R.R. Varma Ambikalayam, Warriam Road Kochi - 682 016...

ADDRESS FOR ALL CORRESPONDENCE: Dr. Meena Chakrabar ti, Editor KJO, Chakrabar ti Eye Care Centre, Kochulloor,Medical College PO, Trivandrum 695 011, Ph-0471-2555530, 2449599 Fax:- 0471-2558530, E-mail: [email protected]

SUBSCRIPTION RATE

Annual : Rs. 600 (4 issues)

Single Copy : Rs. 150

Subscription should be sent by demand draft in favour of

Kerala Journal of Ophthalmology payable at Trivandrum

addressed to the Editor, KJO

The Kerala Journal of Ophthalmology is the official scientific publication of the Kerala Society of

Ophthalmic Surgeons and 4 issues are published every year.

It welcomes original articles, interesting case reports, update articles, book reviews, journal abstracts

and research papers in Ophthalmology. Dates of the upcoming conferences and CME’s are also published.

Original articles are accepted on condition that they have not been published in any other journal.

EX- OFFICIO MEMBERS

Dr. R.R. Varma (President)

Dr. Rajagopalan Nair (Past President)

Dr. T.A. Alexander(Immediate Past President)

Dr. Sahasranamam(Past Secretary)

Dr. Sasi Kumar(Secretary)

ADVISORS

Dr. Shobhana Mohandas

Dr. Thomas Cherian

Dr. Sai Kumar S.J.

Dr. Giridhar A.

EDITORIAL BOARD

Dr. Rajiv Sukumaran (Kollam)

(Associate Editor)Dr. Charles K. Skariah (Thrissur)

Dr. Sonia Rani John (Trivandrum)

Dr. Mini Jayachandran (Kollam)

Dr. Mohammed Haneef (Alapuzha)

Dr. Bindu Das (Kozhikode)

Dr. Merine Paul (Thrissur)

Dr. Leila Mohan (Kozhikode)

Dr. Meenakshi Dhar (Kochi)

Dr. Amitha Varghese (Thiruvalla)

Dr. Sunil (Kasargode)

Dr. Reena Rasheed (Trivandrum)

Dr. Ashley Thomas (Kozhencherry)

KERALA JOURNAL OF OPHTHALMOLOGY

VOL. XXI ISSUE 3 SEPTEMBER 2009

EDITOR

Dr. Meena Chakrabarti

President

Dr. R.R. Varma

Ambikalayam, Warriam Road

Kochi - 682 016

Ph: 0484-2352010 (R)

Mob: 94471 52010

U

KERALA SOCIETY OF OPHTHALMIC SURGEONS(Registered under Societies Registration XXI of 1860. No.387/2003)

General Secretary

Dr. Sasikumar

Ambadi, Adayath Lane,

Ravipuram, Kochi 680216

Ph: 0484-2357135 (H)

Mob: 9447475101

Treasurer

Dr. Radha Ramanan

LF Hospital, Angamaly

Ernakulam

Ph: 0484 2452546 (H)

Mob: 9447006421

President Elect

Dr. B.V. Bhat

Asoka Hospital

South Bazar

Kannur

Ph: 9846139715

Vice President

Dr. A. Giridhar

Giridhar Eye Institute

Ponneth Temple Road

Kadavanthara, Kochi - 682 020

Ph: 9895377899

Scientific Committee Chairman

Dr. Sai Kumar S.J.

Giridhar Eye Institute

Kochi - 682 020

Ph: 0484-2312303 (H)

Mob: 98470 40840

Joint Secretary

Dr. Arup Chakrabarti

Chakrabarti Eye Care Centre

Kochulloor, Trivandrum 695 011

Ph: 0471-2555530

Mob: 9946410540

Web Site Editor

Dr. Thomas George

RIO, Red Cross Road

Trivandrum - 695 035

Mob: 93493 18711

Journal Editor


Chakrabarti Eye Care Centre

Kochulloor, Trivandrum – 695 011

Ph: 0471-2555530

Mob: 9946410541

Immediate Past President

Dr. P. Rajagopalan Nair

Raj Bhavan

Palakkad - 676 013

Ph: 0491-2535676 (R)

Mob: 94476 45676

Dr. T.A. Alexander

Thottumughath, Kusumagiri

Kakkanad, Kochi - 682 030

Ph: 0484-2721161

Dr. George Thomas

T.C. 4/1040-1, Near Kowdiar Jn

Trivandrum - 695 003

Ph: 0471-2431143, 2433333

Mobile: 9847315150

Dr. E.J. Mani

Little Flower Hospital

Angamali - 683 572

Ph: 0484-2608919

Immediate Past Secretary

Dr. Sahasranamam

No. 30, Vinayaka Nagar

Trivandrum 695 018

Ph: 0484-2490421 (R)

Mob: 9846020421

Managing Committee Members

Dr. Anthrayose Kakkanat


Executive Committee Members

Dr. Suresh BabuKasargode

Dr. P.P. KunhiramanKannur

Dr. Baburaj N.P.Kozhikode

Dr. Mohammed Swadique

Malappuram

Dr. Rajesh Radhakrishnan

Palakkad

Dr. Babu Krishnakumar

Thrissur

Dr. Davis Akkara

Ernakulam

Dr. C.K. Mathew

Alapuzha

Dr. Varghese Joseph

Pathanamthitta

Dr. Seshadrinathan

Kottayam

Dr. S Venugopal

Kollam

Dr. Biju John

Trivandrum

C O N T E N T SKJOEDITORIAL

241 In the Grip of the Python: Medicine’s Dependence on the

Pharmaceutical Industry


MAJOR REVIEW

243 Retinoblastoma

Dr. Mahesh P. Shanmugham

ORIGINAL ARTICLES

248 Ocular Manifestations of Intracranial Space Occupying Lesions –

A Clinical Study

Dr. K.V. Raju, Dr. Anju Abdul Khader

253 Capsulo-Cortical Adhesions (CCA) and Phacoemulsification (PE)

Dr. Arup Chakrabarti, Dr. Sonia Rani John, Dr.Valsa Stephen,


258 Efficacy of Combining Intravitreal Bevacizumab Monotherapy (IVB) with

Panretinal Photocoagulation (PRP) in Early Stages of Neovascular Glaucoma

(NVG)

Dr. Meena Chakrabarti, Dr. Arup Chakrabarti, Dr.Sonia Rani John

264 Ophthalmic Manifestations in Children with Delayed Milestones –

A Clinical Study

Dr. Reena A, Dr. Lekshmy S.R, Dr. Lekshmi H, Dr. Bindu K. Appukuttan

270 An Outcome Analysis of Posterior Capsular Rent (PCR) In the Hands of

A Senior Phaco Surgeon

Dr. Arup Chakrabarti, Dr. Meena Chakrabarti, Dr. Sonia Rani John,

Dr. Valsa Stephen MS DNB

OPHTHALMIC SURGERY

274 Lens Surgery in Marfan’s Syndrome

Dr. Somdutt Prasad

OPHTHALMIC INSTRUMENATION

280 The Eyesi: Ophthalmic Surgical Simulator

Dr. Meena Chakrabarti, Dr. Sonia Rani John, Dr. Arup Chakrabarti

OCULAR PHARMACOLOGY

285 Nepafenac

Dr. Sonia Rani John, Dr. Meena Chakrabarti, Dr. Arup Chakrabarti

289 Recent Advances in The Back of the Eye Drug Delivery


C O N T E N T SKJOCURRENT CONCEPTS

294 Care and Maintenance of Contact Lens – An Overview

Dr. Pravin Tellakula

CASE REPORT

304 A Case Report of Colobomatous RD

Dr. Arya A.R, Dr. Biju John

306 Vasoproliferative Tumour of The Retina – A Case Report

Dr. Tulefa Shafi, Dr. Natasha Radhakrishnan, Dr. Gopal S Pillai,

Dr.Roshan George

COMMUNITY OPHTHALMOLOGY

309 Go Green for a Healthier Life


PHOTO ESSAY

312 Masquerade Syndrome


315 CONSULTATION SECTION

319 OPHTHALMIC HISTORY

321 JOURNAL REVIEW

324 BOOK REVIEW

329 UPCOMING CME

331 PG TEAR SHEET

333 INSTRUCTION TO AUTHORS

EDITORIAL

In the grip of the python:

Medicine’s Dependence on the

Pharmaceutical IndustryEverything has either a price, or it possesses dignity.”1 Professionals should be “independent

of the state or commerce” 2. These are two off-quoted quotes, but there is a lingering doubt in

our minds as to the threat of Commercialism and Professional integrity.

Commercialism is such a threat to the professional ethics of individual physicians that

commercialism is incompatible with medical professionalism. Personal financial choices by

physicians at times violate professional responsibilities and the fundamental ethical pact with

society. 3 The conflict between commercialism and professionalism is precisely about the

appropriate and inappropriate (not legal vs illegal) ways that physicians should make money

and contribute to society. 5 If medicine loses professionalism or the public perceives that

physicians are not behaving as professionals, it is no wonder that medicine will surrender its

influence and status in society. Can the medical profession and, specifically, peer-reviewed

literature survive the challenges posed by the secular culture of commercialism and at the

same time maintain the public trust? 5-7

For both academic institutions and individuals, receiving gifts, meals, books, or free continuing

medical education creates the presumption of bias. The further acceptance of invitations to

join speakers bureaus, to serve on boards, to consult on marketing issues, to receive payments

for enrolling in clinical trials, and to participate in research studies with payment in stock

pushes this presumption of bias into fact.3-12 Other enticements, sometimes for spouses,

sometimes at the request of the physicians themselves, are immoral, and some are illegal.

Those who do not believe this bias exists are denying scientifically established patterns of

human behavior and deceiving themselves. The “rule of reciprocation,” one of the

strongest tenets of human social behavior, holds that we should try to repay what another

person has provided to us.3 The ability of physicians to remain neutral under the present

barrage of industry largesse is questionable.

Companies target academic “key opinion leaders” 13 -16 (a marketing term) to populate

scientific advisory committees, join speakers bureaus that sometimes aggressively promote

drugs or devices, and participate on manuscript writing committees that support industry

marketing themes 16. Although key opinion leaders seem convinced of their own impartiality,

Carl Elliott, a moral philosopher at the University of Minnesota and author of Better Than

Well: American Medicine Meets the American Dream, 17 strongly disagrees with them, as do

their own colleagues. 18 The practice of key opinion leaders consulting with multiple companies

to present the appearance of objectivity is even more misleading 19,20,21

242 Kerala Journal of Ophthalmology Vol. XXI, No. 3

A generation of new physicians has grown up with the mistaken belief that professional values

can be replaced with marketplace values and that medical care is just another economic service.

Financial success has become the dominant standard of measurement or value even for most

academic medical centers. 21 Young professionals are reminded that these commercial activities

were previously considered unprofessional. 5

There is tremendous value in the cooperation between academia and industry, but the

engagement should be at a distance, with both sides maintaining their own standards and

ethical norms. 4 Although academic medicine and the health care industry seem intertwined

at present, the profession needs to be reminded that the goals of the medical profession are

very different from the goals of the commercial industry. We must seek ways to disentangle

the two and not just use “disclosure” as the mechanism to cleanse the system; “reader or

buyer beware” should not be the mantra of a profession 22 - 24.

There are serious questions about the reliability of some of the commercially funded trials,24

raising very significant moral and ethical questions for some physicians and a dilemma for

journals. In reality, it is the physicians who have permitted the pharmaceutical and biotech

industries to manipulate medical science through these financial relationships. 19

Many researchers have delayed publication of their results by several months to allow for

patent application,25 - 29 to protect their scientific lead, or to slow the dissemination of results

that would hurt sales of their sponsor‘s product,19 and in some instances scientists at top

research universities have completely refused to share results with their colleagues.30 The

reporting of trial outcomes is also sometimes incomplete, biased, and inconsistent with

protocols. 31 Published articles, as well as reviews that incorporate them, may therefore be

unreliable and overestimate the benefits of an intervention; meta-analysis simply amplifies

erroneous results and is much less powerful or valuable than assumed. To ensure transparency

and avoid the overbearance of commercial industry, planned clinical trials must be registered

and protocols should be made publicly available prior to trial completion. Many major journals

will not permit submission of clinical studies that have not been registered

Journals are hampered by this assault of commercialism on publishing. The only tools editors

have in their efforts to enforce policies on full financial disclosure or to control excess

commercialism and bias is the instigation of a full investigation following complaints by

informed readers. When this happens, the journal is dedicated to clarifying the situation for

the reader, albeit indirectly, by involving the relevant institutional review board because journals

do not have formal investigative or enforcement functions.

There is reason for hope, however, as resistance begins to mount against commercial influence

in medicine, as evidenced by suggested changes in the relationship between academic

medical centers and industry.16, 32-33 There are also new and influential parallel initiatives from

academic medical centers themselves, and from think tanks addressing continuing medical

education (the education environment is even more permissive in fostering biases than is

publishing).34-37 Time will tell whether professionalism will rein over commercialism in

medicine.

Dr. Meena Chakrabarti MS DO DNB

Editor, KJO

September 2009 Kerala Journal of Ophthalmology 243

M A J O R

REV I EW

RetinoblastomaDr. P. Mahesh Shanmugam DO FRCSEd PhD

Head, Vitreoretinal and Ocular Oncology Services, Sankara Eye Hospitals,

Bangalore

Retinoblastoma occurs in approximately 1 in 14,000-

34,000 live births. 1-3 No predisposition to race, sex or

laterality of the eye is noted. The majority of cases of

retinoblastoma are sporadic (no family history and no

affected family members on ophthalmic examination).

Retinoblastoma occurs as a result of loss of the tumor

suppressor gene located on band 14, on the long arm

of chromosome 13 (13q14). 4,5 In genetically

transmitted disease, the abnormality results in the

development of usually bilateral, multifocal tumors in

relatively younger patients. This deletion also

predisposes these children to other non-ocular tumors

such as osteosarcoma in later stages of life. In contrast,

sporadic tumors occur in older children and tends to

be unifocal and unilateral. However, 10-20% of

unilateral disease can also be genetically transmitted.

The average age at diagnosis of retinoblastoma in

American children is 18 months, and evidence indicates

that Asian children present later than their western

counterparts 1,6-8. Bilateral cases are diagnosed earlier

than unilateral cases. 1,9

Clinical Features

The most common presentation of retinoblastoma is

leukocoria (61-70 %) (Fig 1) and strabismus

(22-48%) 1,10,11.

On fundus examination retinoblastoma appears as a

slightly white, flat, translucent lesion in the sensory

retina (Fig 2).

Moderately advanced lesions may present as unilateral

or bilateral leukocoria (Fig 3).

Fig. 1.-3. Common modes of presentation of retinoblastoma

Fig. 1. Leukocoria

Fig. 2. White, flat, translucent lesion in

sensory retina

Fig. 3. Advanced Leison


Based on the growth pattern, the tumor can be classified

into endophytic, exophytic, mixed (both endophytic and

exophytic) and diffusely infiltrative tumors.

Spontaneous regression of retinoblastoma occurs in

about 1 percent of patients. It is often seen in eyes with

phthisis bulbi and following an episode of severe

inflammation.

Local spread to the orbit, distant metastasis to brain,

spinal cord, skull bones, distant bones, viscera and

lymph nodes may occur in advanced retinoblastoma.

On ocular ultrasonography retinoblastoma appears as

an irregular mass lesion with high surface reflectivity

and high internal reflectivity resulting in orbital

shadowing all due to the presence of calcium.

Computerized tomography and magnetic resonance

imaging allow detection of extraocular disease,

intracranial metastasis and pinealoblastoma.

Retinoblastoma appears as an intraocular mass with

calcium on CT scan; it appears as a hyperintense to

vitreous lesion in T1 weighted image and hypointense

to vitreous in T2 weighted images on MRI. (Fig 4)

be well differentiated or poorly differentiated. Poorly

differentiated retinoblastoma consists of small to

medium-sized round cells with hyperchromatic nuclei

and scanty cytoplasm. High mitotic figures are often

observed. A well-differentiated tumor may show:

(i) rosettes, or (ii) fleurettes. Seventy percent of

retinoblastomas are known to contain rosettes.

Rosettes are of two types:

Flexner-Wintersteiner rosette

Homer-Wright rosette

In a Flexner-Wintersteiner rosette, columnar cells

are arranged around a clear central lumen. The nuclei

of the cells are arranged near the base of the tumor.

The lumen contains hyaluronidase resistant

glycosaminoglycans, which are found between

photoreceptor and retinal pigment epithelium.

In a Homer-Wright rosette, the cells are arranged

radially around a central tangle of neural fibers.

Fleurettes represent further differentiation and present

as flower bouquet-like aggregates of tumor cells with

bulbous eosinophilic processes projecting through the

fenestrated membrane. They are seen in 6-10 percent

of the retinoblastoma cases.

Differentiation of the tumor does not have prognostic value.

Management

Management options in retinoblastoma include

enucleation, in an eye without visual potential, if more

than half the globe is involved by the tumor, or in the

presence of glaucoma and anterior chamber

involvement. Eyes with visual potential (unilateral/

bilateral cases) are managed conservatively

with modalities that include cryotherapy, laser

photocoagulation, transpupillary thermotherapy (TTT),

thermochemotherapy, chemoreduction, plaque

brachytherapy and external beam radiotherapy1,13.

International classification of

retinoblastoma 14:

As early classifications were deemed insufficient in this

era of chemoreduction of retinoblastoma, a new revised

classification has been devised to offer prognosis of the

affected eye.14

Rarely cytology by fine needle aspiration biopsy may

be necessary to confirm the diagnosis.

In advanced cases with extraocular disease, metastatic

work-up that includes lumbar puncture, CT / MRI scan,

bone marrow biopsy, bone scan and routine blood

investigations will be necessary 12.

Histopathology

Retinoblastoma appears as a basophilic mass with

lightly eosinophilic areas due to necrosis of tumor and/

or multiple dense basophilic foci (due to calcification)

within areas of necrosis may be seen. The tumor may

Fig. 4. MRI Scan in a child with unilateral retinoblastoma

September 2009 P. Mahesh Shanmugham : Retinoblastoma 245

GroupTumor characteristics

A Small tumor (≤ 3mm)

B � Larger tumor (≥ 3mm)

� ≤ 3 mm from foveola

� ≤ 1.5 mm from disc

� Subretinal fluid ≤ 3mm from margin

C Focal seeding

� Subretinal and or vitreous seeds

≤ 3 mm from tumor

D Diffuse seeding

� Subretinal and or vitreous seeds

≥ 3 mm from tumor

E � Tumor >50 % globe

� Neovascular glaucoma

� Opaque media due to intraocular hemorrhage

� Postlaminar optic nerve invasion, choroid

(>2 mm), sclera, orbit anterior chamber

involvement

Treatment of retinoblastoma 1, 15

Management of retinoblastoma confined to

the eye: Eyes with visual potential (unilateral/bilateral

cases) are managed conservatively. Primary or recurrent

tumours anterior to equator, ≤ 4 mm in diameter and

less than 3 mm thickness, confined to the retina are

treated with triple freeze thaw cryotherapy. Tumors

3-4 mm in diameter, 2 mm thick confined to the retina

are treated with 2 rows of deep laser burns around the

tumor. Slightly larger tumors confined to the retina can

be treated with transpupillary thermotherapy, which is

increasing the tumor temperature by 6-80 C above body

temperature.

Larger tumors or those with vitreous or subretinal seeds

are treated with external beam radiation delivering

3500-4000 cGy, 200 cGy fractions delivered over a

4-5 week period. Plaque brachytherapy with episcleral

plaque applicators (Iodine - 125 or Ruthenium - 106)

can be used to treat tumours ≤ 15 mm in diameter and

6-8 mm in height, at least 2 mm from optic disc and

fovea with or without localized vitreous seeding. Plaque

therapy has the advantage of limited radiation to

normal tissue, thereby limiting complications. Radiation

in any form is associated with complications such as

retinopathy, cataract and in bilateral germinal tumors,

the increased risk of second malignant neoplasms in

later years 16. The risk of second malignant neoplasms

is highest when the child subjected to radiation less

than 1 year of age. Hence it is preferable to avoid

radiation and CT scan in retinoblastoma infants less

than one year of age.

Contemporary management of large tumors, tumors

close to optic nerve (Fig 5) / fovea or those extending

beyond the retina involves using chemoreduction.

Triple drug chemoreduction using vincristine, etoposide

and carboplatin are used in multiple cycles to

“chemoreduce” the tumor and the residue is destroyed

using focal treatments such as laser photocoagulation,

cryotherapy etc., The tumor is replaced with

chorioretinal atrophy and calcific residue with

chemoreduction and local treatment. (Fig 6, 7) Current

focus is on local chemotherapy and one of the avenues

being explored in cannulation of the ophthalmic artery

and melphalan infusion through the same.

Fig. 5. Large tumor mass filling the globe

Fig. 6. Regressed retinoblastoma showing chalky whiteareas of calcification and chorioretinal atrophy


Subconjunctival carboplatin chemotherapy is also used

as an adjunct to systemic chemotherapy.

This shift from radiation to chemoreduction is primarily

aimed at reducing the increased risk of second

malignant neoplasms associated with the use of

radiation.

Enucleation is indicated in retinoblastomas involving

more than half the globe, presence of glaucoma and

anterior chamber involvement. A long optic nerve

stump (≥10 mm in length) should be obtained during

enucleation. If post enucleation histopathological

tumor, excision of the tumor followed by additional

chemotherapy and radiation to the affected part.

Intracranial involvement is treated with intrathecal

chemotherapy in addition to CNS radiation and

systemic chemotherapy.

Prognosis

The overall 5-year survival is around 90 percent in

retinoblastoma. Patients with germinal mutations are

more likely to die due to second nonocular tumors,

which develop at a later age. Involvement of the cut

end of the optic nerve indicates poor prognosis and

possible intracranial metastatic disease if adequate (at

least 10 mm) length of the optic nerve stump was

obtained during enucleation. Tumor invasion into the

ocular coats, extensive choroidal invasion and anterior

chamber seeding are associated with an increased risk

of subsequent metastatic disease. Extraocular, central

nervous system involvement and hematogenous spread

carry a poor prognosis.

References

1. Shields JA, Shields CL. Retinoblastoma. Clinical and

pathologic features. In: Intraocular tumours: A Text andAtlas. WB Saunders, Philadelphia, 1992, pp 305-331.

2. Senft S, al-Kaff A, Bergqvist G, et al. Retinoblastoma.The Saudi Arabian experience. Ophthalmic PaediatrGenet 1988;9:115-119.

3. Kock E, Naeser P. Retinoblastoma in Sweden 1958-1971.

A clinical and histopathological study. Acta Ophthalmol1979:57:344-350.

4. Francke U. Retinoblastoma and chromosome 13.Cytogenet Cell Genet 1976;16:131-134.

5. Yunis JJ, Ramsay N. Retinoblastoma and subbanddeletion of chromosome 13. Am J Dis Child 1978; 132:

161-163.

6. Shanmugam MP, Biswas J, Gopal L, Sharma T,

Nizamuddin SH. The clinical spectrum and treatmentoutcome of retinoblastoma in Indian children. J Pediatr

examination shows tumor invasion beyond lamina

cribrosa, anterior segment involvement (Fig. 8) or extensive

choroidal invasion, adjunctive chemotherapy is necessary

to decrease risk of subsequent metastatic disease.

Involvement of the cut-end of optic nerve with tumor

has to be treated aggressively with adjunctive

chemotherapy and radiation.

Management of extraocular retinoblastoma:

(Fig 9 – showing orbital recurrence of retinoblastoma)

Extraocular retinoblastoma is managed with a multi-

modal approach of chemoreduction to reduce the

Fig. 7. Regressed retinoblastoma showing extensive chorioretinal atrophy and flecks of calcification

Fig. 8. Advanced tumor showing anterior segmentinvolvement

Fig. 9. Orbital recurrence of tumor following enucleation

September 2009 P. Mahesh Shanmugham : Retinoblastoma 247

Ophthalmol Strabismus. 2005 Mar-Apr;42(2):75-81;quiz 112-3.

7. Vemuganti G, Honavar S, John R. Clinicopathologicalprofile of retinoblastoma in Asian Indians. InvOphthalmol Vis Sci 2000;41(S790);4.

8. Sahu S, Banavali SD, Pai SK, et al. Retinoblastoma:problems and perspectives from India. Pediatr HematolOncol 1998;15:501-508 .

9. Rubenfeld M, Abramson DH, Ellsworth RM, et al.Unilateral vs. bilateral retinoblastoma. Correlationsbetween age at diagnosis and stage of ocular disease.Ophthalmology 1986;93:1016-1019.

10. Kayembe L. Retinoblastoma: 21-year review. J FrOphthalmol 1986;9:561-565.

11. Mathew L, Miale TD, Rao S, et al. Retrospective analysisof 58 children with retinoblastoma. Ophthalmic PaediatrGenet 1984; 4:67-74.

12. Mohney BG, Robertson DM. Ancillary testing for

metastasis in patients with newly diagnosed

retinoblastoma. Am J Ophthalmol 1994;118:707-711.

13. Epstein J, Shields CL, Shields JA. Trends in the

management of retinoblastoma: evaluation of 1,196

consecutive eyes during 1974–2001. J Pediatr

Ophthalmol Strabismus. 2003;40:196–203.

14. Shields CL, Shields JA. Basic understanding of current

classification and management of Retinoblastoma. Curr

Opin Ophtalmol 2006;17:228–234.

15. Shields CL, Mashayekhi A, Demirci H, et al. Practical

approach to management of retinoblastoma. Arch

Ophthalmol. 2004;122:729-735.

16. Abramson DH. Retinoblastoma in the 20th Century: Past

Success and Future Challenges The Weisenfeld Lecture.

Inv Ophthalmol Vis Sci. 2005;46:2684-2691


Ocular Manifestations of Intracranial Space

Occupying Lesions – A Clinical StudyDr. K.V. Raju MS, Dr. Anju Abdul Khader MS

nuclei are associated with the eyes besides the vagus

and the sympathetic. This research work covers the

assessment of the incidence of ophthalmologic

manifestations in intracranial space occupying lesions,

and to correlate the ocular manifestations and the site

of the brain tumours as well as the study of the visual

field defects caused by space occupying lesions.

Aim of the Study

To study the incidence of ophthalmologic

Abstract

Aim

� To study the various ophthalmologic manifestations in intracranial space occupying lesions.

� To correlate the ocular manifestations and the site of the brain tumors.

� To study the visual field defects caused by space occupying lesions.

Materials and methods

The study included fifty CT/MRI proven cases of intracranial space occupying lesions who underwent

detailed ocular, neurological and systemic examination.

Results

Female patients in the 40-50 yrs age group were commonly affected. Headache was the common

symptom [63.3 %] followed by defective vision.VII Cranial nerve was most commonly involved.

Papilloedema was the most common fundus finding. Visual field defects correlated with the

site of tumour. Most common histological subtype was neuroepithelial tumours.

Cerebellopontine angle tumours were most common according to the site of tumour.

Keywords. Ocular manifestations, intracranial space occupying lesions, visual field defects.

Introduction

Ocular features sometimes form an early manifestation

of intracranial space occupying lesion, which helps us

to diagnose the condition earlier and decrease the

morbidity and mortality of the patient. How far the

ophthalmologist’s effort can be useful to the neurologist

can be judged from the extensive distance the optic

pathways cover in the brain from pole to pole, and from

the fact that six of the twelve cranial nerves with their

Regional Institute of Ophthalmology, Calicut Medical College

ORIGINAL

ARTICLE

September 2009 Raju K.V. et al. - Ocular Manifestations of ICSOL 249

manifestations in intracranial space occupying lesions,

to correlate the ocular manifestations and the site of

the brain tumours and also to study the visual field

defects caused by space occupying lesions.

Methods

The materials for the study were collected from the

patients who attended Regional Institute of

Ophthalmology, Calicut Medical College, during one

year period [May 2005 - May 2007]. Most of the

patients were admitted in the Neurosurgery Department

and the ophthalmologic evaluation was done in the

preoperative period. Patients with CT or MRI proved

intracranial space occupying lesions were taken up for

the study. Those patients who were uncooperative on

account of very young age, deteriorating general

conditions or marked behavioural disorders were

excluded from the study.

Fifty patients with brain tumours and eye

manifestations were included in the study. In each case

clinical evaluation was done after obtaining a detailed

history. Ophthalmologic assessment included

routine ocular examination with special reference to

ocular movements, corneal sensation, pupillary

abnormalities and nystagmus. Ocular fundus was

examined in detail and visual fields charted in all cases.

A complete examination of the central nervous system

which included examination of the higher functions,

cranial nerves, motor system, sensory system and

cerebellar signs were made.

Observation and Discussion

1) Age distribution [Table :1]

The age of patients ranged from 11- 65 years. The

maximum incidence in the present study was in the

age group between 40 to 50.1 This is in accordance

with other studies by Rao et al, which showed a 52 %

incidence in the 3rd & 4th decade.

2) Sex distribution:

The present study showed a female preponderance

of 60 %.

3) Area of involvement of brain tumors and

histopathological types of brain tumors.

[Table :2]

In the present study according to the site of tumor most

common was cerebellopontine angle tumors [20 %].

According to the histology the most common tumor

found in our study was neuroepithelial tumors [34 %]

like astrocytoma, oligodendroglioma, ependymoma etc.

4) Presenting symptoms:.

In this series maximum no of patients presented with

headache. Headache as initial symptom occurred in

30 % and along with other symptoms occurred in

63.3 %. S.Sood et al also made similar observation.

Defective vision occurred during the course of the

disease in 50 % of the patients. Seizures either

generalized or focal occurred in 3.3 %. Behavioural and

psychiatric changes were noted in patients with parietal,

frontal & temporal lobe tumors. Other symptoms

included vertigo, paresis, dysphasia, dementia,

deafness, tinnitus ataxia, and diplopia etc.

5) Pupillary abnormalities

Among the 50 patients examined 6[12 %] had

abnormal pupillary reaction. All of them had afferent

pupillary defect due to optic atrophy. Although

Wernicke pupil has no significance according to the

literature one patient in this study with left parietal

meningioma and homonymous hemianopia showed the

defect.

6) Papilloedema

Uhthoffs [1914] study of bilateral papilloedema showed

the etiology in 71 % as brain tumors, 12 % cerebral

syphilis, 3.6 % cerebral oxycephaly, brain abscess and

meningitis 2.2 % each. In this study 56 % of the patients

had papilloedema during presentation. Posterior fossa

tumors presented with papilledema earlier where as

cortical & pituitary tumors presented late. Optic nerve

fibres are compressed by elevated cerebrospinal fluid

pressure in the subarachnoid space of the intraorbital

portion of the optic nerve. Subsequent swelling of axons

and leakage of water, protein, and other axoplasmic

Table 1: Age distribution.

Age group Percentage

<10 6 %

10 to 20 6 %

20 to 30 22 %

30 to 40 20 %

40 to 50 30 %

>50 16 %


contents into the extra cellular space causes venous

obstructions, nerve fibre hypoxia and vascular

telangiectasis of the disc as secondary events.

Therefore, papilledema is primarily mechanical rather

than a vascular phenomenon. Normally the disc edema

takes 1-4 days to develop after the increase of CSF

pressure.

7) Cranial nerves [Table:3]

Expanding supratentorial mass lesions displaces cerebral

tissues to compress the brainstem structures. During

this process the nerves innervating the extraocular

muscles are stretched resulting in false localizing sign.

VI nerve may be stretched over the petrous tip between

its point of emergence from the brainstem and its dural

attachment to the clivus. This is due to the downward

descent of the brainstem and may occur with posterior

Table 2 : Area of Involvement & Histopathological subtypes

Area of lesion Histopathology Percentage

Parietal lobe Meningioma-2

Malignant Ependymoma-1 14 %

Glioblastoma multiforme-1 Astrocytoma-2

Epidermoid cyst-1

Fronto parietal Astrocytoma-1 6 %

Meningioma-2

Frontal Meningioma-3

Glioblastoma multiforme-2 12 %

Abscess-1

Fronto temporal Astrocytoma-1

Oligodendroglioma-1 6 %

Glioblastoma multiforme-1

Temporal Pilocytic astrocytoma-1 4 %

Caver. Haemangioma-1

CP angle tumour Acoustic neuroma-7 20 %

Meningioma-1

Glioma-2

Parieto occipital

Astrocytoma-1

Glioma-1 6 %

Abscess-1

Perichiasmatic Pituitary tumours-3

Craniopharyngioma-5 18 %

Tuberculum Sellae Meningioma-1

Cerebellum Medulloblastoma-1 4 %

Glioma-1

Ventricle Colloid cyst-3 8 %

Epidermoid-1

Corpus callosum Glioma-1 2 %

Table 3: Distribution of cranial nerve palsy

Cranial Nerve Palsy Percentage

IIIrd nerve 3.12

VI nerve 21.86

VII nerve 31.2

VIII nerve 18.74

IX, X nerves 6.25

V nerve 18.74


fossa tumours. Bilateral palsy of VI nerve may be a false

localizing sign. Cranial nerves were involved in 64 %.

Cerebellopontine angle tumors were associated with

cranial nerve involvement [5, 7, 8 cranial nerves

involved in 100 % & 9, 10 cranial nerves involved in

6.25 %]

8) Hemiparesis

Pyramidal tract involvement with some form of hemi

paresis was seen in seven patients.

9) Cerebellar signs

All cases of cerebellopontine angle tumors were

associated with cerebellar signs.

10) Optic atrophy [Table:4]

Optic atrophy was seen in 9 patients. 3 patients had

primary optic atrophy [all cases were

craniopharyngiomas]. Post-neuritic optic atrophy

following papilledema was seen in rest of the cases.

accounts for the characteristic visual field defect. It was

seen in 2 cases of craniopharyngioma and one

tuberculum sellae meningioma. (c) Homonymous

hemianopia occurs in optic tract lesions due to tumors

in temporal, frontal, parietal & occipital lobes. It was

seen in 6 cases -2 parietal lobe lesions, 2 frontoparietal

& 2 temporal lobe lesions. (d) Homonymous superior

quadrantanopia was seen in one case of temperofrontal

meningioma due to involvement of the inferior fibres

in the optic radiation. (e) Homonymous inferior

quadrantanopia was seen in one case of parietal tumour

due to involvement of superior fibres in the optic

radiation passing through the parietal lobe.

Frontal lobe tumors

Patients with frontal lobe tumors showed behavioral

abnormalities, dementia, seizures & urinary

incontinence. Three out of the nine had convulsions.

Gliomas were the most common tumors of the frontal

lobe. 9 % of the frontal lobe tumors showed

homonymous hemianopia and 50 % showed peripheral

constriction of visual fields.

Temporal lobe lesions

Temporal lobe involvement was seen in 6 out of the

50 patients. 20 % of the cases showed superior

quadrantanopia & 25 % showed homonymous

hemianopia.

Cerebellopontine angle tumours

There were 10 cases with CP angle tumours. All of them

had deafness, ataxia, impaired corneal sensation,

papilledema and 7th and 8th nerve palsies. Other features

Table 4: Percentage of optic atrophy.

Optic Atrophy Percentage

Primary optic atrophy 2

Secondary optic atrophy 12

Total 18

Table 5: Distribution of visual field defects

Field defect Percentage Cases

Bitemporal hemianopia 7.14 Craniopharyngioma, tuberculus sellae meringroma

Homonymous hemianopia 21.43 Parietal astrocytoma, Parietal epidermoidFronto parietal meningioma Tem parietal oligodendroglioma Tem.pilocystic astrocytoma

Homo.superior quadrantanopia 3.57 Fronto temp.meningiomaHaemangioblastoma cerebellum

Homo.inferior quadrantanopia 3.57 Glioblastoma multiforme

Parietal lobe

Blind spot enlargement 53.57

Peripheral constriction 28.57

11) Visual field defects [Table:5]

Visual field testing helps in localizing and lateralizing

the intracranial lesions. Most field defects of

neurophthalmic significance are located in the central

30-degree field. 56 % of the patients in this study

showed field defects. (a) Blind spot enlargement was

the most common. (b) Bitemporal hemianopia - The

partial decussation of nerve fibres in the optic chiasm


include gaze induced nystagmus, brun’s nystagmus,

tinnitus and dysphasia. In the present study the

incidence of raised ICT as evidenced by papilledema

was seen in 80 % of cases. Papilledema occurred

secondary to hydrocephalus as a result of aqueductal

obstruction by the tumour. Papilledema may sometimes

result due to increased protein secretion by the tumour.

Optic atrophy is secondary to papilledema. In the

present study nystagmus is seen in 20 % of cases of CP

angle tumours.

Conclusion

Ocular manifestations occur very frequently in

ICSOL,which in some cases helps us to diagnose the

condition. Headache was the most common symptom

followed by defective vision. Cranial nerve involvement

was seen in many cases, most common of which was

sixth nerve palsy. Papilledema was the most common

fundus finding followed by optic atrophy. Visual field

abnormality was seen in majority of cases out of which

blindspot enlargement was most common followed by

bitemporal hemianopia, homonymous hemianopia,

superior and inferior quadrantanopia. Distribution of

brain tumours showed CP angle tumours to be most

common followed by parietal lobe, frontoparietal,

frontal, frontotemporal, temporal and parieto-occipital

lobe. This study emphasizes the importance of ocular

manifestations in the localization, extent of the lesion,

prognosis for vision and life of the patient, in the case

of brain tumours.

References

1. Rao KV, Subramanyam M, Rao BS. Papilledema. IndianJournal of Ophthalmology 1982; 30: 465-7.

2. Sood NK, Sharma M, Nada A, Dutt RC, Nagpal.Correlation between CT Scan and Automated Perimetryon Supratentorial Tumours. Neurology India. June2002, 50; 2: 158-161.

3. Duanes Clinical Ophthalmology, Vol.2, 1996. WillaimTasman, Edward A, Jaeger.

4. Duke-Elder, Sytem of Ophthalmology, Vol.XII,Neuroophthalmology, 1967.

5. Hayreh SS. Pathogenesis of Edema of Optic Disc. BJO,48: 522-543, 1964.

6. Huber A, Eye Signs and Symptoms in brain tumours.Blodi FC. 3rd Edition, St.Louis, C.V.Mosby, 1976.

7. Smith JL. Homonymous Hemianopia: A review of 21patients. Arch. Ophthalmol. 96; 656-663; 1978.

8. Miller NR. Walsh and Hoyt ClinicalNeuroophthalmology 3rd Edition, Vol.I&III. 1984.

9. Chamlin M et al. Ophthalmologic Changes Producedby Pituitary Tumours. Am. J. Ophthalmology 40: 353;1955.

10. Adler’s Text Book of Physiology.


Capsulo-Cortical Adhesions (CCA) and

Phacoemulsification (PE)Dr. Arup Chakrabarti MS, Dr. Sonia R John DNB, Dr. Valsa T Stephen MS DNB,

Dr. Meena Chakrabarti MS DNB

One of the basic requirements of modern techniques

of phacoemulsification is free rotation of the

nucleus 1, 2, 3. A freely mobile nucleus 4 is a sign that it is

totally separated from the capsular bag and subsequent

maneuvers of the nucleus are likely to place minimal

stress on the zonules. Rotation is achieved by cortical

cleaving hydrodissection 5 which separates the nucleus

from the capsular bag.

Sometimes it may be difficult or impossible to rotate

the nucleus despite meticulous cortical cleaving

hydrodissection. If faulty technique of cortical cleaving

hydrodissection has been ruled out, it is usually the

presence of capsulo-cortical adhesions that makes

nucleus rotation difficult.

Capsulo-cortical adhesions are characterized by

adhesions between the capsule and cortex (Figures 1a

and 1b). These adhesions may be anterior, posterior,

equatorial or any combinations of the above. Unlike in

a cortical cataract, there is no definite area of

translucence visible between the capsule and the

underlying opaque cortical layers in capsulo-cortical

adhesions. Opacity exists in the outermost layers of the

cortex that is adherent to the lens capsule. These

adhesions can be assessed at the slitlamp as well as the

operating microscope, to a certain extent.

This prospective study was conducted to look into the

peculiarities and difficulties faced by the surgeon while

operating on cataracts with capsulo-cortical adhesions.

The goal was to prepare a guideline for safe

management of these cases.

Patients and Methods

86 consecutive patients with capsulo-cortical adhesions

scheduled for phacoemulsification (Group A) were

included in this prospective study. The diagnosis of

capsulo-cortical adhesion was made intraoperatively

just before starting the surgery with the patient under

the operating microscope after prepping and draping

of the patient. The intraoperative findings were

matched with the slitlamp examination findings

documented in the casesheet during preoperative

evaluation. All these patients had been preoperatively

assessed at the slitlamp with a fully dilated pupil.

Exclusion criteria included patients with prior ocular

surgery, ocular disease, complicated cataract and

nondilating pupils. 20 consecutive patients with

routine uncomplicated cataract, scheduled for

phacoemulsification were also included in the study

as controls (Group B). The exclusion criteria,

Fig. 1a. Capsulo-cort icalAdhesion on diffuseillumination

Fig. 1b. Capsulo-corticalAdhesions on

retroillumination

Chakrabarti Eye Care Centre, Kochulloor, Trivandrum 695 011 E-mail:

[email protected]

ORIGINAL

ARTICLE


surgical technique and protocols were the same in each

group.

Phacoemulsification was performed by a single surgeon

(AC). All surgeries were performed under topical

anesthesia with 2 % xylocaine jelly through the

temporal clear corneal approach. The anterior capsule

was stained with trypan blue dye (0.06 %) under an

air bubble. Continuous curvilinear capsulorhexis was

performed under 2 % hydroxypropyl methyl cellulose

using a 26 gauge bent needle. A three-site cortical

cleaving hydrodissection (3,9 and 6 o’clock) was

performed by injecting BSS through a 26-gauge cannula

attached to a 2 ml syringe. The cannula tip was

advanced under the anterior capsule approximately till

the capsular fornix, the anterior capsule tented and BSS

was gently injected until a complete fluid wave was

observed between the lens and the posterior capsule.

The shallowing of the anterior chamber was also

considered as one of the endpoints of cortical cleaving

hydrodissection. The capsular bag was decompressed

by gently tapping on the anterior lens capsule with the

hydrodissection cannula itself. The anterior chamber

was refilled with viscoelastic and nucleus rotation was

attempted with a Sinskey hook through the side port.

If the nucleus did not rotate freely, no effort was made

to attempt a forcible rotation. Additional multiquadrant

hydrodissection was performed in two more sites that

also included the area of capsulo-cortical adhesion. The

cannula was also passed subcapsularly in an attempt

to lyse the anterior capsulo-cortical adhesions by

employing the concept of hydrofree dissection. Nucleus

rotation was attempted again and the surgeon noted

down the subjective difficulty encountered during

nucleus rotation. If the nucleus did not rotate, another

round of cortical cleaving hydrodissection was repeated

once again at two different points. Subsequently,

phacoemulsification was performed. A phacochop or

stop and chop phacotechnique was employed using the

Bausch and Lomb Millennium phaco unit. The surgeon

looked out for any peculiarity or uniqueness in these

cases. All cases were recorded in a DVD. Subsequently

each of the recorded cases was analysed for a) the total

duration of the actual surgical procedure, b) the total

time required to perform rhexis and c) the total time

required for cortical cleaving hydrodissection.

Results

86 patients were noted to have capsulo-cortical

adhesions at the start of the surgery. The average age

Different types of CCAs seen on diffuse illumination (a),retro illumination (b) and slit beam illumination (c)

Table 1: Patient Profile

Group A Group B(N = 86) ( N = 20)

Age (Years)

Upper limit 87 82

Lower limit 46 32

Mean 67 61.7

Sex

Male 43 11

Female 43 09

Associated systemic disease

Nil 19 (22.09 %) 53 (61.63 %)

Diabetes Mellitus 5 (25 %) 10 (50 %)

September 2009 Arup Chakrabarti et al. - CCA and PE 255

of the patients was 67.1 years (range 46 years to

87 years). The sex distribution was even with

43 patients in each category (Table 1).

19 patients had no systemic illnesses with diabetes

mellitus being the commonest systemic association

resistance was always encountered while performing

the rhexis in the area of the capsulo-cortical adhesion.

Nucleus rotation could be performed after the first

sequence of cortical cleaving hydrodissection in

83 cases. However in 5 of these cases (5.81 %) the

rotation was difficult and stressful though no untoward

damage like zonular dialysis was noted. It could be

completed only after the second sequence of cortical

cleaving hydrodissection. In 3 cases (3.49 %) the

nucleus could not be rotated. Milky turbid fluid

(Figure 2) was noticed to originate from the area of

the capsulo-cortical adhesions in 10 patients (11.63 %)

at the stage of nucleus decompression during cortical

cleaving hydrodissection. There were no significant

intraoperative complications like posterior capsular rent

or zonular dialysis in any of these patients. Visual

recovery of 6/9 or better on the 5th postoperative day

was seen in 76 patients (88.37 %).

Discussion

Free and easy nucleus rotation is an important

prerequisite in all the modern techniques of

phacoemulsification.It considerably reduces the stress

placed on the zonules and capsular bag during removal

of the nucleus or nuclear fragments. Cortical cleaving

hydrodissection is a step, which is aimed to completely

separate the nucleus from its adhesions rendering it

freely mobile within the capsular bag. This separation

may be difficult or stressful and is at times impossible

in the presence of capsulo-cortical adhesions (CCA).

It is therefore important to be able to detect the

presence of capsulo-cortical adhesions before the

cortical cleaving hydrodissection step. A meticulous

dilated slitlamp evaluation preoperatively helps to a

great extent in diagnosing the presence of this

condition. One should also look for this condition with

the patient in extreme gaze. However one may miss

the diagnosis of capsulo-cortical adhesion in the

presence of a nondilating pupil or a dense cataract.

Even if the condition is missed during the preoperative

evaluation (for cataract surgery) a surgeon aware of

this entity should be in a positon to make a diagnosis

of capsulo-cortical adhesion intraoperatively. There

were 13 cases (15.12 %) of capsulo-cortical adhesions

which were undetected preoperatively and detected

intraoperatively in the current study.

Type of Cataract Group A Group B(No .86) (No. 20)

1. Anterior Subcapsular +Posterior Subcapsular 12 (13.95 %) 3 (15 %)

2. Anterior Subcapsular +Nuclear 4 (4.65 %) 2 (10 %)

3. Anterior Subcapsular +Posterior Subcapsular + White 6 (6.98 %) -

4. Anterior Subcapsular +

Posterior Subcapsular+Nuclear 64(74.41 %)15 (75 %)

(61.63 %) in those with concurrent systemic illness.

The type of cataracts associated with capsulo-cortical

adhesion are given in Table 2.

The mean total duration of the surgical procedure as

defined by the time from first incision till the application

of the eye pad at the conclusion of surgery was 22.68

minutes (range: 47.16 minutes to 14.23 minutes). The

mean duration of time when the surgical steps were

actually performed was 14.91 minutes (range: 36.14

minutes to 9.11 minutes). The mean time taken for

rhexis was 1.39 minutes (range: 4.51 minutes to

0.46 seconds). The mean time taken for cortical

cleaving hydrodissection was 2.13 minutes

(3.35 minutes to 0.13 seconds) (Table 3).

Group A Group B(N = 86) (N = 20)

Elapsed Phaco Time (min) 1.16 1.03(5.1 to 0.52) (2.48 to 0.34)

Absolute Phaco Time (min) 0.16 0.10(1.3 to 0.01) (0.24 to 0.03)

Average Phaco Power (%) 21.46 22

(70 to 40) (27 to 5)

The capsulo-cortical adhesions encroaching into the

pupillary area tended to render the red fundal glow

(whenever present) a bit dull as opposed to rest of the

central areas with a brighter red reflex. Trypan blue

staining of the anterior capsule enhanced the visibility

of the capsular tear at the zone of the adhesions. Some


Cortical cleaving hydrodissection should be performed

meticulously. The cannula tip should tent the anterior

capsule and the fluid injection should be performed

close to the capsular fornix. Mechanical lysis of the

adhesion with the same cannula or a cyclodialysis

spatula may be attempted. Signs of successful

hydrodissection include a fluid wave across the

posterior capsule, shallowing of the anterior chamber

due to forward bulging of the nucleus, a prominent

capsulorhexis edge and release of trapped fluid from

the rhexis margin when the nucleus is tapped back.

We routinely perform 3 - quadrant cortical cleaving

hydrodissection even in our standard cases before

attempting nucleus rotation. The same strategy was

adopted in the study too, and this is more likely to lyse

the adhesions than a one-point hydrodissection. This

explains the high success rate of nucleus rotation in

our study after the first sequence of cortical cleaving

hydrodissection. No additional force is to be used to

rotate the nucleus in the event of any difficulty and a

repeat 3 quadrant cortical cleaving hydrodissection is

called for.

Sometimes, inspite of a good cortical cleaving

hydrodissection, where the posterior fluid wave has

been visualized and focal lysis of the capsulo-cortical

adhesions has been performed, it may be difficult to

rotate the nucleus. It could be due to the presence of

equatorial adhesions and further multiquadrant

hydrodissection should be done before attempting to

rotate the nucleus.

The milky fluid (Figure 2) seen to emanate from the

area of capsulo-cortical adhesions (in 10 patients,

11.63 %) while decompressing the capsular bag at that

area seem interesting. The furry epinuclear surface

(Figure 3) present focally at the area of the adhesions

were noted in many cases and could be a result of lysis

of the fibrous adhesions between the anterior capsule

and underlying cortex.

Time required to perform rhexis as well as cortical

cleaving hydrodissection was more in the patients with

capsulo-cortical adhesions when compared to the

control group.

In conclusion, a thorough preoperative dilated slitlamp

evaluation should be performed to detect capsulo-

cortical adhesions. Intraoperative evaluation also helps

to detect some cases of capsulo-cortical adhesions not

detected by prior slitlamp examination. Before any

attempt at nucleus rotation a 3-point cortical cleaving

hydrodissection as well as focal and hydrofree

dissection are strongly recommended.

Reccomendations

• Detection of Capsulo cortical adhesions is

important before hydrodissection

• Meticulous dilated slitlamp evaluation

preoperatively is mandatory

• Capsulo cortical adhesions may be missed in non

dilating pupil or dense cataract

• Can be diagnosed intraoperatively even if missed

initially

• Meticulous cortical cleaving hydrodissection in

presence of Capsulo cortical adhesions

– Fluid injection after tenting of anterior capsule,

close to capsular fornix

– Mechanical lysis with cannula or cyclodialysis

spatula

• Signs of successful hydrodissection

– Fluid wave across the posterior capsule

– Shallowing of anterior chamber

– Prominent capsulorhexis edge

– Release of trapped fluid from the rhexis margin

when nucleus is tapped back.

• In presence of equatorial adhesions, further

multiquadrant hydrodissection to be done before

attempting nucleus rotation.

• Milky fluid emanating from area of adhesions-

could be result of lysis of adhesions

Fig. 3. Furry epinuclearsurface indicating thepresence of capsulo-cortical adhesions

Fig. 2. Milky turbid fluidfrom the area of

c a p s u l o - c o r t i c a ladhesions.

September 2009 Arup Chakrabarti et al. - CCA and PE 257

Guidelines in Patients with Capsulo

cortical adhesions

CCA is a frequent phenomenon and often underdiagnosed

• Establish diagnosis preoperatively. (caution to be

exercised in total cataract/small pupils)

• TB staining of the anterior capsule

• Meticulous cortical cleaving hydrodissection.

• Hydrofreedissection may be beneficial

• No forcible nucleus rotation

• Capsular tension ring/Injector to be kept handy

Conclusion

• Thorough preoperative dilated slitlamp evaluation

mandatory

• Intraoperative evaluation to detect missed cases.

• Increased suspicion when lens milk visualized in

preoperatively undiagnosed cases.

• A 3 point cortical cleaving hydrodissection and

hydrofree dissection to be performed before

attempting nucleus rotation.

References

1. Gimbel HV. Divide and conquer nucleofractis

phacoemulsification: development and variations. J

Cataract Refract Surg 1991; 17:281-291

2. Shepherd JR. In situ fracture. J Cataract Refract Surg

1990; 16:436-440.

3. Vasavada AR, Singh R. Step-by-step chop in situ and

separation of very dense cataracts. J Cataract Refract

Surg 1998; 24:156-159.

4. Gimbel HV. Hydrodissection and hydrodelineation. Int

Ophthalmol Clin 1994;34(2):73-90.

5. Fine IH. Cortical cleaving hydrodissection. J Cataract

Refract Surg 1992; 18:508-512.


Efficacy of Combining Intravitreal

Bevacizumab Monotherapy (IVB) with

Panretinal Photocoagulation(PRP) In Early

Stages of Neovascular Glaucoma (NVG)Dr. Meena Chakrabarti MS DO DNB, Dr. Arup Chakrabarti MS, Dr. Sonia Rani John DNB

Anterior Segment neovascularisation results from

several ocular and systemic diseases that predispose

patients to retinal hypoxia and ischemia with

subsequent release of angiogenesis factors such as

vascular endothelial growth factor. Bevacizumab

(Avastin), a recombinant antibody against vascular

endothelial growth factor (VEGF), has been shown

to effectively reduce neovascular activity and

vascular permeability in ocular tissues. Administration

of intravitreal Bevacizumab in the early stages of

neovascular glaucoma (characterized by

presence of neovascularisation of iris and

angle, elevated IOP by the open angle

mechanism) may dampen the neovascular trigger.

When combined with panretinal photocoagulation

(on the same day) control of the ischemic process is

ensured and further progression to advanced secondary

angle closure neovascular glaucoma may be prevented.

Clinical Objective: To study the efficacy of

combining intravitreal Bevacizumab (Avastin)

injection with same day panretinal photocoagulation

in eyes with early neovascular glaucoma (Stage II,

Open angle mechanism prior to development

of peripheral anterior synechiae and angle

closure)

Primary Outcome Measures: Regression of

neovascularisation of iris, and neovascularisation of the

angle were the primary outcome measures that we

studied.

Brief Review of Pertinent Literature:

1. Oshima et al1 reported a series of seven eyes with

neovascularisation of iris (NVI) secondary to

proliferative diabetic retinopathy. The NVI

regressed in all patients at one week and repeated

injections stabilized the recurrence in 2 eyes that

was seen 2 months after the initial injection. IOP

was controlled in 6 eyes throughout the follow

up period with no inflammation and

complications.

2. Tripathi et al2 have shown that patients with NVG

had significantly increased levels of VEGF in the

aqueous humor. They discussed the possible role

of ciliary epithelium, in addition to the retina, in

the production of VEGF and the complementary

functions of basic fibroblast growth factor and

other growth factors.

3. Davidorf et al3 described the regression of

NVI and NVA in a patient with choroidal

melanoma and diabetes (treated with TTT and

PRP), following intravitreal injection of

Bevacizumab.Chakrabarti Eye Care Centre, Kochulloor, Trivandrum 695 011 E-mail:

[email protected]

ORIGINAL

ARTICLE

September 2009 Meena Chakrabarti et al. - Combination therapy in NVG 259

4. Mason et al4 proposed the use of IVB for patients

with NVG, recurrent hemorrhage from NVI and

for those who despite PRP develop NVI. Tube

drainage procedures may be avoided by giving

intravitreal Bevacizumab injection as it causes

regression of iris and angle neovasularisation and

better IOP control medically.

5. Iliev et al5 described six consecutive NVG patients

with refractory symptomatic elevation of IOP who

received intravitreal Bevacizumab injection.

A marked regression of NVI, substantial IOP

reduction in 3 eyes, and symptomatic relief in all

eyes were observed in 48 hrs.

6. Grisanti et al6 described the regression of NVI in

6 eyes with PDR and NVG following intracameral

injection of Bevacizumab. As early as Day 1

decrease in leakage form the iris vessels was

observed by iris fluorescein angiography. No

inflammation or relapse was observed at 4 weeks.

7. Avery et al7 demonstrated the regression of retinal

and iris neovascualrisation due to PDR, following

the administration of IVB.

8. Vatavuk et al8 reported regression of iris and angle

neovacularisation with reduction of IOP in an eye

with NVG following CRAO.

9. Luis Amselemab9 et al have demonstrated the

efficacy of using Intravitreal Bevacizumab in

patients with ocular ischemic syndrome and

neovascular glaucoma. Although there was

regression of NVI and no recurrence on follow

up, no substantial IOP lowering effect or change

in vision could be demonstrated.

10. Ehlers et al evaluated the efficacy of combining

intravitreal Bevacizumab and panretinal

photocoagulation in the treatment of neovascular

glaucoma. Their results effectively showed that

combination therapy resulted in more rapid

decrease of IOP,increased frequency and rapidity

of regression of neovascularisation.

We conducted a prospective interventional study in

38 eyes with early stage II neovascular glaucoma that

underwent one of the three modes of intervention.

1) Isolated PRP (15 eyes); (2) IVB

Monotherapy (12 eyes) and combined

IVB and PRP ( 11 eyes)

a. Inclusion Criteria:

i. Presence of peripupillary neovascularisation of iris

and early neovascularisation of angle

ii. Elevated Intraocular Pressure

iii. Good fundus view

iv. H/o Laser Photocoagulation (for PDR:

Proliferative Diabetic Retinopathy/: Ischemic

Central Retinal Vein Occlusion) more than 3

months prior to enrolment.

v. Adequately controlled systemic co.morbid

conditions.

The randomization for enrolment into the various

treatment groups was biased in that high risk patients

with a history of prior thromboembolic episodes, or

coronary artery disease were advised to enroll in the

PRP group (Fig. 1). Likewise patients with higher

baseline IOP were enrolled into the combination group.

b. 38 eyes were studied and in bilateral cases

(3 patients) one eye received panretinal

photocoagulation and other eye received a

combination of intravitreal Bevacizumab and

panretinal photocoagulation.

c. Patients were age and gender matched as both

groups had patients with ages ranging from

48-75 years.

d. There was no control group and all patients

underwent one of the three methods of

intervention.

e. Methods of collecting patients: Patients attending

our out-patient department who satisfied our

inclusion criteria were included in this study.

Exclusion Criteria:

1. Florid NVI and presence of Peripheral anterior

synechiae (PAS.)

2. Advanced NVG

3. Corneal Changes, Hyphema, Cataract with

poor fundus view


3. Combined IVB + PRP group: included new

cases with no prior laser who presented with early

NVG and untreated retinopathy. PRP I was given

on the same day as the intravitreal injection and

the second sitting was given on the next day.

Recurrence in this group were treated by repeat

IVB injection (Fig. 2)

We evaluated the patient for any systemic adverse

effects especially thromboembolic episodes or acute

coronary events. Local side effects evaluated were:

vitreous hemorrhage, retinal detachment,

endophthalmitis and recalcitrant glaucoma.

The systemic adverse effects were evaluated by a

detailed history and by consultation with the treating

internist. Ocular side effects were assessed by post

treatment ophthalmic examination and follow up.

Outcome assessments: Outcomes were assessed in

all patients by (VS) and (SRJ). At each follow up

visit the following evaluations were performed.

1. Best corrected visual acuity

2. Non Contact Tonometry (Pulsair, Keeler)

3. Slit lamp examination of the anterior

segment.

4. Gonioscopy

5. Indirect Ophthalmoscopy

The parameters assessed were regression of NVI, by

slit lamp biomicroscopy and gonioscopy for regression

of NVA. The IOP was measured at each follow up visit

and a dilated fundus examination was performed.

All the patients were followed up at weekly intervals

for a period of 12 weeks ,at monthly intervals for 6

months, and 4 monthly for 1 year. All 38 patients

adhered to the follow up schedule.

The primary treatment outcome that we assessed was

for the regression of NVI Table:1 compares the effect

of intervention on the primary outcome ie time to

regression of NVI under the three different interventions

In the PRP group the mean time to regression of NVI

was 107.4+/- 19.3 in the PRP group, 51.5 +/-sd 14.5

days in the IVB Group, and 14.1+/-4.7days in the

combination group.Comparison of the time to NVI

regression under the three different interventions was

least in the combined group and was statistically

Therapeutic Intervention

1. PRP alone (15 eyes): underwent either primary

PRP in 2 sittings if they were unlasered or fill in

additional PRP if they had already undergone laser

photocoagulation previously. They were followed

up at weekly intervals and at each visit the best

corrected visual acuity, slit lamp examination,

applanation tonometry, gonioscopy and fundus

examination were performed. The regression of

NVI and the time to regression, presence or

absence of recurrence were carefully noted.

Repeat treatment for recurrence was by additional

PRP or by combining PRP with IVB.

2. IVB monotherapy (12 eyes) who had

undergone prior laser photocoagulation were

included in this group. Recurrences were treated

by fill in PRP or repeat IVB.

Fig. 1. Bar diagram showing distribution of cases in each groupbased on associated co-morbid condition

Fig. 2. Showing regression of NVE, NVI and decreased leakagein fluorescein angiography in a patient with NVGfollowing Ischemic Central Retinal Vein Occlusion


significant .(p=o.ooo ) using the Scheffe multiple

comparisons test.

Effect of intervention on the secondary outcome ie

control of intraocular pressure is given in Table : 2a-c.

The effect of intervention in controlling IOP was seen

in all the 3 groups at 2 weeks and sustained at 12 weeks.

However a further IOP lowering effect was seen at 12

weeks (p=0.002) in the combination group which was

statistically significant using the paired “ t” test.

Discussion

1) Effect of intervention in causing regression of NVI

and reducing the time to regression was most

significant in the group which received combined

PRP and IVB ( p = 0.000)

2) Effect of intervention in controlling the intraocular

pressure was maximum in the group which

received combined PRP and IVB at both 2 wks

and 12 weeks post intervention ( p=0.000 &

p= 0.002)

3) Recurrence occurred in 53.3 % of patients who

received PRP alone and 20% in the combined

group.

4) There was also a reduced need for repeat injection

in the combination group when comparing the

group that received IVB monotherapy versus

combination group (3.5 injection Vs 1.8 injection)

b) Limitation or Inherent Bias in the study design

1) The randomization for enrollment into the

various study groups was biased with respect

to co- morbid conditions. High risk patients

with history of prior thrombo-embolic

episodes or coronary artery disease received

only pan retinal laser photocoagulation. This

Table 1a Comparison of Time to NVI regression under three different interventions

Type of intervention Mean Time SD N F Sig. Scheffe Multiple Comparisons

(days) Pair Mean Diff p

PRP (A) 107.4 19.3 15 121.96** 0 A &B 55.94** 0

IVB (B) 51.5 14.5 13 A & C 93.30** 0

IVB + PRP (C) 14.1 4.7 10 B & C 37.36** 0

Effectiveness of intervention on IOP

Table 2a Effectiveness of treatment on IOP in PRP group

Stage Mean IOP SD N Group mean difference paired ‘t’ p

BT (A) 27.6 4.7 15 A Vs B 4.8 5.04** 0

post 2 wk (B) 22.8 4.2 15 A Vs C 4.73 3.06** 0.008

post 12 wk (C ) 22.9 5.9 15 B Vs C 0.07 0.06 0.955

** : significant at 0.01 level

Table 2b Effectiveness of treatment on IOP in IVB group

Stage Mean SD N Group mean difference paired ‘t’ p

BT (A) 27.5 4.6 13 A Vs B 4.15 5.67** 0post 2 wk (B) 23.4 3 13 A Vs C 4.62 4.21** 0.001

post 12 wk (C ) 22.9 4.6 13 B Vs C 0.46 0.61 0.553


Table 2c Effectiveness of treatment on IOP in IVB + PRP group

Stage Mean SD N Group mean difference paired ‘t’ p

BT (A) 34.8 7.3 10 A Vs B 8.4 4.71** 0.001post 2 wk (B) 26.4 5.1 10 A Vs C 12 5.75** 0

post 12 wk (C ) 22.8 3.7 10 B Vs C 3.6 4.32** 0.002



group also included patients with ocular

ischemic syndrome.

2) Patients who received combined PRP + IVB

were newly detected cases of vascular

retinopathy presenting to our centre with

early NVI and did not have a history of prior

laser photocoagulation.

The efficacy of combining intravitreal Bevacizumab

monotherapy with pan retinal photocoagulation in early

neovascular glaucoma prior to secondary angle closure

glaucoma alone was studied. This may not be applicable

to patients with 20 angle closure neovascular

glaucoma where prior IVB injection is necessary in

association with maximal medical therapy to control

the ocular inflammation & quieten the eye before laser

photocoagulation.

Comparison of our results with a similar study was

favourable with respect to regression of

neovascularisation of iris and angle and adequate

control of intraocular pressure. (Table : 3)

Thus combining intravitreal bevacizumab injection

panretinal laser photocoagulation can be considered

as a first line therapy for patients with early stage of

neovascular glaucoma

References

1. Oshima Y, Sakaguchi.H et al. Regression of iris

neovascularisation after intravitreal injection of

Bevacizumab in patients with proliferative diabetic

retinopathy. Am. J. Ophthalmol 2006; 142:155-8.

2. Tripathi RC, Li.J, Tripathi BJ, Chalam KV et al. Increased

levels of vascular endothelial growth factor in the

aqueous of patients with neovascular glaucoma.

Ophthalmology 1998; 105:232-7.

3. Davidorf FH, Mouser JG et al. Rapid improvement of

neovasularisation and of iris from a single Bevacizumab

injection. Retina 2006; 26:144-6.

4. Mason JO, Albert MA, Mays A et al. Regression of

neovascular iris vessels by intravitreal injection of

Bevacizumab. Retina 2006; 26:839-41.

5. Iliev MF, Domig D, Wolf – Schnurrbursch U et al.

Intravitreal Bevacizumab injection in the treatment of

neovascular glaucoma. Am.J. Ophthalmol 2006;

142:1054-6.

6. Grisanti.S. Biester S, Peters.S et al for the Tuebingen

Bevacizumab study group. Intracameral Bevacizumab

for iris rubeosis. Am. J.Ophthalmol 2006; 142:158-160.Table

3:

Com

pari

son

wit

h a

noth

er

pu

bli

sh

ed

stu

dy

Au

tho

r /Y

ear

No

Gra

de

Sta

ge

of

PR

PP

RP

+IV

BR

egre

ssio

n

T

ime

to N

VI

Reg

ress

ion

P v

alu

eIO

PP

of

NV

IN

VG

Gp

of

NV

IC

on

tro

lv

alu

e

PR

PP

RP

+IV

BP

RP

PR

P+

IVB

Eh

lers

JP

et

al2

3N

ot

men

-N

ot

men

-1

211

211

12

7d

ays

12

day

P<

0.0

00

111

P=

0.0

3

Ret

ina

28

(5)

20

08

tio

ned

tio

ned

P(

<0

.00

01

)

Pre

sen

t st

ud

y3

8G

r II

Op

en a

ng

le1

511

15

11

10

7 d

ays

14

.1d

ays

P=

0.0

00

11

P=

0.0

00

1

gla

uco

ma

stag

e II


7. Avery RJ. Regression of Retinal and irisneovascualarisation after intravitreal Bevacizumabtreatment. Retina 2006; 26: 352 - 4.

8. Vatavuk Z, Bencic.G et al. Intravitreal Bevacizumab forNVG following CRAO. Eur.J.Ophthalmol 2007; 17:269-271.

9. Luis Amselemab, Javier Montero et al. IntravitrealBevacizumab injection in Ocular Ischemic SyndromeAm.J.Ophthalmol 2007;Vol 144(1): 122-124.

10. Ehlers J, Lam, Samuel Micheal, William Tasman et alCombination Intravitreal Bevacizumab/Pan retinalPhotocoagulation versus pan retinal photocoagulationalone in the treatment of neovascular glaucoma. Retina2008; 28(5): 696-702


Ophthalmic Manifestations in Children with

Delayed Milestones- A Clinical StudyDr. Reena A. MS, Dr. Lekshmy S R MS, Dr. Lekshmi H MS, Dr. Bindu K. Appukuttan MS

ABSTRACT

A cross -sectional study of 150 children aged between 6 months and 3 years with delayed

developmental milestones was conducted at Child Development Centre, Sri Avittam Thirunal

Hospital and Regional Institute of Ophthalmology,Trivandrum over a period of 18 months.The

study aimed at identifying the various ocular manifestations in children with developmental

delay,the treatable causes of visual handicap among them and the associated antenatal and

perinatal factors. A complete systemic examination in consultation with a paediatrician and

a detailed ophthalmic evaluation including assessment of refraction was performed.The

collected data was analysed by statistical methods. CONCLUSIONS :Ocular manifestations

were present in 64 % of selected children. Refractive errors( 41.3 %), Stabismus (40 %) & Optic

Atrophy(9.3 %)were identified as the major causes of visual impairment.The chief treatable

causes were Refractive errors(41.3 %), Squint(40 %), Cataract (2.6 %) and Retinopathy of

Prematurity(4 %).Visual impairment and ocular manifestations like squint and optic atrophy

were more in children with global developmental delay.The importance of ophthalmological

examination in children with developmental delay was highlighted in the study.

Introduction

Development delay is estimated to be present in about

10% of pediatric population. Development may be

impaired due to a variety of factors like maternal,

genetic, perinatal, post-natal and social factors. Visual

development is a highly complex maturation process

involving structural and functional changes in both the

eye and the CNS.The burden of visual handicap in

childhood especially in a child with developmental

delay is of enormous importance because of the life

long impact of the handicap on other areas of

development. Early recognition of the problem may

expedite treatment or other forms of management

where the condition is not treatable. Developmental

delay may be associated with delayed visual maturation

where infants fail to develop fixation for upto 6-12

months but may later develop normal visual behaviour.

These children may have a totally normal eye but have

poor fixation due to the delay in maturation of the visual

system. In these cases, supportive treatment and

reassurance is required until the visual attention

becomes as expected.

Aim of the Study

� To study the various ocular manifestations in

children with delayed milestones.

� To find out the treatable causes of visual handicap

in these children.Regional Institute of Ophthalmology, Trivandrum

ORIGINAL

ARTICLE

September 2009 Reena A. et al. - Ophthalmic manifestations in children with developmental delay 265

� To study antenatal and postnatal factors in these

children.

� To study type of developmental delay whether

isolated or global delay.

� To highlight the importance of detailed

ophthalmic examination in children with

developmental delay.

Materials and Methods

Study Design : Cross Sectional Study

StudySetting : Child Development Centre, SAT

Hospital, Medical College,

Trivandrum, and

Regional Institute of

Ophthalmology, Trivandrum

Sample size : 150 (calculated based on

prevalance of Developmental

Delay in South Kerala)

Study period : 18 months

Study Population : Children between 6 months and

3 years with delayed developmental

milestones

Methodology

A cross- sectional study of 150 children between

6 months and 3 years of age with delayed developmental

milestones attending Child Development Centre,

SAT Hospital, Trivandrum and RIO, Trivandrum was

conducted. Proforma was prepared for recording

data of each patient separately. General examination

including systemic examination in consultation with

a pediatrician & ophthalmic examination consisting

of visual acuity assessment, anterior segment

examination, dilated fundus examination & retinoscopy

were done.

Developmental delay was assessed by Denver

Development Screening Test. The milestones were

assessed in terms of ‘Personal Social’, ‘Gross Motor’,

‘Fine Motor’ and ‘Language’. Children who did not

achieve milestones by the indicated ages were

considered to have developmental delay. Delay may be

present in either social, gross motor, fine motor or

language milestones or in all the four areas, ie, global

developmental delay.

In children <1year, visual acuity was assessed by CSM

method of fixation pattern and by indirect methods

like assessing the red reflex and resistance to occlusion.

Candy Bead test was used to assess visual acuity in

1-2 year age group or alternatively by CSM method if

needed. Sheridan Letter test was used in 2-3 year

age group. Additional investigations including baseline

blood investigations were done if indicated. Children

detected to have ocular features were managed

accordingly. Children who were found to have visual

acuity inappropriate for age or who were not fixing

and following despite normal ocular examination were

followed up after 6 months to see if there was any

improvement in visual acuity. Data collected was then

subjected to thorough descriptive statistical analysis.

Proportions of all relevant study variables were

calculated; such as demographic variables, clinical

variables such as antenatal illnesses in others, mode of

delivery of the babies, neonatal illnesses, neonatal

oxygen administration, types of developmental delay,

refractive errors, squint, nystagmus, optic atrophy,

delayed visual maturation, cortical visual impairment

Retinopathy of Prematurity, papilloedema

Results

Sex Distribution

Of the 150 children with developmental delay included

in study, 83 were males and 67 females.

Age Distribution

Children < 3 years were included in study.Among them

65 were between 6 months-1year,45 were between

1-2 years and 40 in 2-3 year age group.

Consanguinity

History of consanguinity was present only in 4 cases

while the remaining 146 were nonconsanguinous.

Antenatal Period

Antenatal period was uneventful in 133 mothers,

Pregnancy Induced Hypertension (PIH) was present in

5, fever with rashes in 5, 3 had history of trauma, 2

had Gestational Diabetes Mellitus and 2 had history of

threatened abortion.


Delivery

125 were full term and 25 were preterm. Caesarian

section was mode of delivery in 23,vacuum assisted in

2 while 125 had normal vaginal delivery.

Table 1 Postnatal Period

Post Natal Period

YES NO

Neonatal Jaundice 7 143

Birth Asphyxia 25 125

Oxygen administration 12 138

Seizures 19 131

Type of Developmental Delay

Out of the 150 children, 53(36 %) showed global delay,

45(30 %) had only motor delay, 33(22 %) had delay in

motor as well as language milestones, 14(9 %) had

isolated language delay and 5 children (3 %) showed

delay in motor & personal social milestones.

Ocular Manifestations

Table 2. Ocular Manifestations

Number of Cases Percentage (%)

Ocular manifestations 97 64.6

Normal but poor VA 24 16

Normal with good VA 29 19.4

Of the total 150 children with developmental delay,

97 (64.6 %) had ocular manifestation, whereas

29 (19.4 %) had normal ocular examination and good

visual acuity, whereas 24 (16 %) had normal ocular

examination but were not fixing and following light or

had poor visual acuity [Table 2].

Distribution of Ocular Manifestations

The various ocular manifestations seen in children

with developmental delay are refractive errors,

squint, optic atrophy, delayed visual maturation,

cortical visual impairment, retinopathy of

prematurity, papilloedema, nystagmus, and cataract.

(Fig. 1)

Visual Acuity Assessment [Table 3]

Table 3 Visual Acuity Assessment

Visual Acuity Number of Cases

By CSM method

NFNF 25

GEF 1

UCF 24

CSF 16

CSF-MP 16

CSM 13

By Sheridan Letter Test

6/60 -6/36 3

6/24 -6/18 2

6/12 -6/6 30

Refractive Errors

Refractive Errors(seen in 41.3 %)) were the most

common manifestation in these children on retinoscopy.

27 children had significant hypermetropia (>+3D)

18 had myopia and 17 showed astigmatism.

Squint [Table 4]

Table 4. Stabismus

Exotropia 90(60 %)

Esotropia 19(13 % )

Latent 39(26 % )

Hypertropia 2(1 % )

Fig. 1. Aetiologic Classification


Delayed Visual Maturation

24 children who had visual acuity inappropriate for

age or were not fixing or following light despite normal

ocular examination were followed up after 6 months

to look for any improvement.It was seen that 15 of

them showed some improvement in visual acuity while

it remained status quo or worsened in 9 cases.

Vison and Delayed Milestones

Severe visual impairment (< 6/60) and majority of

ocular manifestations like squint and optic atrophy were

seen more in children with global developmental delay.

of cerebral palsy alone and found ocular abnormalities

in 28 %. Regarding the sex distribution, 55 % in this

study were males and rest 45 % were females. In study

by Wu H.J et al 68 % were males and rest females.

Mean age range 1.58+/-0.9 years.In Wu H J et al study

mean age range was 3.53+/-2.25 years.3,6

Consanguinity was seen in only 2.7 %. Antenatal history

was uneventful in 133 cases whereas 17 cases had either

history of pregnancy induced hypertension, gestational

diabetes, trauma, threatened abortion or maternal

infections. History of pre-term delivery was present in

only 25 cases.In a study by Chen et. al 13.95 % had

pre-term delivery and 13.45 % had neonatal insults. In

the post natal period, history of neonatal jaundice was

present in 7 cases (4.7 %), birth asphyxia in 25 cases

(16 %), oxygen delivery in 12 cases (8 %) and seizures

in 19 cases (12.6 %). In a study by Nielson et. al, it was

found that visual impairment was due to prenatal

factors in 11 %, perinatal factors in 6 % and postnatal

in 1.4 %.7,4

On assessing developmental delay, 36 % of cases

showed global delay, 30 % only motor delay, 22 % both

motor and language delay, 9 % isolated language delay

and 3 % showed delay in both motor and social

milestones. In the study by Chen et. al, 51.2 % had

global delay, 21.9 % had speech delay and 13.95 had

motor delay. 7

� In this study ocular manifestations were seen in

64.6 % cases. On examining 150 children, refractive

errors were seen in 62 cases (41.3 %), strabismus

in 60 cases (40 %), optic atrophy in 14 cases

(9.3 %), ROP in 6 cases (4 %), cortical visual

impairment in 9 cases (6 %), nystagmus in 7 cases

(4.6 %), cataract in 4 cases (2.6 %), papilloedema

in 1 case and delayed visual maturation in 15 cases

(10 %). In a study by Wu H J, Tsai et al, optic atrophy

and strabismus were the two most common

manifestations. Bankes et al studied 200 children

with developmental delay & found refractive errors

in 49 %,squint in 37 %, nystagmus in 7.5 % and

other features like cataract,optic atrophy and

retinopathy. 3,5

Refractive Errors(41.3 %) were the most common

manifestation in this study of which 18 % had

significant hypermetropia (> +3D) 12 % had myopia

Fig. 2. Treatable Causes

Table 5 Delayed Milestones and Ocular Manifestations

POOR VISION SQUINT OPTIC ATROPHY

GLOBAL 27 28 10

MOTOR + SPEECH 10 12 3

MOTOR 11 12 1

MOTOR + SOCIAL 2 3

SPEECH 1 4

Treatable Causes of Visual Disability

Among the various ocular manifestations, the various

treatable causes identified were refractive errors

(41.3 %), Squint (40 %), ROP (4 %) and cataract

(2.6 %) (Fig 2)

Discussion

Of the total 150 children with developmental delay

examined at CDC and RIO Trivandrum,97(64.6 %)

had ocular manifestations.A study by Wu H J etal on

41 children with developmental delay showed ocular

manifestations in 56.1%. Lagunju et al studied 149 cases


and 11 % astigmatism. In a similar study by Nielson

et al, 15.3 % had hyperopia>+3D, 10.8 % were myopic

and 20.6 % had astigmatism. 4

On assessing Visual Acuity severe visual impairment

(<6/60) was seen in 51 cases(34.6 %) Lagunju et al

studied 149 Cerebral palsy cases and found that

61.9 % were completely blind.Fazzi et al found that

prevalence of reduced vision in children with CNS

damage was about 86.7%. 6, 8

29 children (19.4 %) had normal ocular examination

and good visual acuity while 24(16 %)had normal

ocular examination but had poor vision or were not

fixing or following light.These children were followed

up after 6 months.On follow up,15 cases showed

improvement in visual acuity whereas 9 cases showed

no improvement.

On analyzing the severity of developmental delay and

ocular manifestations, it is found that poor vision

(ie inability to fix and follow or unsteady fixation) was

seen in 27 children with global delay and majority of

ocular manifestations like squint (28 cases) and optic

atrophy (12 cases) were seen in children with global

developmental delay. In a study by Nielson et al, it was

found that refractive errors and squint correlated with

the level of IQ 4

Conclusions

� Of the 150 children with developmental delay

examined at Regional Institute of Ophthalmology

and Child Development Centre, SAT Hospital,

Trivandrum,over a period of 18 months,

97 children (64.6 %) had ocular manifestations.

� Most common mode of presentation was that the

child was not looking at objects.

� In this study, Refractive errors (41.3 %) was

the major cause of visual impairment,followed by

squint (40 %) and optic atrophy (9.3 %).

� 10% children showed delay in visual maturation.

� Visual impairment and ocular manifestations like

Squint and Optic Atrophy were more in children

with Global Developmental Delay.

� The major treatable causes were Refractive

errors (41.3 %), Squint (40 %), Cataract (2.6 %)

and Retinopathy of Prematurity (4 %).

� Consanguinity was present in 3 % cases.

� Antenatal risk factors were identified in 10 %

cases. They were Pregnancy induced Hypertension

(3 %),Fever with rash (3 %), Trauma (2 %),

Gestational Diabetes (1 %) and Threatened

abortion (1 %).

� There was history of Preterm delivery in 17 %,

Birth Asphyxia in 16.7 %, Neonatal seizures in

12.6 %,history of Oxygen administration in 8 %

and Neonatal jaundice in 4.7 %

� Global Developmental Delay was seen in 36 %

children,whereas 30 % showed delay in motor

development, 9 % showed delay in language and

22 % showed delay in both motor and language

development.

� A full ophthalmic examination should be an

essential part of evaluation of all children with

developmental delay even when no gross ocular

abnormalities are noticed by the attending

Paediatrician. Early identification of such defects

may prove crucial in institution of therapy in all

cases which are amenable to treatment.

� Delayed visual maturation is closely associated

with developmental delay. Occasionally infants fail

to develop visual fixation for upto 6-12 months

but develop normal visual behaviour at a later

stage. Supportive treatment and reassurance is

vital in such cases.

References

1. O.P.Ghai,Essential Paediatrics-5th edition Chap1 pg1-2

2. Uemura Y, Agucci Y, visual developmental delay,Ophthalmol pediatric Genet 1981; 1:4-11

3. Wu H.J Tsai R K,Dept of Ophthalmology,KaohsingUniversity, Taiwan, Kaohsing J Med Sci2000 Aug 16(8)422-428

4. Neilson LS, Skov L, Jensen H, University of Copenhagen,Acta Ophthalmol Scand 2007 Mar 85(12) 149-56

5. Bankes et al Child health dev 1975 Sep-Oct; 1(5)325-333

6. Lagunju I.A et al Dept of Paediatrics University CollegeHospital, Nigeria Afr J Med Sci 2007 Mar; 36(1):71-5

7. Chan Gu. Chen IC, Chen CL, Wong MK,Chung CY, Deptof Rehabilitation Chang Gung Memorial hospital Taipei,

Taiwan, ROC. Med J, 2002 Nov; 25(11)743-45

8. Spectrum of visual disorders in children with cerebralvisual impairment. Fazzi E, Signorini SG, Bova SM,


La Piana. Dept of Child Neurology and psychiatry,IRCCS C. Mondino Institute of Neurology, Universityof Pavia, Italy.

9. Dev Med Child Neurol.1991 Feb ;33(2):181 Delayedvisual maturation: ophthalmic and neurodevelopmentalaspects. Tresidder J.Fielder AR,Nicholson J.Universityof Leicester.

10. Br J Ophthalmol. 1982 Jan;66(1)46-52.Visual disordersassociated with cerebral palsy.Black P

11. Br J Ophthalmol. 1999 May; 83(5):514-518 Risk factorsfor strabismus in children born before 32 weeksgestation. Pennefather PM, Clarke MP. Strong NP,Dutton J, Dept of ophthalmology, Royal VictoriaInfirmary, Newcastle.

12. Trans Ophthalmol Soc UK.1985;104(Pt 6):653-61.Delayed visual maturation.Fielder AR,Russell-EggittIR,Dodd KL, MellorDH.

13. Ocular Abnormalities associated with cerebral palsyafter pre term birth. Pennefather PM, Tin W. Departmentof Ophthalmology, Royal Victoria Infirmary, New Castle

14. Peadiatric Ophthalmology and Strabismus-Kenneth W.Wright Chap 9, Pg.119-121

15. Sondhi N. Archer S.M, Helveston E.M: Development ofnormal ocular alignment. J Pediatric ophthalmolStrabismus 25; 210-211,1988

16. Teller D.Y, Mc Donald N, Visual Acuity in Infants andchildren the acuity card procedure.

17. Cole G. F.Jones RD, Delayed visual maturation. ArchDis child 1984; 59:107-110

18. Lambert S.R, Kriss A, Taylor D, Delayed visualmaturation Ophthalmol 1989;96: 524 529

19. Fern K.D and Manney R.E Visual Acuity of pre schoolchildren : a review Am J Ophtalm, physio optics 63;314-345, 1986

20. Paedriatic Ophthalmology Current aspects-KennithWyaber and David Taylor

21. “Visual Behaviours and Adaptations Associated withCortical and Ocular Impairment in Children ; Jan, J.E;Groenveld, M; Journal of Visual Impairmnet and Blindness,April 1993, American Foundation for the Blind.


An Outcome Analysis of Posterior Capsular

Rent (PCR) In The Hands of A Senior

Phaco SurgeonDr. Arup Chakrabarti MS, Dr. Meena Chakrabarti MS DNB, Dr. Sonia Rani John DNB, Dr. Valsa Stephen MS DO

Introduction

Posterior capsular rent is a common complication of

cataract surgery including phacoemulsification. Though

occurrence is higher with beginners, it can also occur

in the hands of a senior phaco surgeon. This study

analyses the predisposing risk factors, intraoperative

events, mode of occurrence, management strategy and

eventual outcome of Posterior capsular rent during

phacoemulsification by a senior cataract surgeon.

Materials and Methods

This was a retrospective review of 8 consecutive patients

who developed posterior capsular rent with or without

vitreous disturbance during phacoemulsification over

a period of 36 months from Dec 2005 to Dec 2008.

Posterior capsular rent was defined as an unintended

iatrogenic break in the posterior capsule occurring

during any stage of phacoemulsification cataract

surgery. Patients with zonular dialysis or preexisting

posterior capsular rent were excluded from this study.

Records of the patient and then surgical video tapes

were reviewed to accumulate data concerning the

nature, cause, surgical management and outcome of

the surgery. All surgeries were done by a single surgeon

using the Bausch and Lomb Millennium surgical unit.

Preoperative work up and preparations were routine.

All surgeries were done under topical or peribulbar

anesthesia. Direct chop or Stop and Chop were the

standard phaco techniques employed. In the event of a

posterior capsular rent, a stable anterior chamber was

maintained and if vitreous presented, an automated

anterior vitrectomy was performed by a dry or bimanual

technique. Triamcinolone acetonide staining of the

vitreous was used whenever appropriate. The data

analyzed from the case sheets and videos were : patient

profile, associated clinical features including

predisposing risk factors if any, surgical details, and

intraoperative events leading to posterior capsular rent,

management of the posterior capsular rent as well as

the postoperative outcome.

Results

Of the 8 patients who developed posterior capsular

rent, 6 were females (75 %) and 2 were males (25 %).

(Table 1). The mean age group was 72.4 yrs (Range 48

– 87 yrs). 6 of the 8 patients (75 %) had hard cataract

(Grade 4 nuclear sclerosis). One patient had an

intumescent cataract, 1 had pseudoexfoliation and one

had undergone parsplana vitrectomy. In 3 patients

visibility was poor, due to poor mydriasis in 2 and

corneal opacity in 1 (Table 2) (Fig. 1).

In 6 patients, a clear corneal incision was used.

In 2 patients a scleral tunnel incision and in 1 patient

the incision had to be extended.

In the post parsplana vitrectomy cataract, posterior

capsular rent occurred during the end stage of phaco.Chakrabarti Eye Care Centre, Kochulloor, Trivandrum 695 011 E-mail:

[email protected]

ORIGINAL

ARTICLE

September 2009 A. Chakrabarti et al - Outcome of PCR 271

In the intumescent cataract, extension of the

capsulorhexis resulted in posterior capsular rent. Thus,

in a total of 6 cases posterior capsular rent occurred at

the end stage of phacoemulsification. Two cases had

an incomplete capsulorhexis with posterior capsular

rent occurring during irrigation / aspiration (Table 3).

In one case nucleus drop occurred requiring parsplana

vitrectomy. Anterior vitrectomy was required in 5 cases.

IOL could be inserted in the capsular bag in one case

while 6 received PCIOL in the sulcus. 1 eye was left

aphakic. Additional surgical procedures performed

included triamcinolone acetonide (Fig 2) staining of

the prolapsed vitreous to facilitate anterior vitrectomy

in 4 cases, bimanual anterior vitrectomy in 5 dry

vitrectomy (Fig 3), residual cortex aspiration with 26

gauge cannula in 8 and posterior capsulorhexis in 2.

All patients were evaluated on the same day of surgery,

at 1 week, 2 weeks and 2 months postoperatively.

Refraction was done at the 2nd week postoperatively.

On the first postoperative review 4 patients had raised

intraocular pressure which resolved in one week with

routine single topical antiglaucoma medication. Only

one patient required systemic antiglaucoma medication.

4 patients had moderate corneal edema and 2 had mild

corneal edema which resolved by the second

postoperative week. 75 % of the patients regained best

corrected visual acuity of 6/12 or more of which 83 %

Table 1: Sex Distribution

Male Female Total

No 2 6 8

% 25 % 75 % 100 %

Table 2: Associated factors

Associated Factors No

Hard cataract 6

Intumescent cataract 1

Pseudoexfoliation 1

Post PPV 1

Corneal Opacity 1

Traumatic 1

Steps of Phaco No

End stage of Phaco 6

I / A 2Fig. 3. Dry Vitrectomy

Fig. 4 (a) Intraoperative still photographs of PC rent

Fig. 2. Triamcinolone assisted anterior vitrectomy

Fig. 1. Preoperative Findings

Fig 4b. Postoperative anterior segment photographs showingwell centred PC I0L


had vision of 6/9 or more Fig 4 a & b. One patient who

had nucleus drop had a vision of less than 6/ 60 which

could be attributed to the preexisting corneal opacity.

Discussion

Posterior capsular rent during phacoemulsification

cataract surgery remains an important complication

because it may lead to poor visual outcome. Posterior

capsular rent though more common in beginners can

also occur in the hands of the most experienced of

surgeons.

In our study, posterior capsular rent was seen to occur

in association with certain risk factors especially with

hard cataract, intumescent cataracts, in the presence

of pseudoexfoliation and when there was poor visibility.

In uncomplicated routine cases no posterior capsular

rent occurred.

Posterior capsular rent was found to occur during

Irrigation Aspiration and end stage of phaco surgery in

our study. Studies show that posterior capsular rent is

rarer in the initial stages (capsulorhexis,

hydrodissection) and mostly appears in the middle and

final stages (phacoemulsification, Irrigation Aspiration,

IOL implantation and posterior capsular polishing) 1,2

Gimbel et al 3 reported that posterior capsular rent arose

most frequently during phacoemulsification. While Bast

et al 4 reported 72 % occurred during Irrigation

Aspiration. Taskapiliet al 5 reported that posterior

capsular rent most frequently occurs during

phacoemulsification in 59.56 % followed by Irrigation

Aspiration in 28.8 %.

Corneal edema is the most frequent cause of reduced

vision in the early postoperative period. This is generally

temporary. Varying rates of corneal edema ranging from

11.6 - 59 % had been reported 4, 5 6, 7.

High postoperative IOP is another complication

reported in patients with posterior capsular rent.

Viscoelastic material remaining in the anterior chamber,

preoperative glaucoma, trabecular blockage by

dispersed lens particle and iris pigments and mechanical

damage in the trabecular meshwork may lead to this

postoperative event. In our study 50 % developed

raised IOP compared to other studies which reported

13-40 percent 4, 6, 7

The most serious complication of posterior capsule rent

is retinal detachment. Rates of up to 3.57 percent have

been reported 4, 5, 6, 7. In our study no patient developed

retinal detachment during the followup period.

Cystoid macular edema is another complication of

posterior capsular rent which can cause decreased

visual acuity. Its incidence varies from 7.86 percent -

16.7 percent in different studies 6, 7, 8. In our study no

patient developed cystoid macular edema. This may

be due to proper management of posterior capsular

rent minimizing the vitreous loss. There may have been

cases of cystoid macular edema in our series which

eventually resolved without being diagnosed clinically.

With proper and timely management, the final visual

acuity of our patients were comparable with those in

other reports which cite 95 % of cases achieved 6 /12

or better visual acuity 3, 7,9,10. 75 % of our patients had

a visual acuity of 6/12 or more of which 83% had vision

of 6/9 or more. Thus, when properly managed a torn

posterior capsule is compatible with an excellent visual

outcome.

Early Recognition of Zonular or Posterior

Capsular Rupture

If a posterior capsular tear is not recognized in time,

subsequent intraocular maneuvers required for

phacoemulsification (viz. nuclear rotation, sculpting,

cracking) and fluctuations in anterior chamber depth

will quickly enlarge the size of the tear. The risks of

vitreous loss and dropped nucleus increase, longer the

rupture goes unrecognized. Early recognition of a

posterior capsular tear and prompt prophylactic

measures5 will prevent expansion of the tear size 5,6.

Signs of early posterior capsular tear or zonular

dehiscence6 include the following 10.

� Sudden deepening of the anterior chamber with

momentary dilatation of the pupil.

� Sudden transitory appearance of a clear red reflex

peripherally

� Newly apparent inability to rotate a previously

mobile nucleus

� Excessive lateral mobility or displacement of the

nucleus and loss of nucleus followability.

September 2009 A. Chakrabarti et al - Outcome of PCR 273

� Excessive tipping of one pole of the nucleus

� Partial descent of the nucleus into the anterior

vitreous space

Early recognition of a posterior capsular rent and proper

management ensures excellent visual outcomes.

References

1. Corey RP, Olson RJ. Surgical outcomes of cataractextracts performed by residents using phacoemulsification.J Cataract refract Surg 1998 24:66-72.

2. Ota I, Miyake S, Miyake K dislocation of the lens nucleusinto the vitreous cavity after hydrodissection. Am JOphthalmol 1996. 121:706-708.

3. Gimbel HV, Sun R, Ferensowicz et al. Intra Operativemanagement of posterior capsular tears inphacoemulsification and intraocular lens implantation.Ophthalmology 2001 108: 2186-2189.

4. Basti S, Garg P, Reddy MK. Posterior capsular dehisionsduring phacoemulsification and manual extra capsularextraction: comparison of outcomes J Cataract RefractSurg 2003; 29: 532-536.

5. Taskpili M, Engin G, Kaya G et al .Single piecefoldable acrylic intraocular lens implantation in thesulcus in eyes with posterior capsule tear duringphacoemulsification. J Cataract Refract Surg 2005; 31:1593-1597

6. Brazitikos DP, Balidis MO, Tranos P et al Sulcusimplantation three piece 6mm optic, hydrophobic,foldable acrylic intraocular lens in phacoemulsificationcomplicated by posterior capsule tear. J Cataract RefractSurg 2002;28:1618-1622

7. Yap-E-Y, Heng W J, Visual outcome and complicationafter posterior capsule rupture during phacoemulsificationsurgery. Int Ophthalmol 1999-2000;23:57-60.

8. Cruz OA , Wallace GW, Gay CA et al. Visual resultsand complications of phacoemulsification withintraocular lens implantation performed byophthalmology residents. Ophthalmology 1992:99:448-452

9. Chan FM, Mathur R, Ku JJK et al. Short term outcomesin eyes with posterior capsule rupture during cataractsurgery. J Cataract Refract Surg 2003;29:537-541

10. Blomquist PH, Rugwani RM. Visual outcomes aftervitreous loss during cataract surgery performed byresidents. J Cataract Refract Surg 2002;28: 847-852.


Lens Surgery in Marfan’s syndromeDr. Somdutt Prasad MS FRCSEd FRCOphth FACS

Introduction:

Management of the subluxed lens in Marfan’s syndrome

presents one of the most challenging situations in

contemporary lens surgery. Conventional approaches

have included intracapsular lens extraction or a pars

plana lensectomy with vitrectomy. Once the lens was

removed, aphakia was corrected by glasses, contact

lenses or an iris or angle supported anterior chamber

IOL or a scleral sutured posterior chamber IOL. Marfan’s

syndrome patients are known to have an increased risk

of glaucoma as well as retinal detachment (upto 11 %

of patients with Marfan syndrome, and 8–38 % in those

who have dislocation of the lens or have undergone

lens surgery) 1. Accordingly, anterior chamber implants

are best avoided in this setting and a surgical approach

which preserves the capsular bag and avoids disruption

of the vitreous, will, at least potentially, reduce the risk

of retinal detachment subsequently.

Considerations in the surgicalapproach:

Ideally one wants to achieve lens extraction through a

continuous capsulorrhexis with preservation of the

capsular bag, re-center the bag and secure it using a

scleral fixation device and place an in-the-bag IOL,

without disrupting the vitreous body.

The anticipated challenges in these cases include:

i) Systemic considerations: These patients need

a full systemic workup, as they have associated

features of Marfan’s which may increase the risk

for an anaesthetic. They may have aortic arch or

valve anamolies or indeed have had heart valve

surgery already, in which case they may be on

Warfarin.

ii) Biometry: Eyes with severely subluxed lenses

need careful biometry to achieve a good refractive

outcome. Remember that the refraction is

influenced by the lens subluxation and may not

correlate with the predicted IOL power.

iii) Achieving a central curvilinear

capsulorrhexis: This is difficult because the lens

is unstable, the outward pull provided by the

zonules is uneven and the young patients capsule

is much more elastic than the adult, leading to a

tendency for the tear to ‘run out’.

iv) Preserving the capsular bag: Even when a

satisfactory capsulorrhexis has been achieved, the

game is not over. The bag of the Marfan’s patient

may sometimes be smaller than that of the normal

eye leading to an increased risk of tear or rip

during implantation of devices to support and re-

centre it 2.

v) Achieve lens extraction, bag re-centration and

fixation and IOL implantation without disrupting

the anterior vitreous face.

vi) Deploy techniques which reduce the risk

of late complications: posterior capsular

opacification and subluxation/dislocation of the

IOL capsular bag complex.

(1) Possible surgical strategies

In any difficult surgical situation experts will often use

different approaches to achieve the same end. ForArrowe Park Hospital, Wirral University Teaching Hospitals, NHS Foundation Trust,

Wirral, United Kingdom, [email protected]

OPHTHALMIC

SURGERY

September 2009 Somdutt Prasad et al. - Lens surgery in Marfan’s syndrome 275

Fig. 1. The Modified Capsular Tension Ring or the CionniRing (mCTR)

Fig. 2. The Capsular Tension Segment or Ahmed Segment(CTS)

Fig. 3. Use of the mCTR (a) a subluxed lens with temporal zonular loss (right in picture) has capsulorrhexis supported by

two ‘iris’ retractors. The bag is thus satbilised allowing completion of phacoemulsification. (b) The mCTR with adouble armed 9-0 prolene passed through its central islet is placed into the capsular bag, the anteriorly displacedcentral segment is positioned in front of the rhexis by a dialling hook, whilst a second instrument is poised to guidethe trailing end in. (c) The CIF-4 (Ethicon) needles are passed behind the iris, but in front of the anterior capsule toemerge 1.5 mm behind the limbus under a previously prepared scleral flap. This secures the mCTR and the Prolene

knot is covered by the scleral flap. A secure in-the-bag IOL is then placed.

subluxed lenses in Marfan’s patients, possible strategies

mainly follow one of two broad approaches.

One may choose to sacrifice the capsular bag, clear the

anterior chamber of all vitreous and then implant an

intraocular lens. Lens extraction can be done by an

anterior or pars plana approach if this strategy is chosen.

A pars plana approach has the advantage of allowing a

thorough vitrectomy along with a full internal search

of the peripheral retina. Whilst a complete vitrectomy

is appealing in this setting, as it would eliminate any

future vitreo-retinal traction, it is technically quite

difficult to induce a posterior vitreous separation in a

young patient, and attempts to achieve this may actually

induce retinal tears during surgery. Because of this a

deep anterior vitrectomy may be preferable. An IOL

can then be implanted in the anterior chamber. Anterior

chamber IOLs, open loop 2,3 or iris fixated (Artisan) 5

are simple and efficient techniques, but risks include

iritis, pigment dispersion, corectopia, glaucoma, and

endothelial loss. Because of these potential problems

many surgeons choose to implant a posterior chamber

lens in the ciliary sulcus, fixated by trans scleral sutures 6.

To avoid the risk of future suture breakage leading to

subluxation or dislocation of the IOL and to achieve

better centration, the elegant technique of sutureless

intrascleral posterior chamber fixation has been

developed 7,8.

Techniques which preserve the capsular bag are

intellectually more appealing, especially if the bag can

be re-centred and secured with an in-the-bag IOL

implanted. If all this can be achieved without disrupting

the vitreous body, then (at least theoretically), the risk

of complications like future retinal detachment can be

reduced. A capsular tension ring (CTR) can be used to

stabilise the capsular bag. However, CTR implantation

in eyes with a subluxated lens does not correct capsular

bag decentration 9. Lam and co authors overcame this

obstacle by implanting a CTR and then suturing it and

the capsular bag to the sclera to improve capsule

centration 10. However passing sutures through the


capsular bag risks tearing it, and therefore may not be

advisable. Cionni proposed the use of a modified (Fig.1)

capsular tension ring (mCTR), as this device avoided

the need to pass sutures through the capsular bag 11.

Ahmed introduced the capsular tension segment (CTS),

this smaller device is much easier to manouvre into

the bag and position as required 12 and avoids the risk

of over stretching or tearing the unstable bag. (Fig.1)

(2) Preferred surgical technique:

For many surgeons today, the preferred approach is to

go for a technique which preserves and re-centres the

capsular bag, allowing in-the-bag implantation and

fixation of the bag to the ciliary sulcus using a

combination of a CTR and a CTS.(Fig.3 a - c)

The first thing to note is that the work up to surgery in

such a case has to be meticulous, involving liaison with

all the physicians involved in the patients care and the

anaesthetist, so that a safe general anaesthetic can be

administered.

Biometry presents some unique challenges in patients

with Marfan’s syndrome. One of the most important

factors to consider when doing the biometry is which

section the axial length measurement is taken through,

i.e. the phakic or aphakic portion and then adjusting

your instrument accordingly, to take into account the

presence or absence of lens material. Depending on the

extent of the subluxation you may need to consider

dilating the patient in order to ensure you are definitely

aiming the beam through the correct portion. If using

the A-Scan ultrasound to measure axial length, you will

be able to confirm the position of the probe by looking

for the echo corresponding to the presence of the lens

boundaries. Using a case of Marfan’s as an illustrative

example: A 13 year old had bilateral subluxed lenses

had an undilated refraction of R:-30.00/+6.00x115 L:-

24.00/+5.00x60. When dilated and using his aphakic

portion his refraction was R:+8.00/+3.50x120

L:+9.00/+2.50x80 achieving the same level of vision

with both prescriptions. His phakic axial length was

RE:26.49, LE:26.01 and aphakic axial length RE:26.36,

LE:25.96. As you would expect the measurement should

be comparable regardless of which portion it’s taken

through, if the instrument is correctly programmed. The

left eye was operated on using this measurement and has

a deviated post-operative spherical equivalent of -0.68DS.

The lens chosen should be a 3 piece lens with a 360

degree square edge, This reduces the risk of post-

opeartive posterior capsule opacification and the 3 piece

designs allows for resturing into the scleral sulcus, should

late breakage of the suture lead to IOL displacement in

future years 13, 14. I prefer a B&L (Bausch & Lomb)

L161AO which is a 3 piece lens with a 360 degree square

edge and an aspheric design. The Sofport injection

system, used for injecting this lens allows it to come

out into the capsular bag in a fairly flat disposition,

minimising the potential for destabilising an already

unstable bag during IOL implantation.

An illustrative case described below is used to

demonstrate the steps in the technique. Surgery is

usually done under a general anaesthetic.

(3) Case Presentation

A 12 year old boy with known Marfan’s syndrome was

referred by a paediatric ophthalmologist who had been

seeing him from the age of two years. He had managed

reasonably with spectacle correction, maintaining good

vision in both eyes. More recently the subluxation in

the right eye had progressed to the point that his vision

was reduced to 6/24 (BCVA). On presentation his vision

was 6/24 in the right eye (-24.50 DS / +9.00 DC x 92

½ and 6/9+3 in the left eye (-3.00 DS / +3.00 DC x

95). In addition he was being bullied at school and

children kept stealing his glasses. Systemic workup

included aortic valve problems for which he was on

Atenolol and antenatal hydronephrosis both of which

were being managed by appropriate specialists. On

examination the right lens was subluxed markedly with

edge of the lens passing through the centre of the pupil

and the left lens subluxed to a lesser extent. Rest of the

eye examination was unremarkable with normal

intraocular pressures, no vitreous in the anterior

chamber and normal peripheral retinal examination.

Axial length measurements through the phakic portion

was RE: 25.50, LE:21.46 and through the aphakic

portion RE:25.29, LE:21.25. Using the aphakic

measurement we calculated a +18.00 Diopter B&L

(Bausch & Lomb) L161AO IOL for emmetropia when

implanted into the capsular bag

Figure 4a shows the pre-operative situation, with a

subluxed and decentred lens. A fornix based

conjunctival flap is made in the zone of maximum


Fig. 4b

Fig. 4c

Fig. 5a Fig. 5b

Fig. 6a Fig. 6b

Fig. 6c

Fig. 4a

Fig. 7

subluxation, followed by the creation of a partial

thickness scleral flap with its base towards the fornix.

The scleral dissection begins at the limbus and extends

peripherally for about 3mm. It is 4 mm wide (Fig 4b).

Two paracentecis incisions are made on either side of

this scleral flap and flexible ‘iris’ retractors are

prepositioned to support the capsulorrhexis as it is later

developed (Fig. 4c).

The capsulorrhexis is begun close to the iris edge at

12 o’clock as this is the centre of the lens (Fig 5a).

Viscoat is used to fill the anterior chamber and

tamponade the vitreous face. The capsulorrhexis is

developed, taking care to keep a 3 mm distance from

the lens equator (this facilitates later placement of CTR

and CTS; an adequate anterior capsule is necessary to

avoid the CTR or CTS flipping forward, out of the bag

and into the anterior chamber later in the operation.).

The tear is developed a few mm beyond the area where

the iris retractor is poised to engage it, and once the

tear is well clear, the ‘iris retractor is used to engage

the edge of the rhexis and gently draw the lens equator

out to the periphery thus helping to re-centre the

capsular bag. The rhexis is developed further and the

second iris hook engaged and drawn centripetally

further re-centres the capsular bag allowing the superior

part of the capsule to come into view (Fig 5b). The

rhexis can then be completed. Gentle hydrodissection,

with small slow waves of fluid is then done.

A CTR is then inserted into the bag to stretch it

(Fig 6a), and thus allow phacoemulsification without

the bag flopping onto the probe, as is possible in a

largely unsupported bag. Once lens matter has been

removed a CTS with a 9-0 prolene on a double armed

Ethicon CIF-4 needle passed through the central islet is

guided into the capsular bag (Fig 6b). The IOL is then

implanted into the capsular bag (Fig 6c) and the needles

are passed in front of the anterior capsule but behind

the iris to emerge about 1.5 mm behind the limbus

under the previously designed scleral flap. The iris

retractors are then released allowing the surgeon to

judge the position of the capsular bag better. The suture

is tightened (Fig 7) and incisions sutured after removing

viscoelastic. Intracameral Cefuroxime was injected at

the end for endophthalmitis prophylaxis.

Two weeks post operatively vision had recovered to

6/18 unaided, 6/12 with a pinhole and at six weeks


vision was 6/6 with minimal refraction (-1.00 DS /

+1.25 DC x 180). The IOL was well centred.

He requested surgery for his other eye.

(4) Surgical pearls

i) Unstability of the anterior chamber must be

avoided at all cost, mainly to avoid vitreous

coming forward. Meticulous fluid – viscoelastic

exchange technique avoids the capsular bag

diaphragm flopping forward and backward. This

means that every time the phaco probe has to be

removed from the eye, this is done by stopping

aspiration, but with irrigation continuing,

viscoelastic is injected through a side port to

support the anterior chamber. Whilst viscoelstic

is being injected, one gradually eases off the

irrigation, and then the probe can be safely

withdrawn whilst maintaining a deep anterior

chamber, and preventing the capsular bag from

coming forward.

ii) Instead of conjunctival dissection and a scleral

flap, a 600 micron limbal incision is made with a

guarded diamond blade in the region of maximal

lens edge decentration. This incision is similar to

a limbal relaxing incision. A crescent blade is then

used to dissect a 4 mm (wide) x 3 mm deep (from

limbus to periphery), partial thickness scleral

pocket. This allows the prolene knot to be buried

under sclera, with conjunctiva undisturbed.

Moreover as the sides of the ‘pocket’ are attached,

there is no real risk of scleral ‘flap’ contraction in

the future.

iii) When the lens matter is soft (as in a young

patient), most of the surgery is done through two

paracentesis incisions (about 1mm each), with all

the lens matter removed using bimanual

irrigation-aspiration (no phacoemulsification).

This allows for greater stability and reduces risk

of vitreous disturbance. Only when all lens matter

has been removed a 3 mm incision is made to

enable placement of a CTS and then the IOL.

Conclusion

I have here presented the evolving techniques for lens

surgery in Marfan’s syndrome. Whilst some aspects are

debatable, I believe that the combination of a CTR and

a CTS fixated transclerally under a scleral pocket allows

secure in-the bag IOL placement and potentially reduces

the risk of future complications. Meticulous surgical

technique is essential to avoid disrupting the capsular

bag and disturbing the anterior vitreous face. When

this is done excellent visual and anatomic outcomes

are attained. At least potentially, this should reduce the

risk of long term complications, time will tell if this

potential is achieved. In a personal series of eleven

consecutive Marfan’s eyes operated on over the last

two years, in the bag placement with a well centred

bag and secure fixation of a capsular tension segment

using a prolene suture was achieved in all cases with

good visual outcomes.

Reference:

1. Maumenee IH. The eye in the Marfan syndrome. Trans

Am Ophthalmol Soc 1981;79:684–733.

2. Bahar I, Kaiserman I, Rootman D. Cionni endocapsular

ring implantation in Marfan’s Syndrome. Br J

Ophthalmol 2007;91;1477-1480

3. Wagoner MD, Cox TA, Ariyasu RG, et al. Intraocular

lens implantation in the absence of capsular support; a

report by the American Academy of Ophthalmology

(Ophthalmic Technology Assessment). Ophthalmology

2003;110:840–59.

4. Morrison D, Sternberg Jr P, Donahue S. Anterior

chamber intraocular lens (ACIOL) placement after pars

plana lensectomy in pediatric Marfan syndrome. J

AAPOS 2005;9:240–2.

5. Lifshitz T, Levy J, Klemperer I. Artisan aphakic

intraocular lens in children with subluxated crystalline

lenses. J Cataract Refract Surg 2004;30:1977–81.

6. Tsai YY, Tseng SH. Transscleral fixation of foldable

intraocular lens after pars plana lensectomy in eyes with

a subluxated lens. J Cataract Refract Surg 1999;25:

722–4.

7. Scharioth GB, Pavlidis MM. Sutureless intrascleral

posterior chamber intraocular lens fixation. J Cataract

Refract Surg 2007;33;1851-1854

8. Badon ACJ, Scharioth GB, Prasad S. Intrascleral

Sutureless Posterior Chamber Intraocular Lens Fixation

Using Scleral Tunnels. Techniques in Ophthalmology

2009 (in press)

9. Dietlein TS, Jacobi PC, Konen W, et al. Complications

of endocapsular tension ring implantation in a child

with Marfan’s syndrome. J Cataract Refract Surg

2000;26:937–40.

10. Lam DSC, Young AL, Leung ATS, et al. Scleral fixation

of a capsular tension ring for severe ectopia lentis. J

Cataract Refract Surg 2000;26:609–12.


11. Cionni RJ, Osher RH, Marques DM, et al. Modifiedcapsular tension ring for patients with congenital lossof zonular support. J Cataract Refract Surg2003;29:1668–73.

12. Hasanee K, Ahmed II. Capsular tension rings: updateon endocapsular support devices. Opthalmol Clin North

Am 2006;19;507-19

13. Buckley EG. Hanging by a thread: the long-term efficacyand safety of transscleral sutured intraocular lenses inchildren [an American Ophthalmological Societythesis]. Trans Am Ophthalmol Soc. 2007; 105:294-311

14. Por YM, Lavin MJ. Techniques of intraocular lenssuspension in the absence of capsular/zonular support.Surv Ophthalmol. 2005;50: 429-462

In a lighter vein

MEMORY

RRV

I had previously written in this column that the most essential quality for a medicalpractitioner is patience. It is true, alright. But equally important is another one –good memory for names and faces. At least some of your patients expect you toremember them when they come back to you – six years after their previous visit.And are very gratified if you do. Some of them even feel insulted if you don’t.

In my school days we had our family doctor who used to manage anything fromallergy to angina and pruritis to pregnancy. Every time one of the family memberswent to him, he used to ask about the others; their marriages; children’s educationalproblems etc. And he never made a mistake. I always used to wonder how he managedto remember each one of his patients with their myriads of profiles and problems.Of course he had a good memory. But when I myself became a doctor, I happened toask him as to his prodigious reminiscental capabilities he laughed and said: “Oh! Imake small notations on the edge of the prescription as to the job or class or wife’sname etc.”

I tried to emulate him when I started practicing. But my memory was never as good;and I couldn’t remember what my notations stood for.

The problem is worst when you think you remember the face but can’t put a name toit. And the patient talks on familiarly and has not brought the old prescription.When the time comes to write the prescription you use various techniques. One is toask him/her what his/her FULL name is. If it is such small and simple name like“Unni”, you are in trouble. Or you ask him/her what the OFFICIAL name is. If theanswer is ‘It is the same one’, again you are in trouble. May be you can ask what his/her initials are. Most of them will say the name along with the initials. Again it won’thelp if he/she answers simply “P.K.” or “C.T.” With ladies I try another ruse. I askwhat their husband’s name is and prefix a ‘Mrs.’; but you are in a fix if she demurelysay “Oh, doctor, but I am not married.” So now a days I take the bull by the hornsand say: “Sorry, but I can’t remember your name”. With young boys or girls I mayadd, “How you have grown up! I couldn’t recognise you”. Do not try this with olderwomen Instead, say: “You appear younger, I couldn’t recognise you.” Fortunately inmy experience, men do not mind being asked the name visit after visit as much as thefairer sex.

A couple of days back I asked a female patient her name and heard the familiar ‘howcan you forget me’ thing. But considering that she was clad in a ‘burkha’ with a clothmesh in front of her eyes, I felt vindicated.


The Eyesi: Ophthalmic Surgical SimulatorDr. Meena Chakrabarti MS, Dr. Sonia Rani John DNB, Dr. Arup Chakrabarti MS

In recent years, the medical community has benefited

from technological advances that simulate surgical

environments. Ophthalmologists now have access to

commercially available virtual reality systems, including

the Eyesi Ophthalmic Surgical Simulator (VRMagic,

Mannheim, Germany). Fig (1)

The ophthalmic training system is based at the Mayo

Clinic’s Multidisciplinary Simulation Center

(www.mayo.edu/simulationcenter), a 10,000-square

foot clinical training facility dedicated to simulation-

based clinical education and research.

Gone are the days when residents first learned the basics

of handling intraocular instruments and a surgical

microscope in the OR or a variable wet lab environment.

Instead, they now complete a structured curriculum

that combines one-on-one instruction and independent

study with the Eyesi simulator. Instructors create

courses that residents repeat and practice until they

achieve passing scores. The surgeons-in-training then

advance to the Eyesi system’s higher levels of difficulty

until they master all of the simulator’s training tasks.

Residents are enthusiastic about the technology and

its constant availability (24 hours a day, 7 days a week)

(Fig 2).

In studies, the Eyesi Ophthalmic Surgical Simulator

demonstrated construct validity (the ability to reliably

distinguish between novice and expert surgeons) for

training tasks in the posterior and anterior segments2, 3.

The device’s stereoscopic view and foot-pedal controls

are excellent proxies for the “real” environment of

cataract surgery.

VRMagic originally developed the Eyesi system to

simulate vitreoretinal surgery. Recently, however, the

company added a training module for the anterior

segment (Figure 1). In addition to simulating the use

of forceps, precise navigational tasks, the capsulorhexis

formation, and phacoemulsification, the Eyesi’s anterior

segment module evaluates the user’s performance and

measures instructor-defined, standardized surgical

tasks in a virtual environment 1.Chakrabarti Eye Care Centre, Kochulloor, Trivandrum 695 011 E-mail:

[email protected]

Fig. 1: The Eyesi: Ophthalmic Virtual Reality SurgicalSimulator.

O P H T H A L M I C

INSTRUMENTATION

September 2009 Meena Chakrabarti et al. - The Eyesi: Ophthalmic Surgical Simulator 281

Using the anterior segment training module and the

built-in forceps tool, residents learn how to manipulate

instruments in the eye, pivot them at the wound, and

avoid inadvertently injuring the cornea or crystalline

lens. The simulator’s scoring system rewards users for

the efficiency of their intraocular manipulations and

the precision with which they complete their tasks. The

capsulorhexis training module is actually more

challenging than “the real thing,” an acceptable and

desirable quality for a surgical training system.

The posterior segment training modules simulate the

manipulation of forceps, the precise movement of

instruments in the posterior segment, antitremor

training/control, and procedures such as vitrectomy,

epiretinal membrane peeling, and internal limiting

membrane peeling. The Eyesi’s retinal simulations can

“suspend reality” quite effectively. For example,

inexperienced surgeons become so engrossed in

virtually peeling an epiretinal membrane that they

actually start sweating.

Hands-on experience in traditional surgical wet labs is

still the gold standard for training residents to perform

corneal and scleral suturing techniques. Currently

available surgical simulators do not attempt to replace

the experience of working with real cadaveric eyes.

Instead, the simulator provides a realistic, repeatable,

and measurable intraocular surgical environment that

is difficult to duplicate in the traditional wet lab setting.

The Eyesi’s on/off setup eliminates the significant time

and effort typically involved in preparing and

dismantling a wet lab. In addition, the surgical

simulator measures and documents the user’s efforts

and performance.

Depending on which module is used during a training

session, the system tracks and scores up to 74 different

performance variables (Table 1). The Eyesi’s screen

displays the data for each trial, which can also be

summarized and graphed at the end of each simulated

surgical session or exported to a spreadsheet program

for statistical analysis. By allowing residents to

repeatedly perform standardized tasks and measuring

their performance in a realistic environment, the Eyesi

system helps us train surgeons to perform cataract

surgery safely and competently without putting patients

at risk.

Surgical training content for EYESi is organized in

software modules. Training is available for cataract and

vitreoretinal surgery. The ever expanding menu of

surgical modules now offers procedures like

Capsulorhexis and Phaco-emulsification or Posterior

Hyaloid Detachment and ILM Peeling. Each training

module includes various tasks with increasing difficulty

levels.

As EYESi is designed to integrate into a residency

program curriculum the system allows for

customisation. Therefore medical educators can create

courses from the assorted modules and levels of

complexity that exist within the surgical training

modules.

The ability to define training content ensures medical

educators can set up individual curricula to meet the

needs of the trainee relative to the trainee’s current

Fig. 2. An Eyesi training session in progress.

stage of skill and experience. Thus dedicated courses

can use easy or difficult levels from the selected training

modules so that both novices and advanced trainees

can refine their skill level.

EYESi provides the medical educator with detailed user

and group management so that a course can be assigned

to an individual trainee or groups of trainees.

After courses are build and integrated into the residency

curriculum a medical educator would logically want to

monitor each trainee’s development. EYESi offers

detailed performance evaluation and all data for a

trainee can be exported via USB as user friendly spread

sheets or graphs.

To further support medical educators EYESi offers a

recorder playback functionality so that an instructor


can review any given simulation session and provide

feedback to the trainee. All videos and screenshots can

easily be exported via USB for later use. An identical

curriculum can be used over time to measure the

learning curve or to compare skill levels of students.

EYESi cataract

For training of anterior segment surgery the EYESi

platform is equipped with a cataract surgery interface

which includes a head with a cataract eye interface,

the cataract instrument set, footpedals and the

corresponding system software. The simulation can be

configured easily for superior or temporal access to the

patient’s eye; the cataract eye is prepared for

corresponding incisions.

According to many instructors and trainees, mastery

of the capsulorhexis and phaco-emulsification are

amongst the most difficult steps in cataract surgery. In

a capsulorhexis the main difficulty lies in controlling

the delicate capsule tissue to tear in the desired manner.

Furthermore the trainee must learn this complex manual

skill within a confined space of the anterior chamber.

EYESi cataract offers extensive training of the

capsulorhexis. It even allows for the training of

complications so that trainees master what to do when

the rhexis runs outwards.

In learning to perform phacoemulsification the

challenge rests in understanding and controlling the

complex physics of the phaco device.

The phaco training modules offer a safe environment

to experiement with phaco machine settings and to

explore the effects of parameter changes. In practical

terms this means a trainee can cause unwanted events

like surge and chatter and learn how phaco parameter

adjustments can eliminate these occurrences.

A step-by-step approach to the “Divide and Conquer”

technique allows for stress free and lasting acquisition

of the required surgical skills. EYESi also enables a

trainee to now pool all the manual skills together that

make up modern phaco techniques as the simulation

requires coaxial use of instruments, use of the

microscope foot pedal, and modulation of the desired

phaco parameters with a phaco foot pedal.

Table: 1 Performance variables tracked and scoredby the Eyesi System

1. Educational open forceps insertion and removal

2. Nonhorizontal instrument insertion and removal

3. Interacting out of focus and light cone

4. Average radius of capsulorhexis

5. Decentration and overall irregularity of capsulorhexis

6. Deviation of capsulorhexis’ radius from target value

7. Instrument insertions

8. Remaining aqueous humor

9. Efficiency Time (after first interaction)

10. Ultrasonic energy

11. Viscoelastic injection

12. Injury Incision stress

13. Injured cornea and lens area

14. Lens displacement

15. Damaged zonular fibers

16. Iris contact

17. Anterior chamber pressure too low

18. Ultrasonic leakage

19. Emulsification of adjacent cortex

20. Cornea and capsule damaged by ultrasonic energy

21. Anterior and posterior capsule torn

22. Target Remaining objects

22. Progress

23. Capsulorhexis completed

24. Lens cracked/removed

Most medical educators and trainees know that learning

to see through a microscope with both hands and both

feet working all at the same time in a deliberate and

harmonious manner takes considerable practice. EYESi

provides a better way to train for anterior segment

surgery as risk is removed when a patient is eliminated

from the training loop and a trainees can safely practice

critical parts of cataract surgery to mastery.

Fig. 3. The Cataract Module

September 2009 Meena Chakrabarti et al. - The Eyesi: Ophthalmic Surgical Simulator 283

EYESi vitreoretinal

For training of posterior segment surgery the EYESi

platform is equipped with the vitreoretinal surgery

interface which consists of a head with the vitreoretinal

eye interface, a vitreoretinal instrument set, foot pedals

and the corresponding system software.

medical educators to use the system as a complete

training platform.

EYESi’s system software enables medical educators to

seamlessly integrate their own courseware into the

platform. Through the secure administration functions

individual courses can be compiled and complemented

with academic text, still images and high resolution

digital video footage. Powerpoint presentations can be

imported and presented on the graphical user interface

of the EYESi simulator. This allows trainees to study

medical background information and then observe

demonstrations depicting how their mentors perform

Fig. 4. A vitreoretinal training session in progress.

Most everyday realities of microsurgery in the complex

vitreoretinal environment are represented in EYESi.

The EYESi microscope renders a stereoscopic view

identical to the real OR microscope. The trainee is

required to establish suitable visualization via the

microscope foot pedal’s zoom, focus, and X/Y controls.

Experienced retina surgeons know observing the retina

requires a BIOM/ SDI hardware so this too is integrated

into the microscope setup.

Assorted training modules are available for EYESi

vitreoretinal. Training sessions include tasks like

inducing posterior hyaloid detachment and performing

peripheral vitrectomies, peeling the internal limiting

membrane (ILM) or the removal of epiretinal

membranes.

To aid trainees in refining precise manual dexterity skills

associated with vitreoretinal surgery EYESi provides a

virtual surgical instrument tray. In the course of

performing virtual surgery a trainee will use an

illumination probe in their non-dominate hand. As in

real retinal surgery EYESi realistically enables the

surgeon’s dominant hand to alternate between

instruments such as vitrector, endolaser, forceps, scissors

etc.

Trainees acquire expert status during training in a

variety of ways. EYESi therefore was developed to allow

Fig. 5. Macular translocation.

any given procedure. If the goal is teaching the

capsulorhexis a trainee can read about the task, observe

how the task is done, and then complete the task in

virtual reality till mastery of the skill is known to have

been obtained.

With the option to combine the practical surgical

training with multimedia presentations of medical

knowledge EYESi represents the modern way of

teaching surgical skills.

Conclusion

Keeping up to date with the rapid advances and

complexity of modern intraocular surgery is a

challenging but ultimately satisfying and rewarding

endeavor. Surgical simulators based in virtual reality

allow residents to develop and hone their surgical skills

so that they provide patients with the safest and highest-

quality surgical outcomes possible. Currently, a barrier

to the Eyesi’s broad adoption appears to be the system’s

cost (between $100,000 and $200,000, depending on

optional features and the date of purchase)


References

1. EYESi Ophthalmosurgical Simulator user guide.

Mannheim, Germany: VRMagic; 2008.

2. Rossi JV, Verma D, Fujii GY, et al. Virtual vitreoretinal

surgical simulator as a training tool. Retina.

2004;24:231-236.

3. Mahr M, Hodge D. EYESI Ophthalmic Surgical

Simulator anterior segment anti-tremor and forceps

training module construct validity: attending versus

resident performance. J Cataract Refract Surg. In press.

To view a video of a simulated capsulorhexis rescue

performed on the Eyesi Ophthalmic Surgical Simulator,

visit the ESCRS’s Video on Demand Web site at

www.conference2web.com/escrs/Videos or aspx#

VRMagic’s Web site at www.vrmagic.com/downloads/

eyesi/videos/ESCRS%20Mahr.zip

September 2009 SR John et al. - Nepafenac 285

NepafenacDr. Sonia Rani John DNB, Dr. Meena Chakrabarti MS, Dr. Arup Chakrabarti MS

surgery and the other is cataract or other intraocular

surgeries. With refractive surgery, NSAID drops are

particularly effective in reducing discomfort both during

and after the procedure. To a lesser extent, they also

reduce inflammation in the eye related to refractive

surgery, particularly in the cornea and conjunctiva.

With cataract and intraocular surgery, topical NSAIDS

offer several benefits. The goals of topical prophylactic

nonsteroidal anti inflammatory drug treatment include

the prevention of intraoperative miosis 3, management

of postoperative inflammation 3, prevention or

treatment of CME 3,4 and reduction of ocular pain 5.

They lessen the patient’s discomfort during the

procedure, which is especially important when using

topical anesthesia in cataract surgery. NSAID also help

maintain pupillary dilation during cataract surgery,

which has been shown to lower the rate of

complications. They help in controlling inflammation

in the first few days after surgery, as measured by the

presence of cells and flare in the anterior chamber.

Finally, NSAIDs inhibit the development of cystoid

macular oedema (CME), which usually occurs 4 to 6

weeks after cataract surgery. Even after a perfect

cataract surgery with the most modern techniques and

the best instrumentation, as many as 12 % of patients

may develop some CME and the use of an NSAID may

significantly reduce this complication.

Four topical ocular NSAIDS are currently approved by

the U.S Food and Drug Administration (FDA) for the

treatment of postoperative inflammation after cataract

surgery. They are Acular (ketorolac 0.5 %), Xibrom

(bromfenac 0.09 %), Voltaren (diclofenac 0.1 %) and

Nevanac (nepafenac 0.1 %).

Ocular inflammation is a common result of cataract

surgery, producing pain and photophobia in many

patients and potentially leading to serious complications

including increased intraocular pressure, posterior

capsule opacification, cystoid macular oedema and

decreased visual acuity. Steroidal agents have been the

standard treatment for ocular inflammation in the past

while the use of topical NSAIDS has increased over the

past two decades. Clinical evidence suggests that the

combined use of NSAIDS and steroids is synergistic 1.

In fact it has become the standard of care to use a

regimen of NSAIDS and steroids before and after

cataract surgery 2.

Prostaglandins are involved in human intraocular

inflammation and released in response to ocular

trauma, including surgery. When present following

trauma, intraocular surgery, or in association with

uveitis, they may contribute to disruption of blood –

ocular barriers and the generation of macular edema.

During cataract surgery, arachidonic acid is released

from phospholipids of cell membranes to provide the

precursor for prostaglandin synthesis. Corticosteroids

affect the cascade by attenuating the expression of

inflammatory mediators that initiate activation of

phospholipase and the release of arachidonic acid thus

limiting prostaglandin production. NSAIDs exert their

effects further downstream of the cascade, directly

inhibiting cylco-oxygenase and the production of

prostaglandins.

There are 2 main settings of ocular surgery in which

ophthalmologists use topical NSAIDS. One is refractive


[email protected]

OCULAR

PHARMACOLOGY


Nepafenac (Nevanac, Alcon Laboratories) is a novel

topical nonsteroidal anti-inflammatory drug, which is

the only prodrug NSAID, having less anti-inflammatory

activity without conversion to its more active state 6.

Each ml of Nevanac (0.1 %) suspension contains 1 mg

of nepafenac. Nepafenac is designated chemically as 2

–amino 3-benzoylbenzene acetamide with an empirical

formula of C15

H14

N2O

2.

Nevanac Ophthalmic suspension is the first and only

topical NSAID structured as a prodrug. This unique

design allows for target specific activity, because its

efficacy is maximized at the intraocular sites of most

concern to ophthalmologists. Once Nevanac penetrates

the eye, intraocular hydrolysis converts the nepafenac

molecule into a potent cyclooxygenase inhibitor called

amfenac, an active drug that has strong anti-

inflammatory capabilities.

Unlike conventional NSAIDs, the active forms of which

tend to accumulate on the ocular surface and decrease

in activity and concentration as they penetrate the eye,

Nevanac is specially designed to maximize intra ocular

efficacy. Its unique prodrug structure allows Nevanac

to achieve optimal distribution through the cornea into

the iris / ciliary body and retina / choroid , providing

superior inflammation suppression. At the same time,

this rapid and targeted distribution may minimize

tolerability issues commonly noted with conventional

NSAID therapies, because the drug doesn’t overload

the ocular surface.

Nevanac uniformly inhibits all prostaglandins of the

iris / ciliary body, retina, PGE2 synthesis, and the

breakdown of the blood–aqueous barrier. Compared

with conventional NSAIDs such as diclofenac,

nepafenac 0.1 % is superior in blocking the production

of prostaglandins in an uniform manner 7. Studies 8

show that nepafenac 0.1 % inhibits 95 % of

prostaglandin formation by the iris / ciliary body within

80 minutes after topical dosing, compared with

diclofenac’s 53 % 9. This fact has important clinical

implications in terms of potential differences in efficacy

between Nevanac and conventional NSAID therapies.

It is believed that CME is caused by surgically induced

prostaglandin formation in the aqueous and vitreous

and / or by the breakdown of the blood – aqueous and

blood – retinal barriers. Even mild CME damages the

retinal pigment epithelium. Such damage is irreversible,

because these cells do not regenerate. Therefore, any

retinal swelling can have a lasting negative impact on

a patient’s vision.

Due to their mechanism of action, NSAIDs have been

shown to be a good line of defense against CME.

Obviously, it is key that the NSAID selected reaches the

target tissues to provide therapeutic anti-inflammatory

activity and thus prevent the processes described.

The target- specific activity of Nevanac hold great

potential for the superior prevention of post-cataract

complication such as CME. Because the highest

concentration of Amfenac occurs in the choroid and

retina, the agent not only decreases inflammation in

the anterior chamber, but should also lower the patient’s

risk of developing CME. Studies 10,11 have shown that

nepafenac 0.1 % inhibits prostaglandin formation in

the vitreous, whereas conventional NSAID such as

diclofenac and ketorolac fail to do so. A study 12

evaluating the suppression of prostaglandin synthesis

of nepafenac 0.1 % versus diclofenac in the iris/ ciliary

body and the retina / choroid showed that a single

topical dose of nepafenac 0.1 % significantly inhibited

prostaglandin synthesis in the iris/ciliary body and

retina choroid. Efficacy was sustained for 6 hours in

the iris / ciliary body and for 4 hours in the retina/

choroids. In contrast, for diclofenac peak suppression

of prostaglandin activity in the iris/ciliary body was

sustained for 20 minutes, with only minimal inhibition

of prostaglandin synthesis observed with diclofenac in

the retina / choroid.

Because nepafenac is a neutral molecule, it has been

hypothesized to have greater corneal permeability than

other NSAIDS which have acidic structures. In a vitro

study of rabbit tissue, nepafenac had 6 fold greater

corneal penetration than diclofenac as well as faster

rate of penetration 13. Similarly in another study,

nepafenac aqueous humor Cmax

values were 3.6 fold

higher than those of ketorolac despite having a starting

concentration 4-fold (0.1 % versus 0.4 %) 14. Nepafenac

Cmax

values were more than 8 fold higher than those of

bromfenac, despite having similar starting

concentrations (0.1 % versus 0.09 %). Thus the results

in various studies support the fact that the prodrug

nepafenac has faster corneal penetration rate than other

conventional NSAIDs.


Intraocular drug concentrations are expected to

correspond with the anti-inflammatory efficacy of a

drug. The near –maximum concentrations of amfenac

is maintained longer than those of Ketorolac suggesting

that Nevanac may have a prolonged duration of action

relative to other drugs in this class. This may be due to

nepafenac prodrug structure which allows it to rapidly

traverse the cornea, reaching Cmax

in the aqueous humor

within 30 minutes.

Nepafenac is a non steroidal anti-inflammatory

pro-drug that potentially inhibits Cox-1 and Cox-2

activity ex vivo following topical ocular administration.

Nepafenac demonstrates low intrinsic cyclo-oxygenase

inhibitory activity in vitro, yet exhibits in vivo efficacy

equal to that of diclofenac in models of anterior segment

ocular inflammation. In addition to its anterior segment

efficacy, nepafenac exceeds diclofenac in its ability to

reduce posterior segment ocular inflammation.

Nevanac has been tested in various concentrations

(upto 15 times its commercial concentration ) and in

short – as well as – long term settings and it was found

to be safe and well tolerated 15,16. Nepafenac penetrates

the target intraocular tissues faster than any other

topical NSAID, thus providing greater efficacy on a

clinical basis. Once inside, it has rapid conversion and

therapeutic onset and a very high level of tissue

concentration. Studies show that its rate of systemic

absorption in approximately 1700 times less than that

of an oral dose.

Nevanac hold the promise of fast, pain-free visual

recovery without the potential common side effects

noted with conventional NSAID therapies. As

mentioned previously, its unique prodrug formulation

ensures optimal intraocular distribution 17 with superior

inflammation suppression. The superior bioavailability

of Nevanac to the retina / choroid also ensures an

unsurpassed potential for preventing CME after cataract

surgery.

Nevanac suspension, which was filed with the FDA for

the treatment of inflammation following cataract

surgery, will provide a novel, target- specific structure

that optimizes penetration throughout the relevant

ocular tissues to deliver enhanced, longer –lasting anti-

inflammatory efficacy all the way to the retina / choroid

which is of particular relevance to ophthalmic surgeons.

References

1. Flach AJ, Nonsteroidal anti-inflammatory drugs.In ; Tarman W, ed, Duances Foundation of ClinicalOphthalmology Philadelphia, PA, Lippincott 1994; Vol3; Chapter 38.

2. O, Brien T.P. Emerging guidelines for use of NSAIDtherapy to optimize cataract surgery patient care. CurrMed Res Opin 2005;21:1131-1137; erratum, 1431-1432.

3. Flach AJ. Topical nonsteroidal anti-inflammatory drugsin Ophthalmology. Int Ophthalmol Clin 2002; 42 (1);1 -11.

4. Miyake K, Marnda K, Shirato S, et al. Comparison ofdiclofenac and fluorometholone in preventing cystoidmacular edema after small incision cataract surgery; amulticentred prospective trial. Jpn J Ophthalmol 2000;44:58-67.

5. Price MO, Price FW. Efficacy of topical ketorolactromethamine 0.4 % for control of pain or discomfortassociated with cataract surgery. Cure Med Res Opin2004; 20:2015-2019.

6. Gamache DA, Draff G, Brady MT, et al. Nepafenac, aunique non steroidal prodrug with potential utility inthe treatment of trauma-induced ocular inflammation.Assessment of anti-inflammatory efficacy. Inflammation2000; 24:357-370.

7. Kim DH, Stark WJ, O’Brian TP, Dick JD. Aqueouspenetration and biological activity of moxifloxacin0.5 % ophthalmic solution and gatifloxacin 0.3 %solution in cataract surgery patients. Ophthalmology2005;112: 1992-1996.

8. Ke T-L, Graffe G, Spellman JM, Yanne JM. Nepafenac, aunique nonsteroidal prodrug with potential utility inthe treatment of trauma induced ocular inflammation.Inflammation 2000; 24:371-384.

9. Tom Wallers, Michael Raizman, Paul Ernest. In vivopharmacokinetics and in vitro pharmacodynamics ofnepafenac, amfenac, ketorolac and bromfenac. JCataract Refract Surg 2007;33:1539-1545.

10. Heaton J, Hiddeman JW, Hackett RB, et al. Oculareffects of Nepafenac ophthalmic suspension followingsix months of topical ocular administration topigmented rabbits. Paper presented at: The ARVOannual meeting ; May 03, 2005; Fort Lauderdale , FL.

11. Walker LM, Rice RL, Heaton JD, et al. Ocular effects ofNepafenac ophthalmic suspension following three

months of topical ocular suspension to cynomolgusmonkeys. Paper presented at: The ARVO annualmeeting; May 03, 2005; Fort Lauderdale, FL.

12. Heier JS, Topping TM, Bauman W et al. Ketorolac versus

predinisolone versus combination therapy in thetreatment of acute pseudophakic cystoid macularedema. Ophthalmology.2000;107:2034-2038.

13. Flach AJ. Discussion: ketorolac versus prednisoloneversus combination therapy in the treatment of acutepseudophakic cystoid macular edema. Ophthalmology2000;107:11:2039.


14. McColgin AZ, Raizman MB. Efficacy of topical Voltarenin reducing the incidence of postoperative cystoidmacular edema. Invest Ophthalmol Vis Sci.1999; 409(Suppl):S289.

15. O’Brien TP. Emerging guidelines for use of NSAIDtherapy to optimize cataract surgery patient care.Curr.Med REs Opin.2005;21:7:1131-1138.

16. Kapin MA, Yanni JM, Brady MT, et al. Inflammationmediated retinal edema in the rabbits is inhibited bytopical nepafenac. Inflammation.2003;27:5-281-291.

17. Gamache DA, Graff G, Brady MT, et al. Nepafenac, aunique nonsteroidal prodrug with potential utility inthe treatment of trauma–induced ocular inflammation:Inflamamtion.2000; 24:4:357-370.


Recent Advances in The Back of

The Eye Drug DeliveryDr. Meena Chakrabarti MS DO DNB

treatment 1,5. Like solutions and particles implants can

also result in unequal drug distribution due to vitreous

heterogenicity and placement of implant peripheral to

retina to avoid disruption of the visual field. Implants

however come close to the zero-order kinetics: ie the

level of administered drug remains constant throughout

the delivery period.

Implants can be either biodegradable or non

biodegradable. Biodegradable implants do not require

surgical removal. Their disadvantages are a variability

in release kinetics due to differing rates of vitreous

turnover and a final burst in drug release profile. Non

biodegradable implants provide a more controlled drug

delivery but require a second surgical procedure for

removal.

Two ocular implants Vitrasert (Ganciclovir 4-5 mg Bausch

and Lomb, Rochester, NY) and the recently approved

Retisert (flucinolone acetonide 0.59 mg, Bausch and

Lomb) are commercially available. Vitrasert releases

ganciclovir for approximately 5-8 months while Retisert

releases flucinolone for up to 30 months and is currently

the only approved treatment for non-infectious uveitis

of the posterior segment 6.

Other implants that have been developed are

1. A novel doughnut shaped biodegradable implant 7

for delivery of ganciclovir and foscarnet. The

central hole assures easier suturing and the

implant does not need removal.

2. Biodegradable posudrex implant (Allergan, Irvine,

CA) for delivery of dexamethasone in treatment

Introduction

Once the active treatment agent that is efficacious in

the management of posterior segment diseases is

determined, the next big obstacle is the back of the eye

drug delivery. Topical eye drops are far superior to all

other routes of administration with respect to safety,

comfort, affordability and ease of use. However topical

medications are least effective in delivering therapeutic

concentrations of the drug to the retina 1. Hence the

majority of developmental efforts in retina therapeutics

is focussed on novel non-topical delivery systems.

Intravitreal injections introduced in 1945 2,3 provides

superior drug bioavailability in the posterior segment

compared to topical and systematically delivered

agents. However this method of drug administration

has several drawbacks which includes frequent

(monthly / bimonthly) outpatient visits, and carry the

risk of serious complications such as vitreous

hemorrhage, retinal detachment and endophthalmitis.

Intraocular implants 4 are designed to provide drug

release into the posterior segment for longer periods

of time (months or even years) compared to particles

or solutions. These implants are usually placed at the

level of the parsplana during a surgical procedure.

Compared to intravitreal injections, drugs released from

implants deliver more consistent levels of the drug,

avoids side effects associated with frequent intravitreal

injections, minimize peak concentrations and result in

smaller quantities of drug being required for


[email protected]

OCULAR

PHARMACOLOGY


of macular edema associated with retinal vein

occlusions.

3. Iluvien (Alimera, Alpharetta, GA) 8 a non

biodegradable implant to deliver flucinolone

acetonide in diabetic macular edema and designed

to sustain therapy for 24-36 months.

In the past few years researchers have developed

intraocular devices with fewer complications, and

relatively safe, sustained and effective localized

administration. These include

1. Particulate polymeric drug delivery systems

(Microparticles / Nanoparticles)

2. Phospholipid bilayer encapsulated drug delivery

system (liposomes)

3. Iontophoresis: where an electric current is used

to drive ionized drugs into tissues.

Microparticles, Nanoparticles and

Liposomes

The main problem that limits the effectiveness of

intravitreal injections is the lack of homogenicity of the

human vitreous caused by gradients. Injected drugs do

not therefore spread throughout the vitreous resulting

in a significant variability in the drug concentration at

the target site. Nano particles or micro particles are

new formations which can spread more uniformly

throughout the vitreous, increase the duration of action,

and decrease the peak concentration.

Injectable nano particles 9 (1nm to 1000 nm in

diameter) and microparticles (1 nm to 1000 nm in

diameter ) made of polymer encapsulated drug are

novel drug delivery systems that aim to increase the

drug penetration and also increase the duration of

action of small molecules.

Particulate system can be in the form of

1. Nanospheres and microspheres: which are

uniform polymer drug combinations in which the

drug is dispersed homogenously throughout a

polymer matrix.

2. Nanocapsules and Microcapsules: where the drug

is surrounded by a spherical polymer capsule and

released throughout its pores.

3. Polycion complex (PIC) micelles that can be laser

activated are in development and have

successfully inserted DNA into rat retinas through

a process called photochemical internalization in

which light induces the transfer of DNA directly

into cells 10.

4. Liposomes: with encapsulated drug can bind to a

cell membrane and facilitate drug transfer across

the membrane. They are less stable than particles

made of polymer. Both hydrophilic and

hydrophobic drugs can be encapsulated into

liposomes. Research have shown that they can

effectively carry genes to the rat retina following

injections.

Almost any drug can be encapsulated. This

method of drug delivery aids in (1) stabilizing the

active form of the drug (2) increases its half life

(3) increases drug absorption due to slower

elimination rate (4) decreases peak concentrations

reducing the risk of toxicity.

One of the major disadvantages of this mode of delivery

is that nanoparticles and microparticles are heavier than

vitreous. So when they are injected they tend to sink

to the bottom of the vitreous cavity. Particles size can

also have a profound effect on the drug bioavailability

after injection with larger particulate system tending

to maintain superior sustained drug release.

Nanotechnology may have an impact on the treatment

of retinal diseases through gene delivery, drug delivery,

cell delivery, retinal neural prosthetics and nano surgery.

Gene delivery has been attempted with viral vectors

but carry the risk of immunogenicity and mutagenesis.

Non viral vectors such as polymers and lipids also have

the ability to carry genes but with lower risk of

immunogenecity, lower cost and greater ease of

production than viral vectors. The electrostatic

interaction of cationic polymers with RNA or DNA

molecules carrying a negative charge results in

condensation and formation of the material into

particles in the nanoscale range. These polymer

nanoparticles can protect genes from enzymes and

mediate their entry into cells. Incani and colleagues 12

found that polyplexes ……………… complexes of

cationic polymer with plasmid DNA can have

transfection efficiencies comparable to adenoviral

September 2009 Meena Chakrabarti - Recent advances in the back of the eye drug delivery 291

vectors but with reduced safety risks. Colloidal nano

particles carrier systems have been tried for sustained

drug delivery for chronic diseases such as glaucoma

and macular degeneration. Nano particles are also

promising for targeted delivery of drugs to intra ocular

tumors. Sustained submacular delivery may be

enhanced by the use of biocompatible film that serves

as a carrier for drug loaded nanoparticle Fig1. For an

extra ocular approach arrays of hundreds of

microneedles that penetrate the sclera to deliver drugs

to the posterior segment have been designed using

microfabrication technology Fig. 2.

Polymer scaffold engineered on the nanoscale can

increase the survival and differentiation of cells for

retinal transplantation 13.

Use of nanoparticles in engineering of retinal prosthetics

is being investigated with the aim of rejenuvating , by

passing, or taking advantage of the residual retinal

function in patients with retinitis pigmentosa and other

inherited degenerative retinal diseases 14.

Iontophoresis and Suprachoroidal drug

administration

Iontophoresis is a method of drug delivery in which an

electrical current drives charged drug molecule through

either the cornea or sclera and into the retina and

vitreous. It offers a non invasive alternative to

intravitreal injections, particles or implants. The current

leader in clinical ocular iotophoresis is Eye Gate pharma

(Waltham, MA) which is currently investigating this

technology for drug delivery. It uses a reusable battery

powered generator and a disposable applicator.

The Eyegate II uses an inert electrode that can

accommodate both positive and negatively charged

drugs. The mechanism of action of the inert electrode

is electrorepulsion of the same charged molecule which

creates high velocity to achieve flux to the targeted

tissue.Fig. 3

The surface area is important in this technology due to

current density. By delivering the current to the sclera,

the surface area is maximized and current density is

lowered increasing the safety profiled of the device.

The Eyegate II 16,17,18 has shown efficacy in delivering

proteins, si RNA, corticosteroids and nanoparticles in

rabbit studies. Safety of this device on human sclera 19

was shown using a buffer solution. Phase 2 study of

EGP - 437, a corticosteroid delivered using this system

for the treatment of dry eye syndrome has been

completed. Phase II study in uveitis, glaucoma age

related macular degeneration etc is underway.

For patients with retinal tumors, iontophoresis is being

researched as a potential alternative to the use of

systemic chemotherapy. In a mouse model, investigators

found that iontophoresis could successfully transport

carboplatin, a cytotoxic compound for the treatment

of retinoblastoma.

The suprachoroidal drug delivery using a 300 mm

microcatheter 21 (i track -400 , i-science Interventional

corporation, Menlo park, CA ), introduced through a small

anterior incision at the parsplana has been shown to be able

to access the suprachoroidal space. The safety, efficacy and

pharmacokinetics with triamcinolone, a combination of

triamcinolone A and Avastin is being investigated.

(Fig. 5 & 6)

Transporter Targeted Drug delivery to the

retina:

This method of drug delivery targets nutrient

transporters on ocular barriers utilizing a prodrug

approach. Nutrient transporters are transmembrane

proteins involved in the transportation of essential

nutrients and xenobiotics across biological membranes,

thereby regulating the supply of essential ingredients

into the cell.

Several transporters for nutrients and endogenous

compounds are expressed on both the apical and

basolateral sides of the epithelial barriers of various

tissues such as intestine, kidney, BBB, BRB and placenta.

To take advantage of the nutrient transport system, the

parent drug must be covalently conjugated to the

nutrient moiety by an enzymatically cleavable bond

generating a prodrug. Prodrugs significantly enhance

absorption of poorly permeable parent drug. These

prodrugs are recognized by the membrane transporters

as substrates and are transported across the epithelial

or endothelial barriers. Subsequently the prodrugs are

enzymatically cleaved to release the parent drug and

the ligand which in most cases is a nutrient, non toxic

and easily eliminated. (Fig. 7)

Super selective intra arterial chemotherapy in

retinoblastoma aims to deliver a high concentration of


Fig. 1. Biocompatible film for drug delivery 20 nm thickbiocompatible film with multiple drug loadednanoparticles for sustained drug delivery. [Adaptedfrom Retina Today May/ June 2009, Vol.4, No.4]

Fig. 2. Microneedle Array. The size of the experimentalmicroneedle array is shown by its placement on theresearcher’s finger. There are 400 needles in the array.[Adapted from Retina Today May June 2009 Vol.4,No.4]

Fig. 3. The Eye Gate II delivery system.

Fig. 4. The EyeGate II applicator is placed directly upon thesclera.

Fig. 5. The Ophthalmic microcathete for suprachoroidaldrug delivery.

Fig. 6. (a) & (b) View of the Microtheter beacon tip in suprachoroidal space

the drug to the trauma and achieve less exposure via a

low dose systemically to the patient. The goal is to

eliminate the need for enucleation and systemic

chemotherapy in children with RB. Under general

anaesthesia, the femoral artery is catheterized with a

microcatheter (450 nm) which is passed up into the

abdominal aorta, thoracic aorta, internal carotid arteries

and into the ophthalmic artery which measures below

550 nm to 1000 nm in diameter in children.

References

1. Hughes PM, Olejnik O, Chang-Lin JE, Wilson CG. Topicaland systemic drug delivery to the posterior segments.

Adv Drug Deliv Rev.2005;57(14):2010-2032.

September 2009 Meena Chakrabarti - Recent advances in the back of the eye drug delivery 293

2. Wu L, Martinez- Castellanos MA, Quiroz-Mercado- Het al. Twelve –month safety of intravitreal injections ofbevacizumab (Avastin): results of the Pan –AmericanCollaborative Retina Study Group (PACORES). GraefesArch Clin Exp Ophthalmol.2008;246 (1) 81-87.

3. Von Sallmann L. Penicillin therapy of infections of thevitreous. Arch Ophthalmol 1945; 33:455.

4. Bourges JL, Bloquel C, Thomas A et al. Intraocularimplants for extended drug delivery: therapeuticapplications. Adv Drug Deliv Rev. 2006; 58(11):1182-1202.

5. Del Amo EM, Urtti A. Current and future ophthalmicdrug delivery systems. A shift to the posterior segment.Drug Discov Today. 2008;13 (3-4):135-143.

6. Hsu J. Drug delivery methods fro posterior segmentdisease. Curr Opin Ophthalmol.2007; 18(3):235-239.

7. Choonara YE, Pillay V, Carmichael T, Danckwerts MP.Syudies on a novel doughnutshaped minitablet for intraocular drug delivery. AAPS Pharm Sci Tech. 2007;8(4):E118.

8. Alimera. Iluvien: addressing the Ophthalmic Crisis ofDiabetes.2008; v. 2009.

9. Csernus VJ, Szende B, Schally AV, Release of peptidesfrom sustained delivery systems (microcapsules andmicroparticles) in vivo. A histological andimmunohistochemical study. Int J Pept ProtienRes.1990; 35(6):557-565.

10. Tamaki Y. [Novel approach for management of age-related macular degeneration-antiangiogenic therapyand retinal regenerative therapy]. Nippon Ganka GakkaiZasshi. 2007;111(3):232-68; discussion 69.

11. Masuda I, Matsuo T, Yasuda T, Matsuo N. Gene transferwith liposomes to the intraocular tissues by differentroutes of administration. Invest Ophthalmol Vis Sci.1996; 37(9):1914-1920.

12. Incani V, Tunis E, Clements BA, Olson C, Kucharski C,Lavasanifar A, Uludag H. Palmitic acid substitution oncationic polymers for effective delivery of plasmid DNA

to bone marrow stromal cells. J Biomed Mater Res A.2007;81 (2):493-504.

13. Tao SL, Desai TA. Aligned arrays to biodegradable poly(-carprolactone) nanowires and nanofibers by template

sysnthesis. Nano lett.2007.;7 (6):1463-1468. doi:10.1021/nl0700346.

14. Caspi A, Dorn JD, McClure KH, Humayun Ms,Greenberg RJ, McMahon MJ. Feasibility study of aretinal prosthesis: spatial vision with a 16-electrodeimplant. Arch Ophthalmol.2009;127398-401

15. EyeGate. Pipeline [Internet]. Waltham, MA, 2009.

16. Blalock T, Gee R, Manzo M, Ruiz- Perez B, Rao R. Single–dose treatment with dexamehazone phosphateresolves concanavalin A – induced dry eye in rabbits.Poster presented at the annual meeting of theAssociation for Research in vision and Ophthalmologymeeting; April 27-May 1 2008; Fort Lauderadale, FL.

17. Ruiz – Perez B, Blalock T, Dowie T, et al. Transscleraldelivery of a 12.4k Da protein by ocular iontophoresis.Poster presented at the annual meeting of theAssociation for Research in Vision and Ophthalmologymeeting; April 27-May 1 2008: Fort Lauderdate, FL.

18. Patane M, Ji Guo, Schubert W, Landosca J. Iontophoreticdelivery of PRINT ® (Particle Replication In non-wetting templates) Nanoparticles using the Eyegate ®II device. Poster presented at the annual meeting of theControlled Release Society , July 12-16,2008; New York.

19. Reddy M, Thimmaiah R, Cohen A, et al. Clinicalexperience with the EyeGate II ® delivery system: safetyand tolerability in healthy male and female adultvolunteers. Poster presented at the annual meeting ofthe Association Research in Vision and Ophthalmologymeeting; April 27- May 1 2008; Fort Lauderdale, FL.

20. Hayden B, Jockovich ME, Murray TG, et al.Iontophoretic delivery of carboplatin in a murine modelof retinoblastoma. Invest Ophthalmol Vis Sci.2006;47(9):3717-3721.

21. Olsen TW, Feng X, Wabner K et al. Cannulation of thesuprachoroidal space: a novel drug deliverymethodology to the posterior segment. Am J.Ophthalmol.2006;142 (5):777-787.

22. Kansara V, Hao Y, Mitra AK. Dipeptide monoesterganciclovir prodrugs for transscleral drug delivery:targeting the oligopeptide transporter on rabbit retina.J Ocul Pharmacol Ther.2007; 23:321-334.


Care and Maintenance of Contact Lens –

An OverviewDr. Pravin Tellakula MS

Care and maintenance is one of the most critical aspects

of contact lens wear. It can influence the success of

contact lens wear and patients’ satisfaction with their

lenses. Choice of lens care regimen depends on factors

such as lens type, lens material, replacement schedule

of lens, lifestyle and specific patient needs.

“The biggest risk factor in Contact Lens wear is the

person wearing them”

- Geoff Wilson

Safe and effective wear depends on synergism of a good

lens, a compliant patient and periodic professional

monitoring. It is imperative that the purposes and

importance of proper care and maintenance be

impressed upon the prospective contact lens wearer as

soon as contact lens wear is considered seriously.

Role of Care and Maintenance

The overall aims of care and maintenance are

� to prevent and minimise microbial contamination

� reduce deposits

� and attain and maintain ready-to-wear state of

lenses

The various products of care maintenance provide one

or more of the following functions: -

� Cleaning

� Disinfection

� Protein Removal

� Wetting / re-wetting

Regardless of the type of contact lens (except daily

disposables), an appropriate care system must be used.

A typical care system consists of the components listed

Components of Care and Maintenance

� Daily cleaner

� Rinsing solution

� Disinfecting solution/unit

� Weekly/protein cleaner

� Lubricating/rewetting solution

� Lens storage case

DAILY CLEANER - Function

Daily cleaners usually contain surfactants and are used

to remove most loosely bound foreign matter on the

lens surface, such as, Cell debris, Mucus, Lipids,

Proteins, Cosmetics, Micro-organisms, and inorganic

deposits.

The main functional component in a cleaner solution

is the surface-active agent(s) also known as

surfactant(s) (e.g. isopropyl alcohol, tyloxapol,

polyvinyl alcohol, poloxamer-407, amphoteric 10,

poloxamine, hexylene glycol, octylphenoxy ethanol,

tween 21). Surfactant molecules emulsify, dissolve

and/or disperse lipid globules, debris and other lens

contaminants. This is accomplished by the surfactant

forming a monomolecular layer over the contaminant

using the polar ends of its molecules to bind the layer

to the contaminant’s surface. The ‘coated’ contaminants

repel one another mutually or exhibit a lowered surface

tension1.Adithya Eye Clinic, Chennai

CURRENT

C0NCEPTS

September 2009 Pravin T. et al. - Contact Lens Care 295

The other main components are Non-ionic or ionic

chemical compounds, to reduce interaction

between the lens and the solution, and anti-microbial

agents, primarily used as preservatives.

The additional components in a cleaner include

Osmolality adjusting agents, a buffer system to

adjust the pH, Chelating agents for removing lens

contaminants and viscosity enhancing agents.

Viscosity-enhancing agents such as polyvinyl alcohol

or methylcellulose also facilitate cleaning.

Hypertonicity and abrasiveness are properties that

have been added to enhance the efficacy of some lens

cleaners. Hypertonicity results in extraction of water

from soft lenses, which may help remove some soluble

contaminants. Polymeric beads in some cleaners

have a mildly abrasive effect on protein and other

surface deposits. Apart from this Alcohol to remove

lipids and Enzymes to digest proteins are also added.

Rubbing also enhances the efficacy of the cleaning

solution’s surfactant properties.

Caution to be observed when using abrasive cleaners.

Excessive rubbing may cause scratches on the lens and

can also sometimes induce minus power 2, 3.

Rinsing Solution

Value of Rinsing- regardless of the type of

cleaner used it is important for the lens to be thoroughly

rinsed to remove the excess Daily Cleaner, Loosened

deposits and Micro-organisms. If the cleaner is allowed

to remain on the lens and placed in the enzymatic

cleaner, it may induce foaming resulting in the solution

bubbling out and leaving the lens in a dehydrated state4. It is also good to rinse lenses after overnight storage.

Buffering agents are included in rinsing solution

formulations so that their pH is approximate that of

tears. The pH of normal tears is, on average 7.2, but is

subject to individual variation. To enhance the

compatibility of solution and tear pHs at lens insertion,

the solution is normally buffered lightly.

Many different types of solutions can be used for rinsing,

such as, Unpreserved Saline, Preserved Saline and

Multi-purpose solutions. Use of buffered isotonic saline

is preferred to un-buffered as absorption of atmospheric

carbon dioxide lowers the pH.

Disinfecting Systems

Purpose of disinfection

Contact lenses may compromise the eye’s natural

defence by:

� Inhibiting tear film washing action

� Introducing more micro-organisms

� Compromising epithelial barrier function

Functions of the disinfecting solution are to kill or

deactivate potentially pathogenic organisms including:

Bacteria, fungi, viruses, amoebas and maintain lens

hydration

Antimicrobial activity can be divided into three levels

of efficacy (Anger and Currie, 1995) 5.

- Sterilization is the killing of all microbial life forms,

a situation impossible to achieve with normal lens care

products and procedures.

Fig: 1 Cleaning Procedure – Rub and Rinse

DAILY CLEANER – Procedure

1. Wash hands and dry them (avoid moisturizing/

perfumed soaps)

2. Place lens in the palm of the hand

3. Place 2-3 drops of cleaner on each lens surface

4. Rub with forefinger for about 15 seconds per side

using a ‘to & fro’ and ‘L-R’ action. Rolling the

forefinger in both directions cleans the lens

periphery

5. Rinse well

Cleaning should be done with all types of lens including

disposables.

The mechanical action of rubbing and rinsing

reduces significantly the amount of loose debris and

the number of microorganisms on a lens.


- Disinfection is a dynamic process, usually preceded

by a cleaning and rinsing step, intended to kill and/or

remove microbial and viral contaminants from contact

lenses.

- Preservation is the killing or inhibition of growth

of a select range of microorganisms to prevent product

spoilage during consumer use. The choice of

preservative is governed to a large extent by the

resistance of the microbial targets and the sensitivities

of the eye exposed to the preservative via contact lenses

or eye drops.

Disinfection Systems Types

The two main types of disinfection systems available

for soft contact lenses are heat and chemical.

1. Heat-based disinfection systems use heat in

the range from 70°C to 125°C to kill or deactivate

living lens contaminants (ideally 80-90 degrees for

10 minutes). The advantage is that it is very effective

and does not cause any allergy or discomfort.

However, heat can cause problems for the patient due

to alterations that occur within the lens following

long-term use. Heat disinfection systems generally

decrease lens life span and eventually cause lens

discolouration. The Optical and physical properties of

the lens can sometimes be altered due to excessive

heating and can result in denaturation of protein in

and on the lens RGP lenses will warp when heated and

hence cannot be used. Recently, a system for thermal

disinfection of contact lenses in a domestic microwave

oven has been released.

2. Chemical disinfection systems vary greatly and

a wide variety of types exist. Included in the chemical

systems category are the current hydrogen peroxide

and multi-purpose solutions. Chemical disinfection can

be subdivided into oxidative (hydrogen peroxide and

chlorine) and conventional cold chemical.

Conventional Cold Chemical Disinfectant-

Based Solutions

The characteristics of the disinfectants should be

such that they are compatible with other ingredients,

non-toxic and non-irritating, stable over time and

effective against a wide range of organisms.

Disinfectants such as thimerosal, chlorhexidine,

benzalkonium chloride and sorbic acid should be used

with caution because of their potential for disinfectant-

induced sensitivity reactions. The various chemicals

used as disinfectants are listed below.

Thimerosal, a mercurial antibacterial, is effective as

an antifungal agent. It has been used extensively in

the past in solutions for both rigid and soft CLs. It is

most effective neutral or slightly alkaline pHs. It acts

by bonding with cell enzymes, inhibiting their activity

and killing the organism. Its concentration in the

solution varies from 0.001 % - 0.2 %. However, it is

reported to have reduced activity in combination with

ethylenediamine tetracetic acid (EDTA or sodium

edetate) and is incompatible with BAK. Thiomerosal

can be decomposed by light. Cytotoxic reactions of the

corneal epithelium have been reported 6.

Chlorbutanol is a chlorinated alcohol preservative

with broad spectrum of action. It is however, slow acting

against and bacteria and has a distinctive odour.

Originally used on PMMA lenses, it is now not a

common ingredient. It is effective in acidic pH and used

along with other preservatives. This unstable and

volatile preservative is used in a concentration of

0.5 %.

Benzyl Alcohol is a disinfectant and preservative for

RGP and PMMA lenses. It is unsuitable for use with

soft contact lenses. It is non-cytogenic and relatively

non-sensitizing. It is a bactericidal and viricidal but

ineffective against Pseudomonas aeruginosa in low

concentrations. Like other alcohols (isopropyl alcohol,

isopropanol, ethanol), it behaves like a lipid solvent.

Chlorhexidine gluconate (CHG - a biguanide

antimicrobial) is used both in hard and soft contact

Fig. 2. Solution induced corneal toxicity


lens solutions. Chlorhexidine inhibits cation transport

and membrane bound ATP in cell membranes. It can

bind on protein deposits on lenses and can cause

irritation. Not compatible with Thimerosal. It is known

to adsorb until saturation and leach from the lens

causing toxic reactions on the cornea.

Benzalkonium chloride (BAK) is a quaternary

ammonium compound and used mainly for PMMA lenses.

It works by adsorbing to cell’s membrane, thereby

increasing its permeability and leading to rupture of

the cell. For this reason corneal exposure to the solution

should be avoided. The concentration of BAK in solution

is 0.001 – 0.01% and is effective at an alkaline pH of 8.

BAK decomposes in light. Long-term use of this preservative

may cause the lens surface to become hydrophobic.

EDTA, Edetate, Disodium edentate, Edetic acid

are not strictly preservatives. They are variously

described as preservative enhancers, preservative

potentiators and chelating agents. EDTA is contained

in most CL solutions. EDTA potentiates the action of

quaternary ammonium compounds against gram-

negative organisms but not gram-positive ones.

EDTA’s action removes, by chelation, divalent cations

such as calcium and magnesium ions from solutions

and/or cell walls of gram-negative organisms. Such cell

wall disruptions slow or prevent cell growth. EDTA does

not bind to lens materials significantly and is normally

used in combination with other preservatives. It has a

synergistic action with BAK, which enhances the

effectiveness of the blended solution.

Sorbic acid has antibacterial and limited antifungal

activity. Its concentration in SCLs has not been shown

to cause death of the corneal epithelial cells but

adherence to contact lenses is facilitated by its organic

reaction with the amino acid (lysine) in tear proteins,

and causes a yellow or brown discolouration.

DYMED : Poly aminopropyl biguanide (PAPB),

Poly hexamethlene biguanide (PHMB) are new

generation of preservatives developed to address the

problems previous preservatives created, like ocular

irritation and hypersensitivity. Dymed is the marketing

name for PAPB. Initially used in anti-malarial water

treatment and swimming pool chemical has now found

a place as an adjuvant in the treatment of

Acanthamoebakeratitis 7.

PAPB selectively binds with negatively charged

phospholipids of the cell walls causing membrane

damage, cell content leakage and ultimately cell death.

It is used in a low concentration of 0.00005 – 0.0005 %.

Polyquad is the marketing name for a high molecular

weight (polymeric) quaternary ammonium compound:

Poly(quaternium-1), polidromium chloride,

onamer M

This type of preservative is used in both rigid and soft

lenses in concentrations of 0.001 – 0.005 %. Its high

molecular weight of 5000 restricts its entry into lens

materials thus minimizing ocular reactions.

Chlorine Systems : The use of chlorine-releasing

tablets in SCL disinfection systems dates back to the

1970s. The recent systems are supplied as convenient

blister packed anhydrous effervescent tablets of either

stabilized halane or halazone benzoic acid. Both tablets

slightly differ in the amount of available chlorine

(4 – 8 ppm). The tablet is dissolved in 10ml of unpreserved

saline to make a disinfecting solution of pH between

5.5 and 7.5.4 hours exposure is recommended. The

antimicrobial activity will depend on the concentration

of undissociated hypochlorous acid. Lenses should be

thoroughly rinsed before re-insertion.

The dissociated hypochlorous acid produces

hypochlorite and chlorine, which are also bleaching

agents. Lenses tinted with reactive dyes can have their

colour altered.

Hydrogen Peroxide based chemical disinfectant

solutions may be either preserved or preservative free

and can be divided into two main types:

� One-step system

� Two-step systems

Hydrogen peroxide systems are normally formulated

Fig. 3. Thiomerosal Toxicity of skin


with a 3 % peroxide concentration whose pH is often

acidic at 3.0 – 4.0 8. For a lens to be wearable following

disinfection, neutralization is required. For the purpose

of neutralization substances like sodium pyruvate,

sodium thiosulphite, catalase and sodium bicarbonate

have been used. Most systems decompose hydrogen

peroxide into saline and oxygen catalytically.

Disinfection in hydrogen peroxide is reasonably

effective in 15-20 minutes.

One-step systems are formulated so that the

peroxide disinfection and neutralization are performed

during the recommended time. With tablet-using

systems a delay is applied to the neutralization phase.

With disc-based systems, no delay is applied to the

neutralization phase. Regardless of which of these

systems is used special vented lens cases are required

to allow the oxygen generated to escape. One-step

systems use either a catalytic (platinum) disc (6 hours)

or a time-delayed catalase tablet (2 hours).

When neutralization is performed as a separate step,

the system is called a two-step system. Very early

systems ‘neutralized’ peroxide using pre-measured

quantities of sodium bicarbonate for a minimum of

10 minutes. In fact, the process was not true

neutralization and usually took longer than 10 minutes.

Rather, the bicarbonate altered the solution pH

(upwards) to levels at which peroxide was inherently

less stable. The peroxide solution then began to

decompose slowly into water and oxygen.

With two-step systems it is recommended that lenses

are stored overnight in the peroxide and neutralized

immediately before lens usage.

Advantages of the hydrogen peroxidase system is

that they are rapid killing large numbers of most

organisms in a short time period, 10-20 minute

soaking time. High anti microbial efficacy and

non-toxic decomposition products are its other

advantages.

Disadvantages being that once it is neutralized, a

peroxide system has no antimicrobial power and can

sometimes cause irritation in the eye if not neutralized

properly. It is not perfectly compatible especially with

high water content, ionic contact lenses in that it can

reversibly alter lens parameters and water content.

Multi-step peroxidase systems can be overly complex

and confuse the patient.

Multi- Purpose Solution

Many modern lens care systems use one solution to

perform the functions of a number of components,

thereby reducing the actual number of solutions

required.

For ease of use and patient convenience, multi-purpose

solutions (one-bottle systems) are formulated to allowFig. 4. Hydrogen peroxide System

Table: Summary of recommended Disinfecting Systems based on Lens Material1

HEAT COLD CHEMICAL PEROXIDE MULTI-PURPOSE

SCLLow Non-ionic Yes Yes Yes Yes

X Yes X YesLow Ionic Some Yes Yes Yes

High Non-ionic X Yes X YesHigh Ionic X Yes Yes Yes

UncommonPMMARGP X Yes Special Yes

Uncommon Formulation

For coloured contact lenses heat or hydrogen peroxide should not be used as it cause bleaching/ fading of the colour.


cleaning, rinsing and disinfection functions to be

combined. More recently even protein removers have

been added to these solutions.

Protein Remover

Protein removers, also known erroneously as enzymatic

cleaners, are included in the care systems for soft

Cleaving

Enzyme tablets act as protein removers by cleaving the

peptide bonds in tear proteins deposited on contact

lens surfaces 1. Since the action of the enzyme tablet

only loosens the protein, it is important to instruct the

patient to clean the lenses by rubbing and rinsing upon

completion of the deproteinizing process.

Rewetting Drops and Lubricants

Lens Lubricants permit lubrication and rewetting of the

lens while on the eye. Typically, they contain a low

concentration of a non-ionic surfactant to promote

cleaning, a polymer to lubricate the lens, buffering

agents and preservatives 10. Lens lubricants are

particularly helpful for wearers of extended wear lenses,

but can also be used with daily wear lenses. The drying

out of the lens on the eye from exposure to wind, low

humidity, and high temperatures may be relieved by

these products. Patients who experience difficulty

removing hydrogel lenses because of dehydration or

who frequently damage their lenses on removal may

also benefit from the use of lubricants. Lubricating and

re-wetting drops are formulated with viscosity-

enhancing agents (commonly polyvinyl alcohol,

methylcellulose, etc.).

Lens Storage and Cases

A poorly maintained contact lens case can be a source

of heavy contamination of contact lenses with

microorganisms. Biofilm or glycocalyx formation on the

surface of contact lens storage cases can harbour

Pseudomonas aeruginosa and Serratia marcereens 11.

The biofilm is produced by the bacteria themselves.

It protects the host bacterial cells from chemical or

preservative attack and traps nutrient particles and

Fig:5 protein deposits source:IACLE

Fig: 7 Dirty lens case

Fig: 6 Calcium deposits

contact lenses, and some RGP lenses, that are not

replaced regularly (>1 month). Not all protein

removers are enzyme-based.

Those that are, are usually supplied in tablet form.

Chemical-based systems are usually supplied as ready-

to-use liquids. These cleaners are effective in loosening

tightly bound protein deposits.

However, they cannot be expected to remove all

proteins.

Prior to protein removal, the lenses should be cleaned

and rinsed before being placed in the recommended

container with the tablet or solution for the

recommended time. Enzyme cleaners are ineffective

in the presence of lipid deposits or other debris. Protein

treatment is usually done weekly or at a frequency

dependent on the rate of patient protein deposition.

Heavy protein depositors, especially ionic high water

material lens wearers, may require an increased

frequency. Frequent use of protein removers are

required if heat is used as a disinfectant.

Lenses should be soaked in the remover for 15 minutes

to two hours, depending on the type of protein

remover used and rate of protein build-up.

Enzymes used include papain, pancreatin,

subtilisin, pronase, amylase, lipase, and

hydroxyalkylphosphonate. It is to be noted that

Papain is not compatible with hydrogen peroxide 9.


organisms. To avoid contamination, the lens case should

be rinsed after use and the lenses should be stored in

fresh solution.

CIBA vision has come out with a unique Pro Guard

lens case, infused with an anti-microbial agent that

helps prevent contamination. The contact lens case

contains silver atoms that have been electrically charged

(ions), and help reduce the possibility of contamination

by up to 40%.

Care of Lens Cases

Discard all the used solution from the case. This

prevents loss of disinfecting efficacy when fresh solution

is mixed with used solutions.

Scrub with a toothbrush and detergent weekly. Oil free

soaps or detergents are recommended for this step.

Rinse with hot water and rub thoroughly with a clean,

dry tissue.

Air dry. Keeping the lens case dry will prevent

colonization by microorganisms such as protozoa that

thrive in moist or wet environments.

It is also recommended that the lens case be replaced

at frequent intervals.

Lens Replacement Schedule and Care

Regimen

Daily Disposables

Because of its single use concept, this lens does not

require use of surfactant cleaner, disinfecting solution

or weekly enzyme. If needed, the patient can use

in-eye re-wetting drops or sterile saline for rinsing prior

to insertion.

Regular Disposables

These lenses are replaced weekly or bi-weekly. Suitable

care includes multi-purpose solutions given as complete

care system. If preferred, lenses can be rinsed with

saline prior to insertion or a lubrication solution used

to re-wet the lenses. No weekly protein removal is needed.

If a multi-purpose solution causes irritation or

discomfort, a surfactant cleaner can be used along with

hydrogen peroxide as disinfectant.

Frequently Replaced Lenses

Clean lenses with a multi-purpose solution or a

surfactant cleaner. Rinse with multi-purpose solution

or a saline solution (unit-dose, aerosol or preserved).

Disinfection may be done with heat, cold chemical,

oxidative or multipurpose systems. The final choice

depends on lens material and patient compliance.

Protein removal is required for 3 and 6 monthly-

replaced lenses but with lower frequency compared to

conventional lenses. It can be avoided in the case of

monthly disposables. Lubricating/re-wetting drops may

be used if required.

Conventional Lenses

Clean lenses with a multi-purpose solution or a

surfactant cleaner. Rinse with multi-purpose solution

or a saline solution (unit-dose, aerosol or preserved).

Disinfection may be done with heat, cold chemical,

Conventional Frequent Replacement Disposable> 6 months 1 month ≤ 3 months ≤ 1 month

Surfactant Cleaner Yes Maybe No

All Purpose Yes Yes Yes

Peroxide· One Step Yes Yes Yes· Two Step Yes No No

Enzyme Yes Maybe No

Clean Lens Cases weekly Yes Yes Yes


oxidative or multipurpose systems. The final choice

depends on lens material and patient compliance.

Protein removal is done weekly. It is performed using a

tablet or liquid form of protein remover which may be

chemical or enzymatic in nature. Some wearers may

benefit from wetting drops especially if they are working

in air-conditioned environment.

For regular wearers of conventional lenses heat or

thimerosal/chlorhexidine-based disinfection is not

recommended.

In-office Maintenance Of Diagnostic (Trial Set)

Lenses

SCL: Use heat if possible, otherwise peroxide

RGP: Use peroxide or store lenses dry

Re-disinfect non-disposable inventory trial lenses at

least once a month.

Multi-purpose solutions should only be applied to trial

lenses used very frequently and are not suitable for

long term storage. Regardless of the storage method,

all trial lenses should be cleaned and rinsed thoroughly

before storage.

In-office Procedures to Clean and Disinfect

Lenses

Various in-office procedures can be used to clean and

disinfect lenses.

Heater/stirrer units with/without:

-special-purpose care products

-oxidizing agents (hydrogen peroxide, sodium

perborate, sodium percarbonate, sodium hypochlorite,

etc.)

-special saline (e.g. saline with a calcium chelating

agent).

Oxidizing agents (e.g. 6 or 9 % hydrogen peroxide

with or without heat).

Standing waves. A lens cleaning system involving

low-frequency agitation of a lens vial containing contact

lenses and a cleaning solution is said to create

turbulence, which in turn dislodges surface

contaminants.

Ultrasound. Ultrasonic (using high frequency audible

waves between 15 and 20 kHz) agitation causes

removal of particulate matter from contact lens surfaces

by cavitation (intense agitation of small bubbles at the

lens surface). Is effective on low water content soft

lenses. If used for longer duration lens can become

opaque.

Ultraviolet. A lens disinfection system using either

direct UV irradiation of microbes or the production of

ozone by a UV-emitting (253.7nm) discharge tube 13.

The ozone is the actual disinfectant. It kills

microorganisms by breaking bonds and cross-links

between nucleic acids. It effectively disinfects SCLs and

RGPs.

Microwaves. This is an alternative form of heat

disinfection 12, albeit high heat. Microwave oven of

2.5GHz, 500 watts and turntable is used. While

undoubtedly effective against microorganisms, the

temperatures involved may also have deleterious effects

on the lenses and decrease their life expectancy. Vented

containers must be used and the lenses should be

re-hydrated in saline after irradiation.

Some systemic medications can cause lens damage and

ocular signs and symptoms, which have to be

differentiated from those of the care products. Some

care products may also not be compatible with certain

systemic medication.

Table: Possible Systemic Medication Interaction with

Soft contact lenses 14.

Clinical Findings

Medication

Lens Discolouration (yellow to orange)

NtrofurantoinPhenazopyridine

Phenophthalein

Rifampin

Rifadin

Sulfasalazine

Tetracycline

Corneal Staining

Tetracycline when used with Thiomerosal

Preserved products

Contact lens-related epithelial irritation


Acetylsalicylic acid (aspirin)

Decreased lens wetting comfort

Antihypertensives

Tricyclic antidepressants

Antihistamines

Belladonnas

Anticholinergics

Current trends in solution and lens care

The trend in contact lens care is toward simpler, less

toxic systems that rely on patient compliance to function

optimally.

Simplified soft Lens Regimens

The common approach to soft contact lens care is to

use a one-bottle system. The leading, simplified

soft lens care products, ReNu (Bausch and Lomb),

SOLO-care (CIBA), Complete (Allergan), Opti-free and

Opti-one (Alcon) are very similar in their low toxicity

and reliance on digital cleaning and rinsing with clean

hands, followed by soaking in a clean case. While these

products have helped reduce toxic and allergic reactions

by using low toxicity preservatives and avoiding

thimerosal, chlorhexidine and exposure to hydrogen

peroxide, there is little evidence that they have led to

better compliance. Fortunately, frequent lens

replacement and the eye’s defence mechanisms have

kept most patients safe most of the time.

Sicca-like syndrome has been sometimes associated

with one-bottle lens care systems that contain

surfactants. These patients need a saline rinse (sorbic

acid preserved or sterile non-preserved) prior to lens

insertion. If stronger measures are needed, switching

to a hydrogen peroxide system can sometimes

dramatically improve comfort.

Hydrogen Peroxide and other Regimens

The more difficult to use and more expensive hydrogen

peroxide systems are often used only as problem-solvers

and have lost market share in the last decade. AOSEPT

one step is quick and ideal product for in-office

disinfection before re-inserting for a patient. Liquid

protein remover Unizyme, a product from CIBA

Vision for use with peroxide products, is said to work

in 10 minutes. For in-office trial lens storage, however

there is no substitute for heat disinfection.

RGP Lens Care

RGP solutions for the most part are not new, but if one

switches from cleaning/disinfecting/wetting/

conditioning/cushioning solution to cleaning/

disinfecting/ conditioning/but not wetting/cushioning

solution it should be made sure that wetting/cushioning

solution is added to the regime. Most of the currently

available products for RGP equally work well.

Allergy Sufferers

For allergic patients pre- and post lens wear use of

topical anti-histaminics or mast cell stabilizers or non-

steroidal anti-inflammatory agents will maximize

comfort.

To summarise while selecting a care regimen the

practitioner needs to consider the wearing schedule of

the patient, the lens type, replacement schedule and

convenience of the patient and ocular sensitivity issues

as well.

It is a good practice to repeat instructions and assess

demonstration by patient. Patients should be instructed

not to mix solution types and brands and to consult

the practitioner before substituting solutions.

The message for care and maintenance can be stressed

with the acronym

CRADLE – Clean, Rinse And Disinfect Lenses

Everytime

References

1. Sylvie Sulaiman, IACLE Contact Lens Course, Module

5: Units 5.1, pg 9, 1998

2. Carell BA et al: The effect of rigid gas permeable lenscleaners on lens parameter stability. J Am Optom Assoc63:193, 1992

3. Bennett ES, Henry VA: PGP lens power change withabrasive cleaner use. Int Contact Lens Clin 17:152, 1990

4. Mandell RB: Lens Handling, care and storage. In ContactLens Practice 4th ed, pp 568-597, 1988

5. Anger, C. B., and J. P. Curie. 1995. Preservation anddisinfection, p. II-187–II-213. In Contact lenses: theCLAO guide to basic science and clinical practice, vol.


II. Soft and rigid contact lenses. Kendall-Hunt, Dubuque,Iowa.

6. Tripathi BJ, Tripathi RC, Kolli SP: Cytotoxicity ofophthalmic preservatives on human corneal epithelium.Lens Eye Toxic Res. 9(3&4): 361-375, 1993

7. Larkin DFP et al: Treatment of Acanthamoeba Keratitiswith Polyhexamethylene biguanide. Opthalmology. 99:185-191, 1992

8. Rogan M: Systems for hydrogen peroxide disinfectionof soft contact lenses. Transactions of the British ContactLens Association, Annual Clinical Conference, May1985, Blackpool, England pp 40-42

9. Campbell R, Caroline P: A strong case for enzymaticlens care compliance. Contact Lens Spectrum 11:56,1994

10. Lowther GE et al: The Pharmacist’s Guide to ContactLenses and Lens Care. Atlanta, CIBA Vision corporation,1988

11. Feldman GL et al: Control of Bacterial Biofilms onRigid Gas Permeable Lenses. CL Spectrum 7(10): 36-39, 1992

12. Harris MG et al: In-office microwave disinfection of softContact Lenses. Optometry Vision Sci. 67(2): 129-132,1990

13. Harris MG et al: Ultra Violet disinfection of ContactLenses. Optometry Vision Sci. 70(10): 839-842, 1993

14. Shovlin J: Systemic Medications and their interactionwith soft contact lenses. Int Contact lens Clin 17: 250,1990

15. Edward S. Bennett and Barry A. Weissman, ClinicalContact Lens Practice text book, Chapters 25, 34 and35

16. IACLE Contact Lens Course, Module 5: 1998

17. Michael A. Ward, The Microbiology of Contact lensWear, Contact Lens Spectrum Journal, Sept. 1997:23-29.


A case report of colobomatous RDDr. Arya A.R MS, Dr. Biju John MS DNB FRCS

A 33 yr old housewife with no history of any systemic

illness presented with sudden onset of defective vision

in left eye 2 weeks back.There is no history of any

significant ocular illness in the past.No history of prior

trauma/seeing flashes/floaters prior to this episode.

Ocular examination revealed a visual acuity of 6/6 in

right eye and perception of light with accurate

projection in left eye.Anterior segment examination of

left eye revealed typical iris coloboma. (Fig. 1) and

microcornea (10 x 9mm)

Regional institute of Ophthalmology,Trivandrum.

Fundus examination revealed colobomatous area in the

inferior quadrant involving the disc along with retinal

detachment. (Fig. 2). No breaks were detected in the

peripheral retina even after careful indirect

ophthalmoscopy and slit lamp biomicroscopy with

3 mirror. It was presumend that location of the

break/breaks was within the colobomatous area.

Blood investigations were with in normal limits

A diagnosis of iris coloboma (typical) with

retinochoroidal coloboma and rhegmatogenous retinal

detachment in left eye was made.

Fig. 1. showing microcornea and iris coloboma in left eyeand normal appearance in right eye.

Fig. 2. showing retinochoroidal coloboma with RD in left eye.

Fundus

Fig: 3,4,5 Arrow showing laser mark.

Management - The patient underwent pars plana

vitrectomy. During removal of vitreous adjacent to the

colobomatous area “schlieren phenomenon” was

observed and this confirmed that the break was within

the coloboma. Internal drainage of subretinal fluid

along with simultaneous fluid air exchange was done

with the help of a silicone tipped cannula positioned

adjacent to the site of the presumed break.Retina

flattened and following this air silicone oil exchange

was done. Subsequently 3 rows of barrage laser burns

were placed all around the coloboma using LIO.

(LE) (RE)

CASE

REPORT

September 2009 Arya AR et al. - Colobomatous RD 305

Post operatively the retina remained attached and vision

was 1/60.She was discharged on the 4th day. Vision

improved to 3/60 by the 2nd post operative month and

the retina remained attached with barrage laser burns

in place.

Discussion

The term “coloboma”was introduced by Walther-

indicates a condition wherein a portion of a structure

of the eye is lacking.It occurs as result of inadequate

closure of embryonic fissure 5-7 wks postconceptional.

Childhood colobomas are important cause of childhood

blindness and visual impairment.

The development of retina lags behind in the region of

embryonic cleft. Initially the inner layer (presumptive

retina) normally grows more quickly than outer

pigmentary layer of optic cup. Normally the lips of

embryonic cleft meet in central part first and then

extends proximally and distally. Proximally the cleft

never closes where hyaloid artery enters and in this

region the eversion of inner layer is present for

sometime so that fusion of 2 outer layers is delayed

and a short nonpigmented strip remains at proximal

end of fissure. It is an accentuation of this process which

cause the formation of coloboma.Then the process of

atrophy and regression affects the retina throughout

the colobomatous area so that the layers disappear and

tend to be replaced by glial and fibrous elements. At

the same time sclera the development of which is largely

dependent on influence of optic cup remains thin &

poorly developed in abnormal region and tend to suffer

ectatic change.

If the process involves whole length of the fissure it

results in complete coloboma. If isolated areas of cleft

succeed in fusing it results in bridge coloboma.

Colobomas are usually inferonasal(typical). It can be

unilateral/bilateral. Even large coloboma which donot

involve the fovea may exhibit relatively preserved visual

acuity. Severe coloboma may be associated with

microphthalmos.

Ocular complications can be

-amblyopia

-refractive error

- choroidal neovascularisation

-retinal detachment.

CHARGE Syndrome-when coloboma is associated with-

Heart defects and other abnormalities such as

-Atresia(coanal)

-Retardation of Growth

-Ear abnormality

D/D

-Trauma

-Chorioretinal scar

Staphyloma-idiopathic

-myopic

associated with connective tissue disorder

-North Carolina macular dystrophy.

OCT can provide insight into the pathology at the

margin of coloboma. Coupled with the knowledge from

histopathological information can guide the

management of RDs secondary to coloboma of choroid

with a high degree of success.

Retinal detachments associated with coloboma of the

choroid present a surgical challenge. Within the

colobomatous area the retinal tissue is thin and

hypoplastic, the choroid and retinal pigment epithelium

(RPE) are not developed and the underlying sclera is

thin and ectatic, producing a staphyloma. The breaks

which are invariably within this area will be difficult to

locate due to the lack of contrast and are often located

correctly during vitrectomy as in our case.

Complete vitrectomy with method to create chorioretinal

adhesion around the coloboma and silicone oil or gas

tamponade provide effective treatment for

colobomatous retinal detachments.

References

1. Stephen J.Ryan-Retina 4th edition

2. System of ophthalmology-Normal andabnormal

development Vol 3.Sir Stewart Duke Elder.

3. Retina &Vitreous2008-2009; AAO.

4. Parsons Diseases of the eye. 20th edition.

5. Jalali S, Das T. Selection of surgical technique for retinal

detachment with coloboma of the choroid. Indian JOphthalmol 1994;42:27-30


Vasoproliferative Tumour of The Retina-

A Case ReportDr Tufela Shafi MS, Dr Natasha Radhakrishnan MS DNB MRCophth, Dr Gopal S Pillai MD DNB FRCS,

Dr Roshan George MS

Retinal tumors are a rarity with peripheral retinal

tumors being still more rare. Here we report a case

where a peripheral retinal tumor presented with a

progressive decrease in vision over a long time due to

cystoid macular edema.

A 37 yr old male presented with history of gradual

painless progressive loss of vision left eye since 2 years,

with no improvement with treatment. On examination,

he had a best corrected visual acuity of 6/6 in the right

eye and 6/18 in left eye. Intraocular pressure in both

eyes was normal. Examination of the right eye including

anterior and posterior segments was within normal

limits. Anterior segment examination of the left eye

revealed 1+ cells and haze in the anterior chamber.

Vitreous showed 3+ cells and 2+ haze with membranes

and strands signifying partial PVD. Fundus examination

revealed hyperemic disc and stereoscopic examination

of the macula revealed the presence of cystoid macular

edema. There was fibrous proliferation and epiretinal

membrane along the arcades. A yellowish pink elevated

mass about 7 to 8 DD in size, with irregular surface

was seen superotemporally beyond the equator. Vessels

traversing and supplying the mass appeared dilated and

mildly tortuous and there were retinal pigment

epithelial changes at the base of the mass all around.

There were some telangiectatic vessels over the mass

along with hemorrhage. The lesion was also associated

with some intraretinal and subretinal exudation

(Fig 1).

Fluorescein angiography showed patchy

hyperfluorescence of lesion with multiple areas of

window defects corresponding to the RPE changes and

staining and blocked fluorescence secondary to the

exudation and mass lesion. The hyperfluorescence

increased in the late phase due to leakage in some areas.

There were areas of blocked fluorescence over the lesion

corresponding to areas of hemorrhage and in the

periphery of the lesion secondary to the RPE

hyperplasia. There was late disc leakage and flower

petal leakage at fovea signifying cystoid macular edema

(Fig 2).

OCT showed macular edema with a cystoid pattern with

a central macular thickness of about 450 microns.

B Scan showed an elevated, acoustically solid mass

about 9.7 x 7.1 x 3.2 mm in size and multiple echoes

in the vitreous suggestive of opacities (Fig 3).

The following differential diagnosis were entertained

1 Vasoproliferative tumour

2 An inflammatory or infective mass

3 Angioma of Von Hippel Lindau disease

4 Coats disease

A complete systemic evaluation was sought to rule out

coexistent systemic infections. Mantoux test was found

to be negative after 48 hours. Peripheral smear showed

normocytic normochromic blood picture. USG abdomen,

CT Thorax and MRI brain (plain and contrast) wereAIMS, Edapally, Kochi

CASE

REPORT

September 2009 T. Shafi et al. - Vasoproliferative retinal tumours 307

normal. Therefore infective or inflammatory mass was

ruled out. However, cholesterol levels were found to

be high (496.4mg/dl).

During the differential diagnosis, Von Hippel-Lindau

was excluded because of absence of grossly tortuous

and engorged blood vessels, absence of family history

for the disease and absence of other features of Von

Hippel-Lindau disease. In VHL even small tumours are

associated with grossly engorged and tortuous blood

vessels. Also the angiographic characteristics of Von

Hippel-Lindau like rapid filling of arteries and rapid

AV transit were not seen.

Coats disease was excluded because that is usually seen

in boys at a younger age, and usually does not cause

tumour like lesions even when exudation is severe. The

exudations in Coats disease are often flat and not

elevated. Besides tumour like lesions, if present in Coats

are accompanied by advanced exudative retinal

detachment.

Our patient showed the typical clinical picture of

vasoproliferative tumour. He had a solitary,

unilateral, yellowish vascularized tumour associated

with intraretinal exudation, RPE hyperplasia at the base,

telengiectasias and hemorrhage over lesion. He had

additional findings of anterior chamber cells, vitreous

cells and cystoid macular edema all of which have been

reported in various literature 1,2,3. We believe these

changes to be a secondary reactionary process to the

presence of tumour in the eye. FFA picture further

helped to confirm the diagnosis. Presence of elevated

levels of cholesterol in patients with vasoproliferative

tumour has been reported in literature 4.

With the diagnosis of vasoproliferative tumour, decision

to treat with multiple sessions of cryotherapy was taken

and patient given first session of cryotherapy. He is at

present on follow up.

Discussion

The term vasoproliferative tumour was coined by

Shields et al in 1995. Previously these tumours were

called presumed acquired haemangiomas, angioma like

lesions and peripheral retinal telengiectasia.

Vasoproliferative tumours of the retina are benign

vascular tumours of unknown origin. These tumours

generally present as yellow pink, one or more retinal

nodules seen usually in the pre-equatorial fundus,

generally in the inferotemporal quadrant but may also

be seen in the upper retinal quadrants 2,5 or even at

posterior pole 6,7. Their feeding and draining vessels

are slightly dilated but not enlarged or convoluted.

These tumours can be associated with additional clinical

changes like intraretinal and subretinal hemorrhages,

intraretinal and subretinal exudation, exudative retinal

detachments, hyperpigmentation of RPE, vitreous and

anterior chamber cells, vitreous hemorrhage, preretinal

macular fibrosis and macular edema 1,2,7. Exudation in

vasoproliferative tumours tends to creep back towards

the fovea and is hence seen in continuity with the

lesion4,7 . However preretinal gliosis can occur remote

from the lesion 7.

The pathogenesis of these tumours has not

been established. In a study of 103 patients, Shields

et al found that these lesions were idiopathic or

primary in 74 % and secondary to congenital,

inflammatory, vascular, traumatic, dystrophic and

degenerative ocular diseases in the rest 1. Primary

vasoproliferative tumours are solitary, unilateral

and generally located in the inferotemporal quadrant

of the retina. Many of the patients with primary

vasoproliferative tumours also have systemic

hypertension. Secondary vasoproliferative tumours

on the other hand are bilateral, multifocal and can

be located in any quadrant of the retina. SecondaryFig. 3. B-Scan ultrasound showing acoustically solid tumour.

Fig 2. FFA showing CMEFig. 1. Fundus pictureshowing thevasoproliferativetumor mass


tumours also tend to be more ill defined and

diffuse 7.

These tumours are believed to represent gliovascular

proliferations with varying degrees of both gliosis and

vascular proliferation. Histopathology of these tumours

shows them to be composed predominantly of

elongated, spindle shaped cells, corresponding to glial

cell origin imposed over a fine capillary background.

Mitotic figures, pleomorphism or cellular atypia has

not been shown to be present.Another important

feature of these tumours is the presence of dilated blood

vessels within the tumour mass 2,5.

Various treatment options have been described for

vasoproliferative tumours like periodic observation 1,2,

cryotherapy 1,2 ,3,4, laser photocoagulation 1,4 and plaque

radiotherapy 1,2,8. Some reports suggest that these

tumours may be treated successfully with photodynamic

therapy. Vitrectomy may also be needed for

complications accompanying these tumours like

vitreous haemorrhage and retinal detachment.

Irvine F et al 9 have suggested that trans scleral resection

be attempted if there is difficulty in diagnosis. This

would give tissue for diagnosis and also avoid

unnecessary enucleation in case of diagnostic dilemma.

In conclusion, vasoproliferative tumours should be

included in the differential diagnosis of any peripheral

retinal tumour. They should be recognized by their

distinctive clinical features and angiographic

characteristics and being decidedly benign their

recognition would avoid unnecessary morbidity for the

patient.

References

1 Shields CL, Shields JA, Barret j, et al. Vasoproliferativetumours of the ocular fundus. Classification and clinicalmanifestations in 103 patients.Arch Ophthalmol1995;113:615-23.

2 Heimann H,Bornfeld N,Vij O,Coupland SE,Bechaakisne,Kellner U, Forster MM. Vasoproliferative tumours ofthe retina. Br J Ophthalmol 2000;84:1162-1169.

3 Bianciotto C, Shields CL. Retinal vasoproliferativetumour with associated cystoid macular edema treatedwith cryotherapy and intravitreal triamcinolone.RetinaToday 2008;77-78.

4 Shields JA . Ocular oncology essentials. Retinalphysician 2006.

5 Jain K, Berger A R,Yucil Y H, McGowan H D.Vasoproliferative tumours of the retina.Eye2003;17:364-368.

6 Dunbar MT. Is only seeing eye now threatened ?. Reviewof Optometry Vol. No: 141: 04 Issue 4/15/04.

7 Shields JA, Shields Cl.Intra ocular Tumours: An atlasand text book 2007;396-398.

8 Cohen VM, Shields CL, Demirci H, Shields JA. Iodine I125 Plaque radiotherapy for vasoproliferative tumoursof the retina in 30 eyes.Arch Ophthalmol 2008;126(9):1245-51.

9 Irvine F, O Donnell N, Kemp E, Lee WR. Retinalvasoproliferative tumours:surgical management andhistological findings.Arch Ophthalmol 2000;118:563-569.


Go Green for a Healthier LifeDr. Meena Chakrabarti MS DO DNB

The news is crystal clear: After decades and decades of

polluting our surroundings, the planet is suffering.

Scientists have been very vocal about the impact our

driving, manufacturing, and consumption is having on

the future environment, like melting icebergs, rising

ocean levels, and a disappearing ozone layer. Indeed,

“global warming” and “greenhouse gases” have become

regular parts of our vernacular.

The most comprehensive modeling yet carried out on

the likelihood of how much hotter the Earth’s climate

will get in this century shows that without rapid and

massive action, the problem will be about twice as

severe as previously estimated six years ago - and could

be even worse than that.

American Meteorological Society’s Journal of Climate,

indicate a median probability of surface warming of

5.2 degrees Celsius by 2100, with a 90% probability

range of 3.5 to 7.4 degrees. This can be compared to a

median projected increase in the 2003 study of just

2.4 degrees. The difference is caused by several factors

rather than any single big change. Among these are

improved economic modeling and newer economic data

showing less chance of low emissions than had been

projected in the earlier scenarios. Other changes include

accounting for the past masking of underlying warming

by the cooling induced by 20th century volcanoes, and

for emissions of soot, which can add to the warming

effect. In addition, measurements of deep ocean

temperature rises, which enable estimates of how fast

heat and carbon dioxide are removed from the

atmosphere and transferred to the ocean depths, imply

lower transfer rates than previously estimated.

Now, the question being asked is can the damage be

reversed? Experts are unsure of a definitive answer,

but they all agree that if individuals assume a certain

level of personal responsibility, the future will be

cleaner.

With more than 200 million cars on the roads, it is

evident that we have a love affair with the automobile.

Whether it is in a luxury sedan, massive sports utility

vehicle, racy speedster, or cost-conscious compacts, we

enjoy driving. That infatuation, however, has come with

a heavy price tag of urban congestion and plenty of

pollution.

The problem develops when gasoline burns because it

produces a byproduct of nearly 20 pounds of carbon

dioxide (CO2) for each gallon of fuel. CO

2 is one of the

dominant chemicals in greenhouse gases and a major

contributor to global warming.

On a closer level, tailpipe emissions react with sunlight

and oxygen to create ground level ozone. Not

surprising, heavy loads of this toxic gas are prevalent

in major cities and so we live in areas with poor air

quality.

First, check out hybrid automobiles. These cars operate

off both gas engines and electric motors. The electric

motor supplies added power during acceleration,

thereby allowing designers to install smaller traditional

engines. Ultimately, they consume less fuel, which saves

you cash and cuts down on CO2 emissions.

If you drive a totally gas-powered vehicle, you can still

minimize the negatives. One of the best ways to

downgrade its polluting potential is to upgrade your

COMMUNITY

OPHTHALMOLOGY


[email protected]


vehicle’s performance. Schedule regular service

appointments to change oil, belts, and filters. For

example, a clogged air filter can decrease your mileage

by 10%.

Also, measure your tire pressure every few months or

before each long-distance trip. Proper inflation saves

you approximately 3% in fuel costs, and provides you

with a safer drive. Under-inflated tires are more

susceptible to damage, such as flats and blowouts—

two things you definitely want to avoid when heading

to a new job. Remember to refer to your car’s operating

manual or contact a trusted mechanic before attempting

any major maintenance. Other simple, but earth-

friendly, motoring techniques include engaging cruise

control on long stretches and avoiding rapid

acceleration or braking If you drive a totally gas-

powered vehicle, you can still minimize the negatives.

For one thing, recycling pays. Items such as paper,

newspapers, cardboard, glass, plastic, and aluminum,

can be broken down and repurposed into other useful

products. And, we use a lot of these substances . Instead

of expending energy and natural resources to create

new containers, recycling one glass bottle saves enough

power to light a 100-watt bulb for up to 4 hours. One

recycled aluminum can has the potential to save enough

energy to run a television or computer for 3 hours.

Fortunately, many municipalities and apartment

complexes have turned recycling into a simple process

by supplying bins dedicated to specific items. All you

have to do is separate the various pieces from the

regular trash. If your apartment organization does not

yet recycle, volunteer to work with the management

to help set up and promote a new system.

You also can go green by turning off and

unplugging. Sure, it is common sense to switch off a

light or television when leaving a room, but it’s even

better to unplug major electronics and appliances when

not in use. Does your coffee pot really need to be

plugged in while you are on duty for 12 hours?

Also, your computer, printer, and cell phone charger

eat up energy when left plugged in and not turned on.

That is a phenomenon known as vampire power,

and is estimated to waste nearly millions in electric

bills each year. Swapping incandescent light bulbs for

the long-lasting, energy-efficient compact fluorescent

type is another money saving and eco-friendly tip. These

are designed to use 75% less energy, and boast of a 10

times longer life cycle.

Energy is not the only commodity you can affect. Water

is another resource in need of conservation—case in

point, several parts of the world suffered devastating

droughts this past summer. While you have no control

over Mother Nature, you can do your part by taking 4-

minute showers, and turning off the faucet while

brushing your teeth or sudsing your hands.

Also, postpone running washers and dishwashers until

you have full loads, and look for phosphate-, petroleum,

and chlorine-free detergents to avoid feeding

unnecessary chemicals into local water systems. Using

either cold or warm water temperature settings can

prevent an estimated 350 pounds of CO2 production

because you minimize the energy used to heat the water.

These simple steps can be followed at home, in

apartment laundry centers, or in coin-operated

Laundromats.

Taking control of your thermostat is yet another green

habit. Researchers believe that for every two degrees

you lower the thermostat, the atmosphere is saved from

approximately 350 pounds of CO2. The general advice

is to set your house temperature for 68 degrees during

winter days, and slightly lower at night and pile on the

blankets. Also, if you have access, clean your heater’s

filters every few months or sooner.

On hot days, the opposite theory applies. Cool off with

an oscillating or ceiling fan, both of which use less

power than an air conditioner (AC). If you must chill

out, limit your AC usage. For a central air system, set

the thermostat high, around 78 degrees, and run

window units for fewer, shorter operating cycles.

To help maintain a comfortable climate, rely on your

curtains or blinds. In the winter, open them up to let

the sunlight warm your rooms, and do the opposite in

summer to keep the heat out.

On your own, follow these simple policies. Start off by

bringing in your own coffee mug or refillable water

bottle instead of choosing disposable cups or plastic

bottles. You can save money and act eco-friendly by

bringing your lunch with you to work on most days. If

September 2009 Meena Chakrabarti - Go Green for a Healthier Life 311

you plan to brown bag it, literally, reuse that bag as

much as possible. Even better, buy a soft insulated

lunchbox. These tend to be easy to clean and keep food

hot or cold. Store food in containers or wash out and

reuse plastic storage bags whenever feasible. A healthy

byproduct? You control what you eat.

What better way to acquaint yourself with a region than

through sampling the local cuisine? Buying locally

grown produce, flowers, and other items helps cut down

on transportation of goods over highways while also

supporting the regional economy. Wherever you grocery

shop, skip the plastic or paper debate and pack up your

own canvas bags. This will reduce the number of plastic

items ending up in landfills.

On everyday items, look for green products. Some

brands promote the fact that they are environmentally

friendly. For others, there are a few simple rules to abide

by, such as choosing pump sprays over aerosols and

picking up brown coffee filters instead of the traditional

bleached white ones. If you do buy something in a

plastic bottle, such as body lotion, flip it over and look

for a number. This is an indicator about which type of

plastic was used to create it. No number means the

item isn’t recyclable.

Finally, put your money where it counts. There are

numerous organizations that work toward protecting

the planet through research, lobbying, and raising

public awareness.

Making it work

The planet’s future is yet to be written, but for

now, the message is fairly clear: Do what you can to

minimize the negative impact. Going green may

take some effort at first, but you will most likely find

that it quickly becomes force of habit, no matter where

you are.

Being Green

• When shopping for a new car, consider

a hybrid model.

• Schedule regular maintenance to change out filters

and oil

• Check tire pressure

• Ease up on the pedals and drive at consistent speeds

• Recycle whenever possible

• Unplug unused electronics and appliances

• Adjust thermostat to seasons

• BYOL: Bring your own lunch (and coffee mug)

• Buy local products

• Use canvas bags when shopping

• Donate to environmental organizations


Masquerade SyndromeDr. Meena Chakrabarti MS DO DNB

Masquerade syndrome includes a group of malignant

and non-malignant systemic or primary ocular disease

that clinically present in the eye as an intraocular

inflammation or uveitis

Uveitis Masquerade accounts for 5 % of patients with

uveitis in a tertiary care centre. An awareness of the

presence of and early recognition of the masquerade is

of utmost importance as Ocular Masquerade may be

the first sign of a life threatening disease.

The various conditions that can manifest in the eye as

a masquerade includes

MALIGNANCIES

Adults:

Primary Central Nervous System lymphomas /

Primary Intra Ocular lymphomas

Systemic NHL Metastatic To The Eye

Metastatic Carcinoma : Breast / Lung / Renal

Uveal Melanomas

Children:

Leukaemia

Retinoblastoma

Medulloepithelioma

Juvenile Xanthogranuloma

NON-MALIGNANT MASQUERADE

Intraocular foreign body / Retinal Detachment /

Retinitis pigmentosa / Pigment Dispersion Syndrome

/ P. Acnes Infection

Many entities present as chronic intraocular

inflammation and a thorough workup to exclude a

masquerade syndrome should be carried out in the

following situations.

1. All undiagnosed inflammatory disease

2. Intraocular inflammations with atypical clinical

features and course

3. Inflammations that do not respond to adequate

medical therapy

4. Age <5 years />50 years

Because of the nature of the underlying disease, which

has detrimental consequences, early diagnosis and

prompt treatment are critical.

This photoessay is on primary intraocular lymphoma

(PIL)

Primary Intraocular Lymphoma is the commonest

condition presenting as an ocular masquerade.PIOL is

a large B cell Non Hodgkin Lymphoma, presenting in

the 5th to 7th decade in immunocompetent persons.

Presentation in an younger age group is seen in the

immunocompromised.This entity is commonly

associated with CNS lymphoma and rarely with visceral

and nodal lymphoma. This condition is bilateral in

80 % of cases. The ocular presentation may be varied

and may manifest as vitritis, sub retinal and sub RPE

creamy white infiltrates, vasculitis, retinitis or as an

uveal mass lesion.

90 % of patients with PIOL develop CNS Lymphoma

while only 5 % of patients with CNS Lymphoma will

develop intraocular manifestations. Hence a detailed

systemic workup, neurological investigations,

PHOTO

ESSAY


[email protected]

September 2009 Meena Chakrabarti - Masquerade syndrome 313

Fig. 1. a-c : (a) Fundus picture at presentation showing optic nerve infiltration in Primary Intraocular lymphoma. (b)Histopathological evidence of large B cells in vitreous biopsy specimen (c)Fundus photograph comparing the lesion

before and after radiotherapy.

like cranial MRI and lumbar puncture are essential.

Vitreous biopsy, sub retinal or subRPE aspirates or a

retinochoroidotomy may be necessary for

histopathological confirmation.

Treatment recommendations depend on whether the

lesions are confined to the eye alone both eye and CNS

involvement or there is recurrence following primary

therapy.

Treatment recommendations:

1. Intraocular Lymphoma alone

XRT to eyes only Systemic Chemotherapy

2. Intraocular and CNS Lymphoma

XRT to eyes + / - BRAIN

Systemic Chemotherapy

Table 1. Scheme of Investigating a patient withchronic Intraocular Inflammation

3. Recurrent Intraocular Lymphoma

Intravitreal salvage chemotherapy with Methotrexate,

Rituximab, Anti CD-20 Monoclonal antibody. Requires


multiple intravitreal injection and carry a very high

recurrence rate on cessation of therapy.

The first case shows regression after radiotherapy in a

biopsy proven case of primary intraocular lymphoma

which presented as disc inflitration, disc edema and

vitritis. Vitreous biopsy specimen showed large B cells

suggestive of PIOL. Note that regression of the lesion

is unfortunately associated with optic atrophy as

evidenced by the disc pallor and functional loss in this

patient. (Fig. 1 a-c)

Fig. 2. a-c . (a) Fundus picture at presentation showing the creamy subretinal infiltrates temporal to the macula in a patientwith PIOL. (b)Hitopathological confirmation of large B cell infiltrates in the chorioretinal biopsy speciemen(c)Comparative fundus pictures before and after systemic chemotherapy showing good resolution and residual RPEscarring

The second case presented as creamy subretinal

infiltrates temporal to the macula in a 55 year old

male patient who attended our clinic with complaints

of defective vision and floaters. Vitreous biopsy

and chorioretinal biopsy specimen showed large

B cells suggestive of PIOL. This patient was managed

by systemic chemotherapy and showed good

resolution of the lesion with residual rpe scarring

(Fig 2 a-c).


Management of A Case of Post-traumatic

Cyclodialysis With CataractDr. Mohan Rajan MS 1, Dr. Andrew Braganza MS 2, Dr. Arup Chakrabarti MS 3, Dr. V. Sahasranamam MS 4,

Dr. Simon George MS 4

A 48 year old diabetic lady was seen in our OPD with

complaints of defective vision right eye following a

closed globe injury (blunt trauma) 3 years back. She

was having moderate visual loss at that time and was

being treated by ophthalmologists at two local hospitals.

Available records show that she was on systemic

steroids for some time.

Presently examination of her right eye revealed a clear

cornea, dilated non reacting pupil, mature (white)

cataract with phacodonesis. IOP recorded was 4mm of

Hg in the right eye and vision was perception of light

with accurate light projection. Gonioscopy revealed

cyclodialysis from 9’O’clock to 2’O’clock. The

cyclodialysis was confirmed by UBM.

B Scan did not show any retinal detachment.

Left eye was normal, BCVA of 6/6.

How would you approach this case?

Dr. Mohan Rajan

Cyclodialysis clefts are due to disinsertion of the

longitudinal fibres of the ciliary body from the scleral

spur. They can occur following blunt trauma or due to

surgery for cataract or glaucoma.The result is a

communication between the anterior chamber and the

suprachoroidal space which results in internal filtration

and therefore hypotony. Hypotony causes choroidal

effusions, macular / optic disc edema and decreased

visual acuity. Later generalised detachment of the ciliary

body occurs which results in decreased aqueous humour

production which further aggravates hypotony.

The goal of treatment is to reverse hypotony and restore

visual function. The indications for treatment of

cyclodialysis include hypotonous maculopathy, macular

folds, choroidal detachment, corneal edema &

worsening vision. A cyclodialysis cleft with hypotony

but without structural or functional abnormalities does

not require treatment. The management algorithm

includes treatment by medical, laser or surgical

methods.

Medical management consists of apposition of ciliary

body against the scleral spur and promotion of

adherence by scar formation. This is enhanced by strong

mydriasis ( 1% atropine eye drops) and minimising /

stopping of steroid medication for up to 6 weeks.

Noninvasive laser methods include treatment by argon

laser to the ciliary body and sclera through a goniolens.

If visualisation of the cleft is difficult due to shallow

anterior chamber, the chamber can be deepened with

viscoelastics prior to the procedure.Joondeph who did

the first argon laser treatment used powers of

400-800mw, 200 micron spot and 0.1-0.2 sec exposure

time. Other noninvasive methods include use of

transcleral yag / diode laser,transcleral cryotherapy.

If medical /noninvasive laser methods do not work then

sugical methods become the next option. Methods

adopted depend on the size of the cleft. Small clefts

<2 clock hours can be approached by direct /indirect

cyclopexy or ciliochoroidal diathermy. Medium clefts1Chennai 2 CMC , VELLORE, 3Chakrabarti Eye Care Centre, Kochulloor, Trivandrum4 RIO, Trivandrum

CONSULTATION

SECTION


of 2-4 clock hours need to be approached by direct

cyclopexy or diathermy. Large clefts >4 clock hours

can be approached by direct cyclopexy or by anterior

scleral buckling. Large chronic clefts are reported to

benefit from parsplana vitrectomy, cryotherapy and gas

tamponade.Delay of treatment for> 8 weeks increases

the risk of loosing 1-3 snellen lines of visual acuity.

With respect to our patient, medical management with

Atropine eye drops and transcleral diode laser in two

rows of contiguous burns 2 to 3mm behind the limbus

or argon laser photocoagulation. Following this since

the patient has mature cataract, phacoemulsification

and implantation of nonfoldable intraocular lens in the

ciliary sulcus will enhance closure of the Cyclodialysis

cleft. If the above treatment fails then direct repair of

the cleft is recomended. In cases of traumatic

cyclodialysis there could be alterations in the

iridocorneal angle which persists after cyclodialysis

repair and therefore regular monitoring of intraocular

pressure is recommended.

Dr. Andrew Braganza

This is a very interesting clinical scenario. One more

piece of information I would like is to know whether

there is a relative afferent pupillary defect in the

affected (right) eye. Even though the pupil is dilated

and non reactive, presumably secondary to traumatic

mydriasis, this information is easily obtained by the

swinging flashlight test and observation of its effects

on the left eye. I assume there is no RAPD and that

therefore there is no significant disc damage in the right

eye.The problems that need addressing are the

following:

1.Cataract

2.Cyclodialysis and hypotony

The traumatic mydriasis may be a problem, but can be

addressed subsequently. Diabetes related ocular

problems is unlikely to be an issue here in view of the

normal fellow eye.

Cataract: The cataract needs to be removed and an

IOL implanted. It is likely that there is extensive zonular

damage, and capsular support for the IOL may be

lacking. I would plan a superior scleral tunnel incision

with the intention of doing a manual small incision

surgery, converting to a sclerally fixated lens if needed.

It is easy enough to pass the sutures needed through

the posterior lip of the tunnel and under a scleral flap

180 degrees away, so that they remain buried under

partial thickness sclera after being tied. Alternatively,

there are techniques available to handle this cataract

by phaco even to the extent of sclerally fixating or iris

fixating a foldable lens. Details of this are outside the

scope of this discussion. Please note that scleral fixation

of the IOL must be done only after repair of the

cyclodialysis

Cyclodialysis: Applying laser treatment or cryo is a

conservative option for a cyclodialysis cleft. With a small

cleft the results are quite good, the advantage of this

approach being that it is non invasive and can be

repeated if it fails, still leaving a surgical option open.

With a large cleft, this treatment is unlikely to succeed;

in this patient, therefore, I would recommend

commitment to a surgical repair, especially as the

cataract surgery has to be done anyway. The technique

involved is similar to scleral fixation of an IOL. A double

armed suture needs to be passed through or just behind

the root of the iris, through the scleral spur and out

under a partial thickness scleral flap and tied, to appose

the dialysed ciliary body to its normal attachment. 10-

0 prolene is a suitable material, though over tightening

must be avoided as the delicate ciliary and iris tissue

cheese-wires quite easily. For a superior cleft like this,

an open-sky approach through a scleral tunnel using

10-0 monofilament nylon on a curved needle is also

possible. The procedure is to some extent blind, as one

cannot directly visualize the exact entry point of the

suture from the inside. But, as with sclerally fixating

an IOL, using external surface anatomy and a 26 or

30G hypodermic needle introduced from outside the

eyeball as a guide, precise placement can be achieved

by railroading the prolene suture through the

hypodermic needle. Many variations of technique have

been described; the reader can study these in detail

and decide for him- or herself which makes the most

sense. With 5 clock hours of dialysis in this patient it is

likely that two separate sutures will be needed for the

repair. If a scleral tunnel incision is being used for the

cataract, it should be possible to pass both these sutures

through the bed of the tunnel without the need for

separate scleral flaps or dissections.

September 2009 R. Sahasranamam et al. - Post-traumatic cyclodialysis 317

Apart from the technical difficulty of the repair, the

challenging part of treating a cyclodialysis is handling

the IOP once the repair is achieved. A steep rise to 40

or 50 mmHg can be expected in the postoperative

period associated with pain and acute danger to the

optic nerve head. Prophylactic administration of

Diamox is obviously not an option in a hypotonic eye.

Early removal of the bandage and checking of IOP

postoperatively, probably within 12 hours of the

procedure is a logical precaution. The initial reversal

and upswing of IOP does eventually stabilize in most

cases, but requires monitoring and treatment; it may

take days to weeks to stabilize and the patient needs to

be closely followed up during this period. Permanent

secondary glaucoma may ensue, and require lifelong

treatment. To my mind this is preferable to macular

damage from hypotony. If surgical control of IOP is

needed later, this would usually take the form of a

glaucoma drainage device, not a trabeculectomy.In this

patient, even assuming that surgery is successful, the

visual prognosis remains guarded. This is because we

don’t know the condition of the macula preoperatively.

Prolonged hypotony may result in permanent damage

and irreversible visual loss.The dilated pupil may cause

the patient problems. If so, an iris implant can be

considered at a later stage.

Dr. Arup Chakrabarti

The given patient presents with a couple of intriguing

problems. The condition of the patient is to be tackled

at two levels.

1. Visual rehabilitation

2. Management of hypotony

Visual rehabilitation

Careful preoperative counseling is mandatory. Patient

is to be informed that non improvement of vision

postoperatively may be related to subtle changes in the

posterior segment which may not be evident

preoperatively in view of the media opacity. Late

postoperative complications may arise because of the

prior trauma unrelated to the cataract surgery. The

extend of subluxation should be evaluated with the

patient in supine position. A scan biometry may be

difficult in view of the hypotonicity. Injection of

viscoelastic through a paracentesis site on the slit lamp

has been recommended prior to gonioscopy. Another

option would be to perform A scan biometry on the

surgical table with sterile precautions. It is preferred

to use peribulbar anesthesia since the surgery is likely

to be complicated and a prolonged one. A temporal

scleral tunnel incision would be appropriate since it

will render conversion to a non phaco technique easier,

should the need arise, due to intraoperative

complications. Anterior capsule must be stained with

trypan blue dye. The capsulorhexis should be performed

with a closed chamber technique preferably with micro

rhexis forceps. Fibrotic anterior capsular plaque may

be seen in similar situations. In difficult situations,

placement of iris hooks may be called for, to support

the capsular bag, during capsulorhexis. Hydrodissection

may perhaps be avoided since this is a traumatic mature

cataract and a preexisting posterior capsular dehiscence

may not be completely ruled out. A good quality

viscoelastic agent should be employed to protect the

endothelium and maintain the anterior chamber depth.

Excessive chamber depth fluctuation should be avoided.

Direct phaco chop would be an ideal technique to

remove the nucleus since it is less traumatic to the

zonules. Vitreous if present should be managed by

automated anterior vitrectomy. A foldable hydrophobic

or hydrophilic acrylic intraocular lens should be

implanted in the capsular bag. After nucleus removal,

it may be a good idea to implant a capsular tension

ring within the capsular bag. A double eyelet Cionni

ring sutured to the sclera may have to be considered if

there is extensive zonular loss.

If the capsular bag stability is inadequate for safe

phacoemulsification, one should think of converting to

a non phaco technique. In that case, the PCIOL may

have to be sutured to the ciliary sulcus (scleral fixation).

There are several techniques available for scleral

fixation and the surgeon can choose a technique he is

comfortable with.

Postoperative evaluation should be intensive since more

than usual post operative inflammation is to be

expected. A thorough evaluation of the posterior

segment should be performed. The postoperative course

may be complicated by retinal detachment as a result

of the prior trauma and the patient should be informed

about it.


Management of hypotony

Patient has to be watched carefully in the postoperative

period. Hypotony is known to have deleterious effects

in the posterior segment including hypotonous

maculopathy. In such a case, the condition may have

to be managed surgically. There are various procedures

described in literature for the treatment of cyclodialysis

clefts which implies that the condition is difficult to

treat. Direct Argon laser photocoagulation through a

gonioprism ( in cases with good visualization) has been

found to be successful by several investigators.

Confluent applications of 100 mm spots at 0.1 to 0.2

sec and 500-1000 mW are delivered to the base of the

cleft followed by postoperative cycloplegics. Repeat

treatment may be required in some cases to

progressively close the cleft. In cases with poor visibility,

the cleft can be treated indirectly from outside by

cryotherapy or photocoagulate it with either a diode

or transcleral Yag laser. All these indirect approaches

require a peribulbar anesthesia for comfort, as well as

post operative cycloplegics.

More aggressive surgical therapy has been described

and involves external diathermy to the bed of the scleral

flap that is created over the cleft. This can be combined

with suturing the cleft with 9-0 or 10-0 nylon through

the scleral bed, either with or without direct

visualization. Recalcitrant clefts may require pars plana

vitrectomy, cryotherapy and tamponade with SF6 gas.

The patient can experience a period of extremely high

pressure and acute pain once the cleft is closed. The

patient should always be warned of this possibility and

prophylactic aqueous suppressants may have to be

prescribed.

In summary, management of this complicated case is

quite complex. Difficulties are expected during cataract

surgery in view of the mature state of cataract,

subluxation and very soft eye. Inspite of a well done

cataract surgery, visual success may not be satisfactory

in view of the posterior segment complications induced

by the blunt trauma. In the event of a persistently low

post operative intraocular pressure affecting structure

and function, cyclodialysis cleft will have to be dealt

with surgically using one of the techniques described.

Compilation

As opined by our expert panel, this is a difficult,

intriguing problem.

Our approach to the problem was, two pronged

1. Tackle the hypotony

2. Visual rehabilitation

In a primary sitting, we planned to take care of the

hypotony. Being a large cyclodialysis cleft, of long

standing , we planned a surgical cyclopexy. Under a

partial thickness sclera flap we did a continuous – 10-

0 nylon(curved needle) suturing of the ciliary body to

its scleral bed. As indicated by our panelists this

procedure, is to a good extent a blind procedure. The

appositioning of the CB to its scleral bed should be

full, to get a desired effect but you can easily cheese

wire through delicate ciliary / uveal tissue. Even a small

cyclodialysis cleft remaining open shall keep the IOP

low and in the other hand you can have raised IOP

post operatively. The balance is delicate. In our case ,

the post op IOP was around 8mm of Hg (1 week and 3

weeks post op).Post-op evaluation revealed

cyclodialysis persisting in one clock hour. Though our

intention was to close the cleft fully,it has not worked

out in one sitting.

Regarding the cataract we planned to deal with it 3

weeks post cyclopexy, but the patient disclosed chicken

pox during this period, which delayed the second

surgery by more than 6 weeks. SICS through a scleral

tunnel made close to the limbus ( to avoid the cyclopexy

site) was done. Through the patient developed a

phacodonesis, intraoperatively, capsulorhexis, lens

nucleus delivery and IOL implantation were uneventful.

The dilated non reacting pupil (traumatic mydriasis)

is persisting. Seen 10 days post op the patient had a

UCVA of 6/36. Fundus examination revealed, normal

disc and vessels with a dull fovea. Post cataract surgery

also, the IOP is in the range of 8mm of Hg.

On 16/9/09 (last follow up, when the patient is

reviewed by her local ophthalmologist at Cochin), the

visual acuity in the operated eye is 6/12 improving to

6/6p with glasses and the IOP is 8.5mm Hg

Compiled by: Dr. V. Sahasranamam and Dr. Simon George, RIO Trivandrum


A Tribute to Charles L. Schepens, MD

The current practice of

ophthalmology owes a great

debt to Charles Schepens’

passion for science, which

revolutionized ophthalmic

practice by combining

clinical practice and eye

research. He is considered by

many to be the father of

modern retinal surgery, not

to mention the grandfather

of the corneal subspecialty.

He was the brilliant inventor of the indirect binocular

ophthalmoscope, and his devices, as well as surgical

techniques such as scleral buckling, have been credited

with raising the success rate of retinal reattachment

surgery to 90 percent.The Belgian-born Dr. Schepens

began his training in mathematics, which led to his

interest in ophthalmic instrumentation. He received his

medical degree from the University of Gand in 1935

and went on to train at Moorfields Eye Hospital,

London, from 1935 to 1937. He then returned to

Belgium to practice medicine, and in 1939 joined the

medical corps of the Belgian Air Force. After the German

invasion of Belgium in 1940, he became a courageous

leader in the French Resistance who masterminded the

escape through the Pyrenees of more than 100 people.

He was later decorated for bravery by both the French

and the Belgian governments.In 1947, Dr. Schepens

emigrated to the United States and took a fellowship

post at the Howe Laboratory of Ophthalmology at

Harvard Medical School. Two years later, he established

and became the first director of the retina service at

OPTHALMIC

HISTORY

Dr. Meena Chakrabarti MS DO DNB

Fig. 1. The old prototype model of the binocular indirectophthalmoscope invented by Dr. Charles Schepens

Fig.2 The technique of placing staggered rows of diathermy

burns on the bed of the dissected seleral flap was avery efficient form of retinopexy during detachmentrepair surgery popularised by Dr. Schepens.

Fig. 3. The ‘MIRA SERIES’ of silicon buckles and spongeshave withstood the test of time and are used for both

implant and explant procedures.Chakrabarti Eye Care Centre, Kochulloor, Trivandrum 695 011 E-mail:

[email protected]


Fig. 4. The meridonal buckles (No. 135 & 137) wereextensively used during inplant procedures forpreventing fish mouthing of a large posterior horseshoe tear.

the Massachusetts Eye and Ear Infirmary, the first of its

kind. In 1950, he established the Retina Foundation, a

center for the intensive investigation of retinal

detachment and allied conditions. This illustrious

organization is now known as the Schepens Eye

Research Institute and is the largest independent eye

research organization in the United States, a living

legacy to the basic biomedical and clinical eye research

Dr. Schepens thought so important.(Fig.1 - 4) He was

the author of more than 340 medical papers and four

books, trained more than 170 vitreoretinal surgeons,

gave countless lectures and courses, and received

innumerable honors during his distinguished career.

In 1999, he was selected as one of the 10 Most

Influential Ophthalmologists of the 20th Century by

his peers—33,000 ophthalmologists in the United States

and abroad—for his innovations and inventions that

have so greatly improved ophthalmology. In 2003, he

was honored as an inaugural recipient of the American

Academy of Ophthalmology’s highest honor, the

Laureate Recognition Award.He had an unlimited

amount of kinetic energy and seemed always focused,

engaged, passionate and driven. He was quite engaging,

and never forgot anything about anyone he ever met.

In his presence, you could feel the energy he radiated—

the fire of so many things to do and questions to be

answered. This energy was contagious, and gave him

the ability to inspire others with his passion and

enthusiasm. He created in every one a sense of the

importance of the projects in which we were involved.

His logical thought processes, attention to detail and

formidable intellect are legendary.Of course, Dr.

Schepens will be missed, but we are fortunate that so

much of his energy and passion persist in the many

physicians and researchers he inspired.

September 2009 Journal Review 321

Photodynamic Therapy for Age-Related

Macular Degeneration : Epidemiological

and Clinical Analysis of a Long –Term StudyJorge Mataix, M Carmen Desco, Elna Palacios.

Ophthalmic Surg Lasers Imaging 2009; 40:277-284

Age related macular degeneration (AMD) is a

degenerative dystrophic disease that goes through

several phases in its natural evolution. Its consequences

range from minor forms of dry AMD to severe forms of

exudative AMD with choroidal neovascularization, in

which more serious loss of vision occurs. CNV is a self

limiting lesion that grows progressively, producing a

serious injury to the retina, until a disciform scar

appears. There are different and multiple treatments

to stop this disease, but photodynamic therapy is the

only one with long term follow up. The clinical results

of PDT can be of great interest and potential concern

to clinicians as a basis of comparative efficacy of new

treatments.

The principal aim of this prospective non randomized

clinical trial from Valencia, Spain was to analyze the

long term results of patients with exudative age related

macular degeneration treated with photodynamic

therapy. 262 patients were included with exudative age

related macular degeneration who were treated with

PDT in accordance with a protocol of the Treatment of

Age Related Macular Degeneration with Photodynamic

Therapy Study. The follow up lasted 48 months.

There was significant loss of visual acuity 3 months

after the first PDT treatment, a slow progressive

decrease of vision until month 12, and then visual acuity

remained stable from months 24 to 48.The choroidal

neovascularization size increased noticeably during the

first 12 months, particularly the first 3 months after

PDT. The higher the classic component of choroidal

neovascularization, the better it responded to PDT. The

evolution of juxtafoveal choroidal neovascularization

was worse than that of subfoveal choroidal

neovascularization after PDT because it grew quickly

towards the fovea and visual acuity loss was greater.

The authors conclude that PDT is a safe, long term

treatment for exudative age related macular

degeneration, but it is not definitive because this

treatment cannot stop the initial growth of the choroidal

neovascularization lesion. Future studies on long term

visual acuity changes for exudative AMD treated with

antiangiogenic drugs will show us the difference with

PDT treatment for this disease.

JOURNAL

REVIEW


Refractive Errors and Strabismus in Children

with Down Syndrome: A Controlled StudyArsen Akinci, Ozgur Oner, Ozlem Hekim Bozkurt.

J Pediatr Ophthalmol Strabismus 2009;46:83-86.

Corneal Collagen Cross Linking Using

Riboflavin and Ultraviolet-A Light For

Keratoconus : One-year Analysis Using

Scheimpflug ImagingDilraj S Grewal, Gagandeep S Brar, Rajeev Jain , Vardaan Sood.

J Cataract Refract Surg 2009; 35:425-432.

There is a mounting evidence of the efficacy of corneal

collagen cross linking treatment using photo sensitizer

riboflavin and ultraviolet-A(UVA) light with wavelength

of 370 nm in halting the progression of keratoconus

and post refractive surgery corneal ectasia with minimal

toxicity. This study from Grewal Eye Institute,

Chandigarh aim to evaluate changes in corneal

curvature, corneal elevation, corneal thickness, lens

density and foveal thickness after corneal collagen cross

linking with riboflavin and ultraviolet-A light in eyes

with progressive keratoconus.

This study recruited 102 patients older than 18 years

with a corneal thickness of atleast 400 μm diagnosed

with progressive keratoconus. All patients had

subjective refraction, best corrected visual acuity(BCVA)

measurement, Pentacam rotating Scheimpflug imaging

and OCT imaging before cross linking and 1 week,1,3

and 6 months and 1 year after cross linking .The mean

preoperative BCVA remained stable from preoperative

levels in all postoperative visits. The mean spherical

equivalent decreased steadily postoperatively to a low

of -4.90±3.52D at 1 year. The mean cylinder vector

was 1.58×7º±3.8D before cross linking and

1.41×24º±3.5D, 1 year after cross linking. There was

no significant difference in mean measurements

between preoperatively and 1 year postoperatively,

respectively for Central Corneal Thickness (CCT)

(458.9±40μm and 455.2± 48.6μm), anterior corneal

curvature (50.6±7.4D and 51.5±3.6D), posterior

corneal curvature (-7, 7±1.2D and -7.4 ±1.1D) apex

anterior (p=.9),posterior corneal elevation (p=.7), lens

density( p=.33) foveal thickness (175.7±35.6μm and

146.4±8.5 μm; p=.1).

Stable BCVA, spherical equivalent, anterior and

posterior corneal curvatures and corneal elevation

one year after cross linking indicate that keratoconus

did not progress. Unchanged lens density and foveal

thickness suggest that lens and macula were not

affected after UVA exposure during cross linking.

Authors admit that this study included limited number

of patients with limited follow up. Long term stability,

indications and contraindications of riboflavin- UVA

collagen cross linking must be evaluated.

Ocular manifestations of Down syndrome have been

well described in numerous studies and include eyelid

anomalies such as prominent epicanthal folds, upward

slanting of palpebral fissures, epiblepharon,

September 2009 Journal Review 323

Compiled by Dr. Reesha, Little Flower Hospital, Angamaly

nasolacrimal duct obstruction, blepharitis, keratoconus,

retinal abnormalities, glaucoma and amblyopia due to

strabismus, refractive errors, and media opacities.

However in all these studies an appropriate control

group was lacking and the authors compared their

findings with previous normative studies. In this study

authors from Boston aim to evaluate the prevalence of

refractive errors, strabismus, nystagmus and congenital

cataract in children with Down syndrome and control

subjects of similar age and socioeconomic group.

Seventy seven children with Down syndrome and 151

control subjects were evaluated for the prevalence of

ocular findings. The diagnosis of Down syndrome was

made through clinical and genetic findings. All children

underwent cycloplegic auto refraction, retinoscopy, or

both, slit lamp biomicroscopy and detailed fundus

examination. Ocular movements were checked and

ocular alignment was assessed by Hirschberg corneal

reflex test, Krimsky prism test or prism cover test. Ocular

findings were discovered in 97.4% of children with

Down syndrome and 42.4% of control subjects

(p<.0001). The point prevalence of nystagmus,

strabismus, hypermetropia, astigmatism and congenital

cataract was significantly higher in children with Down

syndrome (p<.0001 for first four categories, and p<.01

for congenital cataract).

The authors conclude that evaluation , treatment and

regular review of ocular and refractive findings in

children with Down syndrome is essential and likely to

significantly enhance the quality of life of individuals

with Down syndrome.


Manual of SQUINTAuthor Leela Ahuja, Ex- Professor of Strabismology, Ex- Director, Institute of Ophthalmology

Aligarh Muslim University, Aligarh, UP

Published by Jaypee Brothers, New Delhi

First Edition, 2008

Price - Rs; 350/-

Most controversial aspects of certain condition have

been deliberately left out for the sake of easy

understanding. This book includes materials from Duke

– Elder, Kyeth Lyle, von Noordan, Kanski, Muller and

Peymann.

This book gives a reasonable background for

understanding the ocular muscles and their functional

anomalies. The surgeon’s update knowledge of the

subject, efficiency and dedication alltogether can find

solution to the squint problem. Appropriate diagrams,

figures and photographs have been provided in this

book. I do hope the postgraduates are benefited by

going through this work, not only during the course of

their formal study but also, subsequently in their

practices.

A lot of literary works have been done on squint but

still there is a dearth of standard books on strabismus

for post graduate students. No doubt, surgery of squint

is done by many ophthalmologists, but mostly, it is on

cosmetic grounds and that too without the help of

proper orthoptic department. It is also a fact that general

public is reluctant to have treatment, particularly surgical

treatment of squint, as this malady is considered to be

due to displeasure of some goddess. The importance is

not to cure deviation, but to improve binocular function.

The prevalence of squint in Indian population is estimated

to be 3- 4 % and prevalence of amblyopia 1%.

Squint topics are very much comprehensive so the

author has tried to simplify them by providing their

description in simple and easily understood language.

Ophthalmology Secrets In ColorAuthors James F. Vander MD, Janice A. Gault, MD, FACS

Published by, MOSBY ELSEVIER, New Delhi

Third Edition – 2009

Price Rs: 850/-

Much of the information in this book can be found in a

number of other ophthalmology text books. The table

of contents is similar to that of many other books already

in print. So why bother to write a new ophthalmology

text? The value of the book is in the unique manner in

which the material is presented, continuing the tradition

the Secrets Series has established in numerous other

specialties. The question – and – answer “Socratic Method”

format reflects the process by which a large portion of

clinical medical education actually takes place.

This completely updated top – seller in ophthalmology

continues the tradition of the highly popular Secrets

BOOK

REVIEW

September 2009 Book Review 325

Series. From basic science to visual fields and refraction,

from the basic eye exam to discussions of all

ophthalmologic disorders, from contact lenses to

corneal transplantation, problems of the aging eye and

pediatric disorders – this book presents all the key

elements of ophthalmology for clinical use, rounds, and

board preparation.

� Presents figures in full color for enhanced visual

guidance

� Expedites reference and review with a question –

and – answer format, bulleted lists, mnemonics,

and tips from the authors.

� Features a two – color page layout, “Key Points”

boxes, and lists of useful web sites to enhance

your referencing power.

� Includes a chapter containing the “Top 100

Secrets” in ophthalmology, enabling you to quickly

review essential material.

� Comes in a pocket size for easy access to key

information.

No matter what questions arise, whether preparing for

examinations or in practice, Ophthalmology secrets, 3rd

Edition, has the answers you need

Dr. Hoyos’s Step by Step Lamellar

Corneal GraftEdited by Eduardo Arenas, Jairo E Hoyos

Published by Jaypee brothers New Delhi

First Edition-2008

Price Rs: 595/-

The time for lamellar keratoplasty has finally arrived;

an old surgical procedure has always been outshined

by the more glamorous technique of penetrating

keratoplasty. Lamellar keratoplasty (LK) has fallen in

and out of favor, being regarded as a tectonic procedure

or as graft for superficial corneal scars. The editors of

this book, Arenas and Hoyos, are experienced corneal

surgeons, well known writers and editors of scientific

articles. They have seen the need for this publications

and have undertaken the formidable task of putting

together actual information about a variety of

techniques and indications for partial lamellar

keratoplasty, some so revolutionary that they are still

unknown in some medical centers. To this effect, they

have obtained collaboration of a group of

internationally known corneal surgeons to write

specialized chapters.

The numerous papers included in this book illustrate

the multiple techniques and indications for this type of

surgery at the present time. Some procedures were not

even dreamed of a few years back, expect in the minds

of a few that were ahead of their time.

The table of contents shows what pathologists call “sequence

of events”; in this case, how a procedure has been

gradually changed and perfected through the years with

the help of new ideas and technical innovation.

This review of the most recent lamellar keratoplasty

techniques will be informative for the anterior segment

surgeon.


Manual Small Incision Cataract Surgery

(MSICS)Edited by Ashok Garg, Francisco J Gutierrez-Carmona, Luther L Fry, Amulya Sahu, M S Ravindra

Published by Jaypee Brothers New Delhi

First edition – 2008

Price Rs 395/-

This book is mainly dedicated to describe several

manual techniques including nuclear manipulation

or fragmentation, fragment extraction, strategies in

the use of several viscoelastic devices, the use of an

anterior chamber maintainer, etc. A whole chapter on

complications and their avoidance is also included.

In other words, the reader will find many ideas to either

learn or enrich from this manual small incision cataract

surgery mini atlas.

This Mini Atlas on MSICS shall be invaluable

companion to ophthalmologists as ready reckoner

in operation theatre and clinical OPD for quick

review.

Manual Small Incision Cataract Surgery (MSICS) has

improved significantly with the passage of time. Similar

visual results can be obtained as with phaco with much

lesser costs. Being proficient in MSICS not only makes

the ophthalmologists independent of machine technology

but also it has many other advantages as it is very useful

in difficult situations like hard cataracts. Proficiency in

MSICS makes the transition to phaco emulsification much

easy. This Mini Atlas of MSICS contains 15 chapters

covering various techniques of MSICS beautifully by

International Masters of this field. All MSICS techniques

are described with more figures step by step for better

understanding. Video DVD ROM provided with this book

shows various important MSICS techniques by experts

in this field.

Basic OphthalmologyAuthor - Renu Jogi

Published by Jaypee Brothers

Fourth Edition – 2009

Price Rs: 895/-

The need for a textbook for undergraduate medical

students in ophthalmology dealing with the basic

concepts and recent advances has been felt for a long-

time. Keeping in mind the changed curriculum, this

book is intended primarily as a first step in commencing

and continuing the study for the fundamentals of

ophthalmology. In essence, Basic Ophthalmology is both

a ‘text book’ and a ‘note book’ that might as well have

been written in the student’s own hand. The idea is for

the student to relate to the material; and not merely to

memorize it mechanically for reproducing it during an

examination. The past few years have witnessed not only

an alarming multiplication of information in the field

of ophthalmology, but more significantly, a definite

paradigmatic shift in the focus and direction of ophthalmic

research and study. The student will thus find a new

section devoted to a discussion on Visual Display

Terminal Syndrome (VDTS) that is an outcome of excessive

exposure of the eyes to the computer monitor as well

as the use of contact lenses. Two additional sections deal

with the Early Treatment for Diabetic Retinopathy Study

(ETDRS) classification and Scheie’s classification for

hypertensive retinopathy that replaces the pre-existent

taxonomy prevalent for little less than seven decades.

September 2009 Book Review 327

Salient features of this book are:

� Fully revised and updated.

� Written as per syllabi of Indian Universities.

� Presents the basic aspects as well as recent

advances in ophthalmology comprehensively.

� Highlights Visual Display Terminal Syndrome and

Compiled by Dr. C.V. Andrews Kakkanatt, JMMC, Thrissur

ETDRS and Scheie’s classifications of hypertensive

retinopathy as new additions.

� Covers more than 500 MCQs with answers for easy

recall of the concepts.

� Useful for graduate and postgraduate students and

teachers as well as practicing ophthalmologists.

ERRATUM

In the June 2009 issue an error in the names of the authors for the articlein Community Ophthalmology was inadvertently published. We sincerelyapologise for this error

The corrected names of authors are

1. Dr. [Mrs.] R. Jose MD 2. Dr. Sandeep Sachdeva MD, DNB

CME Programmes

STATE CONFERENCES

DRISHTI 2009

36th Annual Conference of Kerala Society of

Ophthalmic Surgeons

27-29 th November 2009

Dinesh Auditorium, Thana, Kannur

Dr.Sreeni Edakhlon

9895618170

NATIONAL CONFERENCES

FOCUS 2009

XXIX th Annual Conference of the Maharashtra

Ophthalmological Society & XVIIth Annual Conference

of the Bombay Ophthalmologists’ Association

25-27th September 2009

ITC Grand Maratha Sheraton, Hyatt Regency and Le

Royal Meridien, Sahar, Mumbai

Dr.Ragini Parekh: 9867872333

Kalpavriksha 2009

National PG CME Programme

October 1-4, 2009

Organizer: Dr.Agarwal’s Eye Hospital, Chennai

VISTA 2009

XIX Annual Conference of the

Glaucoma Society of India

November 6 – 8, 2009

Nimhans Convention Centre

Bangalore

Dr.Gowri J Murthy: 080-26722215

KSOC 2009

28th Karnataka State Ophthalmic Conference

November 27-29, 2009

J.J.M Medical College, Davangere

Dr.Rajesh.P: 9845568791

AIX 2010

68th Annual conference of

All India Ophthalmological Society &

15th Afro Asian Congress of Ophthamology

21-24th January 2010

Science city Kolkata

Dr. Ashish K. Bhattacharya

www.aioc2010.com

INTERNATIONAL CONFERENCES

XXVII Congress of the Europian Society of Cataract and

Refractive Surgeons

12-16th September 2009

Barcelona, Spain

www.escrs.org

AAO-PAAO 2009

24-27th October, 2009

Sanfrancisco

www.aao.org/2009

ASCRS.ASOA

Boston 2010

9- 14th April 2010

www.ascrs.org / www.asoa.org

UPCOMING

CME

Glaucoma Drugs and Dry - Eyes

Complications

Potential ocular and/or systemic adverse effects:

• Prostaglandin Analogues: stinging, blurred vision, eye redness,itching, burning, possible changes in eye color and eyelid skin,.

• Beta Blockers: foreign body sensation, photophobia, itching,ocular irritation, low blood pressure, reduced pulse rate, fatigue,shortness of breath; rarely: reduced libido, depression,

• Alpha Agonists: burning or stinging, fatigue, headache,drowsiness, dry mouth and nose, relatively higher likelihood ofallergic reaction.

• Carbonic Anhydrase Inhibitors: in eye drop form: stinging,burning, eye discomfort; in pill form: tingling hands and feet,stomach upset, memory problems, depression, frequenturination.

Prevalence of Dry Eye in Glaucoma Patients

• Patients with open-angle glaucoma also have symptoms ofconcurrent ocular surface disease.

• Dr Leung studied 101 patients with either open-angle glaucomaor ocular hypertension.

• 60 patients (59 %) reported dry eye symptoms in at least oneeye, and 27 patients (27 %) reported severe dry eye symptoms.

• Schirmer testing - 62 patients (61 %) experienced reduced tearproduction in at least one eye; 35 patients (35 %) had severetear deficiency.

• Twenty-two patients (22 %) showed positive corneal andconjunctival lissamine green staining results

• Break-up time testing - 79 patients (78 %) showed abnormaltear quality, and 66 patients (65 %) had a severe decrease intear quality in at least one eye.

Glaucoma Drugs and dry eye condition

• Dry-eye condition also could be caused by Glaucomamedication.

• Side effects increase with the frequency of instillations.

• Risk of failure of filtration surgery.

• Subtle signs of ocular toxicity (break up time, superficialpunctuate keratitis) have long term consequences.

• Long term use - conjunctival scarring known as drug inducedpemphigoid.

Dry eye symptoms with Preservatives

• Decrease the stability of the precorneal tear film through a

detergent effect

• Decrease the density of goblet cells in the conjunctival epithelium.

• BAK causes toxic or immuno-inflammatory effect on the ocular

surface.

• Topical preservatives cause inflammation, squamous metaplasia,

and subconjunctival fibrosis in the conjunctiva and Tenon’s capsule.

• These changes could probably also concern the trabeculum

structures.

• Except for beta-blockers, all commercially currently available

antiglaucoma eyedrops contain BAK.

• Preservatives decrease the stability of the precorneal tear film.

• They have a detergent effect on the lipid layer, resulting in

increased evaporation.

• Preservatives also destabilise the tear film

• Worsens pre-existing dry eye.

• Surgical treatment failure in patients treated over the long term

with glaucoma eye drops.

• A prospective epidemiological survey was carried out in 1999.

All symptoms were more prevalent with P (Preservative) than

with PF (Preservative Free) eye drops :

– discomfort upon instillation (43 % versus 17 %)

– symptoms between instillations such as

burning-stinging (40 % versus 22 %)

– foreign body sensation (31 % versus 14 %)

– dry eye sensation (23 % versus 14 %)

– tearing (21 % versus 14 %)

– eyelid itching (18 % versus 10 %)

– An increased incidence (>2 times) of

ocular signs was seen with P eye drops.

PG

TEAR SHEET


Dry eye symptoms with beta blockers

• The most common ocular complaints - transient stinging andburning.

• Other commonly reported symptoms

– Transient blurred vision

– Reversible myopia

– Foreign body sensation

– Photophobia, itching

– Ocular irritation

– Cystoid macular edema

• Objective ocular signs:

– superficial punctate keratatis

– keratitis sicca

– corneal hypoesthesia

– lid ptosis and

– allergic blepharoconjunctivitis

Dry eye symptoms with beta blockers

• Timolol, timolol maleate, and benzalkonium chloride (BAK -0 01 %) are used worldwide for lowering intraocular pressure.

• The mean tear turnover using timolol + BAK was significantlylower (32 %) than the value of healthy controls in the study byKuppens et al.

• 50 % of Patients complained of burning or dry eye sensationwhen using Timolol + BAK.Basal tear turnover, intraocular pressure, and tearfilm breakup time

Tear IOP Mean Number of subjectsturnover (SD) with tearfilm

Mean (SD) (mmHg) break up time(%/min)

< 10 > 10seconds seconds

Patients* when 10-7 17-7 4 16using timolol + (3-0) (2-0)BAK 13-2 18-1 5 15

Patients* when using (5-1) (3 0)timolol-BAK Healthy 15-7 14-7 0 2controls (5 3) (2 9)

Ocular complications with prostaglandin analogs

• Hypotensive lipids, named as eicosanoids, include latanoprost,travoprost and bimatoprost.

• Ocular side effects:– hyperemia– foreign body sensation– hypertrichosis– increased lower eyelid pigmentation with darkening of the

periocular skin and “cernes”– and superficial punctate keratopathy

• Allergic reactions occur in 1% of adult patients.

• It can also cause increased eyelash thickness, length and number.

• Can also cause permanent hyperchromia of the iris.

Dry eye symptoms with Prostaglandin analogues

• Prostaglandin Analogues may affect corneal sensitivity.

• Kozobolis VP et al examined that central corneal mechanicalsensitivity (CCMS) significantly reduced at the 5 minute intervalfor all analogs.

• The overall reduction in CCMS score at the 5-minute intervalsignificantly correlated with Schirmer and BUT tests scores.

• Latanoprost caused highest reduction in CCMS, followed byTravoprost

• Bimatoprost caused least reduction in CCMS

• Administration of ar tificial tears in combination withprostaglandin analogs may therefore be considered

Dry eye symptoms with alpha adrenergic agonists

• Apraclonidine and Brimonidine.

• Allergy has been reported in 4 to 26 % of patients.

• Eyedrop allergy and reduction of the tear film production is morecommon with brimonidine.

• Ocular Side effects:

– Rebound hyperemia

– Lid elevation

– Pupil dilatation (for apraclonidine)

– Allergy (up to 26 % for brimonidine, up to 36 % for apraclonidine)

– Uveitis ± allergic conjunctivitis ± IOP increase (brimonidine)

– Conjunctive hyperemia (for apraclonidine, 12.6 %)

– Itching and foreign body sensation (apraclonidine, 6.8 %)

– Tearing (apraclonidine, 4.5 %)

Dry eye symptoms with Carbonic anhydrase inhibitors

• Dorzolamide and brinzolamide.

• Dorzolamide is known to induce stinging and burning uponinstillation in more than one-third of patients.

• For both drugs, allergic reactions may be seen.

• Corneal decompensation may occur in patients with alreadycompromised endothelium and pre-existing corneal edema.

Compiled by

Dr. Sonia Rani John

Other signs of ocular surface damage reported more frequently

in patients treated with Containing Preservaties eye drops:

Presence of conjunctival signs 49% 26 %*Conjunctival redness 41% 20 %*Conjunctival follicles 22% 11 %*Fluorescein staining in the nasal bulbar conjunctiva 13% 5 %*Presence of an SPK 19% 9 %*Superficial punctate keratitisMild 17% 8.9 %*Severe 2% 0.6 %*Presence of at least one palpebral sign 22% 9 %*Anterior blepharitis 16% 7 %*Posterior blepharitis (meibomiitis) 7% 3 %*Eczema 6% 1 %*


GENERAL INSTRUCTIONS TO AUTHORS

The Kerala Journal of Ophthalmology (KJO) is a quarterly; peer reviewed one, devoted to dissemination

of the latest in ophthalmology to the general ophthalmologists as well as to specialists in the various

subspecialties of this discipline. It invites submission of original work dealing with clinical and laboratory

materials.

Authors submitting materials to this journal are requested to adhere STRICTLY to the norms laid down

below. The matter must be typed on one side of the paper. A margin of I” must be left all around and the

material must be double-spaced. A page should contain not more than 25 lines. Two copies of the text in

paper and one copy in a CD must be submitted to the Editor and the corresponding author is advised to

keep another copy with him. The corresponding author must give it in writing in his covering letter that

the same matter will not be submitted elsewhere if accepted. He must also enclose the copyright transfer

of his work to this journal. The papers sent will be subjected to peer review. The accepted manuscripts

become the permanent property of this Journal. The author is informed that, if his work is returned to him

for correction / clarification after peer review, he should effect the same and send the manuscript back to

the Editor within one month. Each manuscript component mentioned here under must begin with a new

page and the pages are to be numbered at the right tip corner starting from the Title page.

1. TITLE: The title of the work must be brief and precise. It should not exceed two lines and 40 characters

(including comma, period) Author (s) full name (s) must be given along with his (their) degree and

the affiliations. Corresponding author’s name, correct address (including e-mail and Fax, if available)

and phone number must be mentioned at the bottom left hand corner of the first page.

2. ABSTRACT: The abstract is to be given in the beginning itself. It should not exceed 200 words. It must

contain the aim, methodology, results and conclusion. For case report, summary / conclusion alone is

to be given.

KEY WORDS (maximum five) in capitals are to be included at the end of Abstract.

3. INTRODUCTION: Describe the aim of the study, along with the hypotheses that were tested. Only

necessary references are to be given

4. METHOD: Give in detail the materials used and the methods employed. Describe the type of study.

Pharmacological names only must be mentioned for the drugs used and, if proprietary name is used,

then the manufacturers name must be given in parentheses. Except for standard, well-accepted

abbreviations (Including SI Units), all others must be introduced in parentheses when the full term is

used for the first time in the article.

5. RESULTS: Give only the results obtained by the study under discussion. State the statistics in the

correct scientific form (P value, mean etc). Results based on assumptions must not be given. Indicate

in the text the place where the tables have to be inserted

6. DISCUSSION: The discussion should be to the point and relevant to the subject under discussion.

This section can be combined with the previous one if the author desires. Avoid speculations. Use

only standard abbreviations or the abbreviations already introduced.

7. ACKNOWLEDGEMENT: This is to be made only to those who were directly and scientifically involved

with the preparation of the paper. Permitting authorities, technicians, photographers who assisted in

the work need not be mentioned.


8. REFERENCES: The references should be given in numerical order in which they first appear in text

and not in alphabetical order (Citation Order System). It should be numbered consecutively in the

text. The references will not be checked by the Editor or by the Peer reviewer and hence the author is

solely responsible for its completeness and the accuracy. Period should not be employed anywhere in

the references. Personal communication, unpublished data and poster references, if mentioned, should

be in the text itself and the source mentioned in parentheses. References should be in the following

form:-

Journal reference: Author(s) full title, Journal name (as abbreviated in Index Medicus), volume number,

pages and year. If there are more than three authors, then mention the first three authors and then ‘et

al’.

Book reference: Authors(s) (& Editor, if any), title of book (and chapter), publisher, place of publication,

page number (s) of the cited portion and year.

9. THE LEGEND: The legend for the illustrations (and tables, if necessary) must be given in a separate

sheet of paper and should be typed double-spaced.

Illustrations: The photos and figures should be prepared in glossy prints with good contrast and of the

size 6” x 4”. Only salient details should be included. On the back of the illustration, the figure number

in text, title of the paper, the first author’s name and the top side (marked with an arrow) must be

specified. Except for arrows, no text is to be on the photos. It is the duty of the author(s) to get the

patient’s written permission when the subject is identifiable in the photo. Submit two sets of illustrations.

Illustrations from other Journals and books are usually not accepted. If used, it rests with the author(s)

to get the copy right permission from the original author / publisher and this permission letter must

be sent to the Editor at the time of submitting the manuscript. For Histological figures the stain and

magnification used should be noted e.g.: - H & E Stain x 70.

10. TABLE: It should be in double space. Each table must have an Arabic numeral (except for single

table) and a title both in a single line. Each column in the table must have a short heading. If a table

is large, then it must be continued in a second page, which also must have the table number and the

title. Avoid vertical lines in the tables. Two sets must be submitted.

The manuscripts are to be sent to The Editor by Courier Mail or by Registered post. The corresponding

author will receive communication from the Editor within two weeks of receiving the manuscript.

11. All manuscripts are subjected to editorial board review.

12. Other Categories of Manuscript

a) Original Articles should generally not exceed 3,000 words or 12 double – spaced pages.

b) Review Articles: can be on topics of relevance to clinical practice, research methodology, community

ophthalmology or investigative work, of relevance to visual science. These articles should include

up to date review of existing literature, and summarize the current status / preferred practice for

that particular topic.

Brief reports are short communication of new instruments, new laboratory techniques or surgical

techniques as well as interesting case reports with unique findings. These should not exceed 1000

words with a maximum of 2 illustrations. They should follow the format - introduction, case, and

discussion. No more than 8 references should be cited. Each brief report must begin with a 75-100

word summary that highlights the significance of the articles.

KERALA JOURNAL OF OPHTHALMOLOGY...President Dr. R.R. Varma Ambikalayam, Warriam Road Kochi - 682 016...

Documents

Transcript of KERALA JOURNAL OF OPHTHALMOLOGY...President Dr. R.R. Varma Ambikalayam, Warriam Road Kochi - 682 016...