Comprehensive Ophthalmology Free Papers - AIOS · PDF fileCOMPREHENSIVE OPHTHALMOLOGY ......

Comprehensive OphthalmologyFree Papers

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Contents

COMPREHENSIVE OPHTHALMOLOGYComparing The fellow Eyes in Patients with Unilateral Pseudo Exfoliation Syndrome -----------------------------------------------------------------------------------------210Dr. Kumar Sambhav

Kayer-Fleischer Ring, A Definitive Diagnosis for Wilson Disease-Case Report ----------------------------------------------------------------------------------------------212Dr. Rajesh Konda, Dr. Chaithra Dembala Aroor

Medical Management of Familial Exudative Vitreoretinopathy ---------------216Dr. Archis Shedbale, Dr. Suhas Haldipurkar, Dr. Haresh Asnani, Dr. Sachin Fegde

Conquered Quest of Lost Muscle: Case Report ------------------------------------218Dr. Trapti Sharma, Dr. Pradhnya Wasule, Dr. Bhudhendra Kumar Jain, Dr. Avinash Bagzai

Pain and Comfort with Single Drop Topical Anaesthesia for Lasik ---------221Dr. Swapna Nair, Dr. Nair Ramachandran K.G.

Oral Omega 3 Fatty Acids(Ω-3 FA) in Blepharitis, Meibomian Gland Dysfunction and Associated Dry Eye --------------------------------------------------223Dr. Rahul Pandey, Dr. Rathore M.K., Dr. Eva Tirkey, Dr. Dwivedi P.C, Dr. Shivcharan Lal Chandravanshi

Results of Screening of APML Patients and Correlation of Ocular and Hematological Findings ---------------------------------------------------------------------226Dr. Aparna Dwibedy, Dr. Haemoglobin, Dr. Sumita Mohapatra, Dr. Nanda Prasanta Kumar

Microbial Contamination of Surface and Needles in Patients Undergoing Intravitreal Injection --------------------------------------------------------------------------229Dr. Bhushan Ghodke, Dr. Pooja Gupta, Dr. Snehal Bonde Chaurasia, Dr. Preeti Kankrej

Scleral Contact Lenses in the Management of Pellucid Marginal Degeneration ------------------------------------------------------------------------------------232Dr. Rathi Varsha Madanlal

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COMPREhENSIVE OPhthAlMOlOGyChairman: Dr. Arun Sethi. l Co-Chairman: Dr. Yogesh Shukla

Convenor: Dr. Sukul R.R. l Moderator: Dr. Dhami G.S.

Comparing The fellow Eyes in Patients with Unilateral Pseudo Exfoliation SyndromeDr. Kumar Sambhav

Pseudoexfoliation is a disorder which is characterized by the appearance of a fibrillary whitish material on the lens surface, the lens zonules, ciliary

body and other parts of the anterior chamber.1,2

It is a clinically important disorder in terms of its association with weakness of the lens zonules leading to zonular dialysis during cataract surgery and late postoperative dislocation of the intraocular lens.3 The reported prevalence of Pseudoexfoliation varies from 0.2% to 30% in different studies.4

There is no established sex predilection for Pseudoexfoliation but a female preponderance has been noted.4,5,6 Unilateral Pseudoexfoliation occurs in 48-76% of patients which becomes bilateral in up to 50% of patients within 5 to 10 years.7,8

Pseudoexfoliation is also associated with poor pupillary dilatation and is a risk factor for zonular dialysis and vitreous loss during cataract surgery. Central corneal thickness (CCT) is known to have an impact on IOP, but there is no consensus on the central corneal thickness in Pseudoexfoliation eyes.

This study was done to compare the corneal thickness and intraocular pressure between the fellow eyes in patients with unilateral pseudo exfoliation syndrome without glaucoma.

MATERIALS AND METHODSThis was a case series of patients with Pseudoexfoliation syndrome who presented at a tertiary eye care. The Institutional ethical committee approval was obtained. Informed consent was taken from all patients.

Exclusion criteria were presence of glaucoma, previous intraocular surgery in the eyes, use of topical/systemic steroids within the last six months, history of ocular trauma, uveitis, corneal scars, and any other ocular pathology. Eyes with hazy media due to cataract, which precluded optic disc assessment, were also excluded from the analysis.

Ocular examination in all patients was performed by a single Ophthalmologist. Slit-lamp examination, Goldmann applanation tonometry, gonioscopy and

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dilated fundus examination using +90 D lens was done in all cases. Visual field assessment was performed using Humphrey’s Field Analyzer. Central corneal thickness was measured by ultrasound pachymetry.

RESULTSForty patients with unilateral pseudo exfoliation syndrome were selected after satisfying the inclusion and exclusion criterion.

There were 15 males and 25 females. The age range was 39 to 74 yrs with a mean age of 51.6 ± 11.5 yrs.

The mean corneal thickness in eyes with pseudo exfoliation was 509.78 ± 41.30 microns while in the other eye was 507.82 ± 32.41 microns which was significant (p value 0.01).

The mean intraocular pressure in the eye was 14.2 ± 2.3 mm Hg in eyes with pseudo exfoliation while it was 14.1 ± 3.2 mm Hg in the other eye. The difference was insignificant with a p value 0.31.

DISCUSSIONThere is an established fact that central corneal thickness affects IOP measurements and according to ocular hypertension treatment study, central corneal thickness is an important and independent risk factor for progression of glaucomatous damage in persons with ocular hypertension.9

In our study, mean corneal thickness in eyes with pseudo exfoliation was 509.78 ± 41.30 microns while in the other eye was 507.82 ± 32.41 microns which was significant (p value 0.01). In another study by Ventura AC et. al., the central corneal thickness of patients with ocular hypertension was significantly higher than in normal (control) individuals or in subjects with normal tension glaucoma, open angle glaucoma or pseudoexfoliation glaucoma with no significant differences between the latter four groups.10 Contrary to our study, many studies have shown that central corneal thickness is less in cases of pseudo exfoliation syndrome compared to normal.

In our study, the mean intraocular pressure in the eyes with pseudo exfoliation was 14.2 ± 2.3 mm Hg while it was 14.1 ± 3.2 mm Hg in the other eye. The difference in intraocular pressure between fellow eyes was insignificant.

This study is first of its kind to compare the ocular parameters in fellow eye in cases of pseudoexfoliation syndrome.

REfERENCES1. Naumann GO, Schlötzer-Schrehardt U, Küchle M. Pseudoexfoliation syndrome

for the comprehensive ophthalmologist. Intraocular and systemic manifestations. Ophthalmology 1998;105:951–68.

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2. Ritch R, Schlötzer-Schrehardt U: Exfoliation syndrome. Surv Ophthalmol 2001;45: 265–315.

3. Belovay GW, Varma DK, Ahmed II. Cataract surgery in pseudoexfoliation syndrome. Curr Opin Ophthalmol 2010;21:25–34.

4. Krishnadas R, Nirmalan PK, Ramakrishnan R, Thulasiraj RD, Katz J, et. al. Pseudoexfoliation in a rural population of southern India: the Aravind Comprehensive Eye Survey. Am J Ophthalmol 2003;135:830–7.

5. Arvind H, Raju P, Paul PG, Baskaran M, Ramesh SV, George RJ, et. al. Pseudoexfoliation in South India. Br J Ophthalmol. 2003;87:132.

6. Karger RA, Jeng SM, Johnson DH, Hodge DO, Good MS. Estimated incidence of pseudoexfoliation syndrome and pseudoexfoliation glaucoma in Olmsted County, Minnesota. J Glaucoma. 2002;12:193–7.

7. Kozart DM, Yanoff M. Intraocular pressure status in 100 consecutive patients with exfoliation syndrome. Ophthalmology. 1982;89:214–8.

8. Henry JC, Krupin T, Schmitt M, Lauffer J, Miller E, Ewing MQ, et. al. Long-term follow-up of pseudoexfoliation and the development of elevated intraocular pressure. Ophthalmology. 1987;94:545–52.

9. Gordon MO, Beiser JA, Brandt JD, et. al. The Ocular Hypertension Treatment Study: baseline factors that predict the onset of primary open-angle glaucoma. Arch Ophthalmol 2002;120714–20.720 discussion 829–830.

10. Ventura AC, Böhnke M, Mojon DS. Central corneal thickness measurements in patients with normal tension glaucoma, primary open angle glaucoma, pseudoexfoliation glaucoma, or ocular hypertension. Br J Ophthalmol. 2001;85:792-5.

Kayer-Fleischer Ring, A Definitive Diagnosis for Wilson Disease-Case ReportDr. Rajesh Konda, Dr. Chaithra Dembala Aroor

Wilsons disease (WD) is an autosomal recessive genetic disorder in which copper accumulates in tissues like liver and brain, resulting in

neurological or psychiatric symptoms and liver disease.1 The disease presents itself as a multisystem disorder. Various medical conditions have been linked with WD like Kayser-Fleischer ring (K-F ring) around cornea which occur in 66% of diagnosed cases.1 The classical ophthalmological finding is the presence of the K-F ring, which is considered pathognomonic of WD.2 K-F ring, also referred to as Fleischer-Kayser ring or Fleischer-Strumpell ring was first described by the German ophthalmologists Bernard Kayser (1902) and Bruno Fleischer (1903) independently in a patient who was then diagnosed to have multiple sclerosis. Fleischer in 1912 recognized it as a part of WD.2 In 1970, Harry et. al., described the electron microscopic appearance of the K-F


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ring as electron-dense deposits of copper of varying sizes lying mainly in the Descemet’s membrane (DM).2 Westphal in 1883 and Gowers in 1888 first suspected the inter-relationship of copper metabolism and WD.3 Cumings (1948) first conclusively demonstrated the inter-relationship of copper metabolism and WD.4 Wilson (1912) first described the clinical findings of rigidity, tremor, drooling and impairment of liver function.5 We report a case of WD and discuss the importance of K.F ring in diagnosing this disease.

MATERIALS AND METHODSA 12-year-old male presented with inability to walk due to weakness of both upper and lower limbs for 6 months. On examination he was found to have enlarged (3 finger) firm and nontender liver, Risus Sardonicus, Dysarthria, Dystonia, Tremors, Gait f reezing. Ophthalmic examination revealed normal visual acuity and field with normal optic fundii. Slit lamp examination showed K.F. rings (3mm width golden-brown deposit at the level of the DM of cornea) on either eye close to the corneal limbus. Investigations revealed, lower Serum Cerruloplasmin (7.2mg/dl), increased 24hr Urinary Copper (135 µg/dL), serum copper level was 9.6 μmol there was no history of convulsion, jaundice, measles or recent vaccination. A diagnosis of Wilson’s disease was made. The patient was treated with d-penicillamine 20mg/kg/day in three divided doses along with pyridoxine 25mg/day and elemental zinc 75mg/day 1 hour before food for 2 months resulted in neurological and performance improvement. Corneal KF rings however remained unchanged.

DISCUSSIONWD is caused by mutation in the copper-transporting gene ATP7B which facilitates the transfer of copper into the Golgi apparatus where it combines with ceruloplasmin or other proteins like cytochrome oxidase. Failure of this process leads to instability and decreased half-life of ceruloplasmin and paradoxical ceruloplasmin deficiency. The free circulating copper (which is toxic as it inhibits enzymatic processes) accumulates in liver cytosol resulting in hepatocyte degeneration and cirrhosis. When the sites for copper binding in the liver are saturated, free copper is released into the circulation and accumulates in other tissues like the eye, brain (basal ganglia) and kidneys amongst others leading to morphological changes, functional derangements and clinical manifestations. K-F ring in the cornea, sunflower cataract in the

Fig.1: Kayser-Fleischer Ring

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lens, tremors and rigidity due to accumulation in the central nervous system, and renal tubular defects due to accumulation in the kidneys.6

The best documented report of deposition of copper in the cornea is that of Uzman and Jakin.7 They demonstrated that the clinically visible copper which accounts for K-F ring is probably present as a protein-copper complex copper chelata. It’s rare association are renal tubular acidosis (causing loss of calcium phosphate and amino acids in urine), nephrocalcinosis and cardiovascular involvement in form of cardiomyopathy and arrhythmias. Infertility and habitual abortion may also occur.8

KF ring is the pathognomic sign of WD. It is present in 98% of neurologically symptomatic and 40% of asymptomatic patients with WD.9 Although it is commonly described to be golden brown or greenish yellow in color, it could be ruby red, bright green or ultramarine blue in color, sometimes interspersed with yellow or smoky brown color. It is usually bilateral and appears initially superiorly at the 10-2 o’clock position, then inferiorly and later becomes circumferential.10,11 It is best detected with slit-lamp examination by an expert, often with the aid of a goniolens.11

The general pattern of the deposits suggests that the copper particles infiltrate into DM through the endothelial cells from the aqueous humour while the larger deposits with a central nidus probably result from coalescence of the smaller particles over a period of time. The question why the copper should react with some normal or abnormal constituent of DM to produce the structural pattern of the K-F ring remains unanswered. Nor is it clear why this ring should be deposited at the periphery. It seems, however, likely that this may be related to the direction of aqueous flow and/or to some functional peculiarity of the peripheral corneal endothelium. Moreover, it may not be just due to passive diffusion but may be attributed to cellular activity, the copper granule production being related to formation of the basement membrane by endothelial cells.[12] An alternative hypothesis that the copper deposits originate from the limbal circulation seems to be less likely.2 Apart from the K-F ring in WD, the cornea is also permeated by ionic copper as demonstrated by spectroanalytic study and X-ray excitation spectrometry, which is independent of the appearance of the K-F ring and may aid in the diagnosis of WD.13

WD is treated with agents that chelate copper and hence the K-F ring could fade or disappear (80-90% cases)14,15 following successful treatment. When using trientine or pencillamine, it is necessary to monitor for drug toxicity, particularly bone marrow suppression and proteinuria. Zinc treatment does not require blood or urine monitoring for toxicity.16 The ring tends to disappear in the reverse order of its formation.2 Others ocular features include sunflower cataract, infrequent blinking, jerky oscillatory movements, involuntary upward gaze, night blindness and pallor of discs and xerophthalmia.17


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K-F-like ring has been reported in many other conditions like cryptogenic cirrhosis, chronic active hepatitis, neonatal hepatitis, primary biliary cirrhosis, cholestatic cirrhosis, hepatocellular disorders (when bilirubin rises acutely above 20mg/dl), alcoholic liver disease, galactosialidosis, multiple myeloma and intraocular foreign body containing copper.18

If there are neurological symptoms, magnetic resonance imaging (MRI) of the brain is usually performed; this shows hyper intensities in the part of the brain called the basal ganglia in the T2 setting.19 MRI may also demonstrate the characteristic “face of the giant panda” pattern.20 Seizures have been reported to occur in 6.5% patients with WD[21] and the reported frequency of seizures in Indian patients with WD varied between 4.9% and 8.3%.22,23

In conclusion, WD in this patient was suspected by the presence of K-F ring and confirmed with investigations. The significance of K-F ring is stressed in this case report in the diagnosis of WD.

REfERENCES1. Ala A, Walker AP, Ashkan K, Dooley JS, Schilsky ML. “Wilson’s disease”. Lancet

2007;369:397-408.

2. Harry J, Tripathi R. Kayser-Fleischer ring: A pathological study. Br J Ophthalmol 1970;54:794-800.

3. Gowers WR-A manual of disease of the nervous system. Vol. 2 T and A Churchill. London. 1888. P 656.

4. Wilson SAK - Progressive lenticular degeneration, a familial nervous system disease associated with Cirrhosis of the liver. Brain 1912;34:295.

5. Cumings JN- The copper and iron content of the brain and liver in normal and in hepato lenticular degeneration. Brain. 1948.;71.:410.

6. Gotto J, Williams R. Wilson’s disease: Diagnosis and current treatment options. Prescriber 2005;16:25-30.

7. Uzman, L. and Jakins, 1957, K. F. Ring A histo¬chemical and electron microscopic study neurology (Minneap), 7, 341.

8. Fatima J, Karoli R, Jain V. Hypoparathyroidism in a case of Wilson’s disease: Rare association of a rare disorder. Indian J Endocr Metab. 2013;17:361-2.

9. Datta S, Datta H. Kayser Fleischer ring. Indian Pediatr 2004;41:744.

10. Kim HB, Kim JC, Byan YJ. Kayser Fleischer ring in Wilson’s disease. J Korean Ophthal Soc 1979;20:129-31.

11. Innes JR, Strachan IM, Triger DR. Unilateral Kayser-Fleischer ring. Br J Ophthalmol 1986;70:469-70.

12. Belkin M, Zeimer R, Chajek T, Friedman G, Melamed E. Non-invasive quantitation of corneal copper in hepatolenticular degeneration (Wilson’s disease). Lancet 1976;1:391-4.

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13. Wiebers DO, Hollenhorst RW, Goldstein NP. The ophthalmologic manifestations of Wilson’s disease. Mayo Clin Proc 1977;52:409-16.

14. Lossner A, Lossner J, Bachmann H, Zotter J. The Kayser Fleischer ring during long-term treatment in Wilson’s disease (hepatolenticular degeneration): A follow-up study. Graefes Arch Clin Exp Ophthalmol 1986;224:152-5.

15. George JB – Wilson disease.Harrison’s Principles of Internal Medicine 17th edition, Mc Graw Hill, 2008.

16. Saiduzzafar H, Ansari Z, Kumar M. Wilson’s disease with special reference to ocular manifestations (A case report). Indian J Ophthalmol 1978;26:37-9.

17. Suvarna J C. Kayser-Fleischer ring. J Postgrad Med. 2008;54:238-40. 18. Roberts EA, Schilsky ML. “A practice guideline on Wilson disease” (PDF).

Hepatology. 2003;37(6):1475–92. doi:10.1053/jhep.2003.5025219. Das SK, Ray K. “Wilson’s disease: an update”. Nat Clin Pract Neurol 2006;2(9):482–93.

doi:10.1038/ncpneuro0291.20. Dening TR, Berrios GE, Walshe JM. Wilson’s disease and epilepsy. Brain

1988;111:1139-55.21. Taly AB, Prashanth LK, Sinha S. Wilsons disease: An Indian perspective. Neurol

India 2009;57:528-40.22. Prashanth LK, Sinha S, Taly AB, Mahadevan A, Vasudev MK, Shankar SK.

Spectrum of epilepsy in Wilson’s disease with electroencephalographic, MR imaging and pathological correlates. J Neurol Sci. 2010;291:44-51.

Medical Management of Familial Exudative VitreoretinopathyDr. Archis Shedbale, Dr. Suhas Haldipurkar, Dr. Haresh Asnani, Dr. Sachin Fegde

Familial exudative vitreoretinopathy (FEVR) is a rare inheritable disorder of retinal vascular development. First described by Criswick and Schepens

in 1969, FEVR is a unique disorder characterized by various combinations of macular dragging, temporal radial retinal folds, retinal neovascularization, preretinal vitreous organization, vitreous hemorrhage, tractional retinal detachment, and subretinal exudation.1 Many of these findings are similar to those observed in retinopathy of prematurity (ROP), and therefore a careful history is necessary to distinguish these two disorders.2 Unlike ROP, affected individuals with FEVR have a normal gestational period and lack a history of low birth weight and exposure to supplemental oxygen therapy. In addition, FEVR tends to be a variably progressive disorder, with detachments often not occurring until the first or second decade of life. When adulthood is reached, however, the retinal manifestations may appear to remain stable.3,4


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Case Report

A 16 year old male presented with history of diminished vision in right eye since childhood. He gave history of injury to left eye by stick about 10 years back. His best correct visual acuity (BCVA) was 6/24 in right eye and no perception of light in left eye.The intraocular pressure (IOP) was 12 mmHg. Anterior segment of right eye was within normal limits. Left eye examination showed band keratopathy and was pthisical. Detailed retinal examination by indirect ophthalmoscopy and slit lamp biomicroscopy of right eye showed peripheral retinal vascular abnormalities, exudation and epiretinal membrane with macular edema. Fundus fluorescein angiography showed temporal peripheral avascular zone, brush like anastomosis and shunts at the border of avascular zone and leaking NVEs. A diagnosis of familial exudative vitreo-retinopathy (FEVR) was made considering the characteristic clinical and FFA features. Prophylactic scatter laser photocoagulation was done for temporal retinal avascular zone in two sittings. At 2nd month and 6th month follow-up, visual acuity was maintained at 6/24 and fundus showed attached retina with regressing NVEs.

DISCUSSIONFamilial exudative vitreoretinopathy is a relatively uncommon disease and its protean manifestations are easily mistaken for other ocular disorders. The inheritance, penetrance, and expressivity of FEVR are highly variable5, Fluorescein angiography is an important tool in confirming the existence of FEVR.6,7 Retinal avascularity per se often requires no treatment; however, it can induce ischemia, leading to neovascularization of the retinal periphery, which can be treated with prophylactic cryotherapy or argon laser photocoagulation to attempt to induce regression of the new vessels.8 In FEVR, the incidence of retinal detachment is quite high, and it tends to be of the rhegmatogenous or tractional type. Vitrectomy is a reasonable and effective method for the treatment of complicated retinal detachment. However, if there is no associated retinal detachment and no vitreo-retinal traction, prophylactic laser photocoagulation leads to considerable stabilization of the disease. In our patient, there was no vitreoretinal traction, hence the case was managed medically (prophylactic laser photocoagulation). Follow-up over a period of 6 months showed stable visual acuity and regression of NVEs.

One of the largest surgical series on FEVR was published by van Nouhuys4 in 1991. The results were somewhat discouraging, with reattachment of the retina occurring only in 50% of the cases after one or more surgeries.

In conclusion, considering the life-long progression and poor outcomes after surgery, early diagnosis, prompt treatment and periodic follow-up are crucial in the management of FEVR.

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REfERENCES1. Criswick VG, Schepens CL. Familial exudative vitreoretinopathy. Am J Ophthalmol

1969;68:578-94.2. Campo RV. Similarity of familial exudative vitreoretinopathy and retinopathy of

prematurity. Arch Ophthalmol. 1983;101:821.3. Ober RR, Bird AC, Hamilton AM, Sehmi K. Autosomal dominant exudative

vitreoretinopathy. Br J Ophthalmol. 1980;64:112-20.4. van Nouhuys CE. Signs, complications, and platelet aggregation in familial

exudative vitreoretinopathy. Am J Ophthalmol. 1991;111:34-41.5. Shastry BS, Trese MT. Familial exudative vitreoretinopathy: further evidence for

genetic heterogeneity. Am J Med Genet. 1997;69:217-8.6. Swanson D, Rush P, Bird AC. Visual loss from retinal oedema in autosomal

dominant exudative vitreoretinopathy. Br J Ophthalmol. 1982;66:627–9.7. Canny CLB, Oliver GL. Fluorescein angiographic findings in familial exudative

vitreoretinopathy. Arch Ophthalmol. 1976;94:1114–20.8. Toomes C, Downey L.Familial Exudative Vitreoretinopathy, Autosomal Dominant.

In: Pagon RA, Adam MP, Bird TD, Dolan CR, Fong CT, Stephens K, editors. GeneReviews™ [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2013. 2005 Mar 21 [updated 2011 Sep 22].

Conquered Quest of Lost Muscle: Case ReportDr. Trapti Sharma, Dr. Pradhnya Wasule, Dr. Bhudhendra Kumar Jain, Dr. Avinash Bagzai

To report a case of iatrogenic lateral rectus(LR) palsy during mass excision and its management.

Case Report

35 yr female came with chief complaint of sudden, non progressive double vision with deviation of LE since 2 months.

Gross examination(LE)

Ptosis with MRD1 –3 mm and Esotropia 15 PD (20 deviation >10) with total abduction limitation( - 4) (Fig. 1-3)

Slit-lamp examination

Revealed symblepheron with conjunctival scar in upper fornix leading to mechanical ptosis.


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Fig. 1 Fig. 2 Fig. 3



Fig. 10 Fig. 11 Fig. 12

Fig. 13 Fig. 14 Fig. 15

Fig. 16 Fig. 17 Fig. 18

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On further history taking, patient elucidated history of LE surgery 2 months back. Documents revealed surgery for mass excision. Histopathology indicated an inflammatory mass.

Diagnosis: Iatrogenic LR disinsertion

Treatment Plan

Surgical exploration with reattachment of LR muscle and symblepheron release with amniotic membrane graft (AMG).

Surgery

On FDT, tight MR was unable to cross midline. (Fig. 4, 5). 3 mm MR recession done. (Fig. 6) LR hooked at 14mm from limbus (attached to sclera and IO). (Fig. 7,8) Dissection with LR advancement done at 7 mm from limbus. (Fig. 9,10) Subconjunctival triamcinolone at LR (prevent further fibrosis) (Fig. 11) Symblepheron release with AMG. (Fig. 12,13)

RESULTS1st post operative day: Diplopia resolved with 70 LE exotropia and abduction improved from -4 to -2 (Fig. 14-16)

1st month follow up: Patient was orthophoric with improved ptosis from MRD1 of -3 to +3 mm (Fig. 17,18)

DISCUSSIONDetached EOM can be iatrogenic or traumatic. During Surgery it may “Slip”- slipped inside muscle capsule, “Snip”- Lost after detachment at insertion or “Snap”- tear away from insertion. While in trauma it is torn either at or away from insertion.

Lost EOM can be located pre-operatively by CT, Cine-MRI while intra-operatively by oculo-cardiac reflex or electromyography and finally surgical exploration along orbital wall.

Iatrogenic torn EOM is reported during strabismus, orbital and vitreo-retinal surgeries, but not reported during other anterior segment surgery as in our case.

It is also common when associated with underlying muscle pathology, prior muscle surgery or botox injection, which was not there in our case.

ConclusionIn spite of having common knowledge about muscle insertions, grave complications like muscle disinsertion can happen during anterior segment surgery due to negligence. General Ophthalmologist should keep it in mind and should identify if muscles involved or if operating in proximity.


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Pain and Comfort with Single Drop Topical Anaesthesia for LasikDr. Swapna Nair, Dr. Nair Ramachandran K.G.

Laser refractive corneal ablation is a commonly performed premium procedure in our country. Under topical anesthesia, this is an extremely

comfortable procedure, even for an excessively apprehensive patient. At the same time, topical anesthesia is known to alter the cellular characteristics of corneal tissue leading to the incidence of epithelial defects that are unwelcome. Our paper looks at the balance that can be struck between these two opposite effects of topical anesthesia.

Aim of the study is to undertook the effects of a drop of topical anesthetic versus multiple drops in patients undergoing lasik by assessing the pain experienced and comfort levels during the procedure, and the occurrence of intraoperative epithelial defects.

MATERIALS AND METHODS60 patients posted for lasik were randomised into two equal groups. The protocol for study was approved by the institutional review board of the hospital and informed consent for the study protocol was obtained from the patients. Prior to the procedure, the patients were briefly explained the steps of the procedure and what to expect. In Group A, a single drop of proparacain topical anesthesia was instilled after getting the patient inside the operating room and immediately prior to draping. In Group B, anesthetic drops were instilled at multiple times, first in the waiting room, then prior to draping and once more prior to the microkeratome run. The Moria microkeratome was used to lift the flap and the Alcon Wavelight Eye Q 400 Hz was used to perform the ablation. Intraoperative epithelial defects were noted.

Following the procedure, the patients were given two forms: the pain assessment visual analogue scale and comfort level scoring questionnaire (Fig. 1 and 2).

------------------------------------------Fold Over Here--------------------------------------Fig. 1: Visual Analogue Scale (VAS) for pain assessment

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-------------------------------------------------------------------------------

0 1 2 3 4 5 6 7 9 10Fig. 2: Comfort Level Scoring chart

On a scale of 1 - 10, please rate your comfort level during the procedure. Uncomfortable Very comfortableDraping 1 2 3 4 5 6 7 8 9 10Flap making 1 2 3 4 5 6 7 8 9 10Laser 1 2 3 4 5 6 7 8 9 10Overall 1 2 3 4 5 6 7 8 9 10

RESULTSOn a pain scale of 0 to 10, patients in Group A reported a pain of 1.5 and those in Group B 0.8. The difference between the groups was not statistically significant ( P=0.87). On responding to the comfort levels during the procedure, patients in Group A experienced a mean comfort of 7.4 and those in Group B 7.8, the difference was not statistically significant (P=0.72). 9 patients (30%) in Group A had epithelial defects on the table of which 2 patients had in both eyes, while in group B only 3 patients (10%) had it and all were unilateral.

DISCUSSIONThe cellular effects of proparacain on the corneal epithelium include decreased permeability of sodium ions blocking nerve conduction, epithelial swelling (ref 1) and disruption of actin rich stress fibres (ref 2) aiding epithelial adhesion. So besides the positive effect of masking pain, the drug inadvertently loosens epithelial integrity so much that a larger number of drops can also be used to peel off the epithelium for procedures like LASEK and collagen cross linking. We found that preoperative counselling and proper explanation of the procedure with clearing of doubts not only reduces the anxiety for the unknown in the patient but also helps the patient cooperate with the surgeon’s instructions. In such a situation the instillation of a single drop of topical anesthetic alleviates sensation during contact and is adequate considering the short duration of the procedure. Though the difference wasn’t clinically significant, in our study, it were such patients that had less pain than those that had multiple drops.

The comfort levels of the patients were very comparable in both groups indicating that it was independant of the dosage of the anesthetic.

The frequency of epithelial defects were higher in those who were dosed multiple times as this would have produced a cumulative effect of disrupting epithelium, especially during the run of the microkeratome and consequent


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shearing, subject to the presence of a relatively less moist cornea. Another factor that could have compounded the effect could have been the presence of inherent poor basement membrane – epithelial adhesion in some of the individuals.

Pain is a subjective factor, the awareness of which and the tolerance to which is highly variable among individuals. Also the effect of pain may be compounded by anatomical factors like the presence of a small palpebral fissure. Such are the issues that confound the outcome of the study.

ConclusionsInstillation of a single drop of topical anesthetic produces adequate anesthesia and reduces the incidence of epithelial defects.

REfERENCES1. Herse P, Siu A. Short term effects of proparacain on human corneal thickness. Acta

Ophthalmol (Copenh). 1992;70:740-4.2. Dass BA, Soong HK, Lee B. Effects of proparacaine on actin cytoskeleton of corneal

epithelium. J Ocul Pharmac. 1988:4:187-94.

Oral Omega 3 Fatty Acids(Ω-3 FA) in Blepharitis, Meibomian Gland Dysfunction and Associated Dry EyeDr. Rahul Pandey, Dr. Rathore M.K., Dr. Eva Tirkey, Dr. Dwivedi P.C, Dr. Shivcharan Lal Chandravanshi

The reported prevalence of blepharitis and MGD varies widely. A striking observation is that the prevalence of MGD appears to be much higher

in Asian populations, often reported as greater than 60% in different Asian population-based studies.1 Echoing it, these conditions have become one of the most common complaints presented by the patients to ophthalmologists in current practice. When the severity of MGD is of a sufficient degree, it may give rise to the second major subtype of dry eye disease, evaporative dry eye.

Inflammation is an integral component of blepharitis, MGD, and the aqueous-deficient dry eye.2 Anti-inflammatory therapies such as topical cyclosporin A and corticosteroids have been successful in the short-term management of MGD.3 Alternative treatments, including dietary supplements, have become an explosive area of investigation. Dietary supplementation with fatty acids (FAs) has been recommended for MGD patients,4 but there is a lack of objective

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clinical studies published in the literature to demonstrate effectiveness. Ratio of omega-6 to omega-3 FA is important in influencing the overall inflammatory state of the body, both of which compete for the same enzyme. Omega-3 FAs decreases proinflammatory markers by competitive inhibition of omega-6 FAs metabolism. Studies have also shown that omega-3 FAs also increase synthesis of meibum and help in clearing and thinning of it thus increasing lipid volume of tears.

Aim of this study was to evaluate and further understand the effect of ω-3 FA as dietary supplement on signs and symptoms of blepharitis, MGD and associated dry eye.

MATERIALS AND METHODSThe study consisted of 208 eyes of 104 patients with simple obstructive MGD and blepharitis seen between August 2011 and May 2013 in a tertiary hospital. Patients having taken systemic medications like oral tetracycline, corticosteroids, antihistaminics or any topical medication other than artificial drops in last 1 month were excluded from the study along with patients having any other ocular disease, eye lash abnormalities, disease of lacrimal sac or duct or history of prior corneal surgery. After taking informed consent, patients were randomized into 2 groups. Group 1 patients (n=54) were instructed to take 2 soft geltabs of omega-3 FA each containing 180 mg Eicosapentaenoic acid (EPA) and 120 mg docosahexaenoic (DHA) daily for 6 months. Group 2 patients (n=50) were given placebo capsules. All patients (group 1 and 2) maintained lid hygiene in form of daily eyelash cleansing with a nonirritating neutral dilute baby shampoo during the course of study. Patients were followed and examined at 1, 3 and 6 months. Primary outcome measures were fluoresceing tear break up time (FTBUT), meibum score, Schirmer test and Ocular Surface Disease Index (OSDI) score for patient’s symptoms. Rest of the parameters were considered as secondary measures. Meibum was expressed with mild lid pressure applied immediately below the lash line. Normal meibum is clear, fluid oil that easily spreads to become the outermost surface of the tear film. Color and consistency of meibum was noted and graded accordingly.

RESULTSAt enrolment the mean values of OSDI score, FTBUT, Schirmer and meibum score for group 1 were 42.1, 5.3s, 4.8mm and 2.9 respectively and those for group 2 were 32.1, 5.1s, 5.2mm and 2.1 respectively. Values of these parameters at last follow up were 29.2, 7.2s, 6.3mm and 1.1 respectively for group 1 and 30.1, 5.3s, 5.5mm and 1.9 respectively for group 2. At 6 months, group 1 had statistically significant improvement (p<0.05) in FTBUT, Schirmer, OSDI and meibum scores whereas group 2 had no significant improvement. 81.6% eyes in group 1 had healthy meibum compared to 27.5% in group 2 at 6 months,


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with similar percentage (26.3% and 22.5% in group 1 and 2 respectively) at baseline. Meibum score of 1.5 or less was considered healthy for analysis.

Number of eyes with healthy meibum at baseline and 6 months.

Group Baseline 6 Month P ValueOmega-3 FA 27/103(26.3%) 84/103(81.6%) <0.05Control 22/98(22.5%) 27/98(27.5%) >0.05

DISCUSSIONWe analyzed the data of all outcome measures (subjective and objective) of all patients at start and end of the study for both the groups. We compared findings of test group with the control group at the last follow up. Our results indicate that omega-3 FA supplementation significantly alleviates signs and symptoms of blepharitis, MGD and associated dry eye as compared to baseline. Control group, practicing only lid hygiene didn’t have significant improvement at the end of study. Quality of meibum, as a measure of meibomian gland health also improved significantly in test group. Marian S. Macsai and Oleñik A et. al. also showed similar results demonstrating the antinflammatory role of omega 3 fatty acids in blepharitis, MGD, and associated dry eye.5,6

From our study we can conclude that nutritional supplementation with omega-3 FAs, either as an alternative or an adjunct therapy holds great promise in the treatment of blepharitis, MGD, and the evaporative dry eye.

REfERENCES1. Nichols KK, Foulks GN, Bron AJ, Ben J. Glasgow, Murat Dogru, Kazuo Tsubota

et. al. The international workshop on meibomian gland dysfunction: executive summary. Invest Ophthalmol Vis Sci. 2011;52:1922–9.

2. Solomon A, Dursun D, Liu Z, Xie Y, Macri A, Pflugfelder SC. Pro- and anti-inflammatory forms of interleukin-1 in the tear fluid and conjunctiva of patients with dry-eye disease. Invest Ophthalmol Vis Sci. 2001;42:2283-92.

3. Rubin M, Rao SN. Efficacy of topical cyclosporin 0.05% in the treatment of posterior blepharitis. J Occul Phamacol Ther. 2006;22:47–53.

4. Miljanović B, Trivedi KA, Dana MR, Gilbard JP, Buring JE, Schaumberg DA et. al. The relationship between dietary n-3 and n-6 fatty acids and clinically diagnosed dry eye syndrome in women. Am J Clin Nutr. 2005;82:887–93.

5. Andrea Oleñik, Ignacio Jiménez-Alfaro, Nicolás Alejandre-Alba, Ignacio Mahillo-Fernández. A randomized, double-masked study to evaluate the effect of omega-3 fatty acids supplementation in meibomian gland dysfunction. Clin Interv Aging. 2013;8:1133–8.

6. Marian S. Macsai. The role of omega-3 dietary Supplementation in blepharitis and meibomian gland dysfunction (An AOS Thesis). Trans Am Ophthalmol Soc. 2008;106:336–56.

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Results of Screening of APML Patients and Correlation of Ocular and Hematological findingsDr. Aparna Dwibedy, Dr. Haemoglobin, Dr. Sumita Mohapatra, Dr. Nanda Prasanta Kumar

Acute Promyelocytic Leukemia (APL) (M3 variant of Acute Myeloid Leukemia, FAB Classification) is unique for its characteristic chromosomal

translocation {t(15;17)} leading to the production of the promyelocytic leukemia (PML)-retinoic acid receptor alpha (RARα) fusion protein.

The PML-RARα protein is responsible for the maturation block of white blood cells beyond the promyelocyte stage and causes them to proliferate rapidly in an uncontrolled way. The Promyelocyte lyse and liberate toxic granules containing procoagulant factors which cause widespread generation of thrombin. The overgrowth of promyelocytes leads to a shortage of RBCs and platelets in the body which also contributes to its clinical spectrum.

Bleeding is the leading cause of death and morbidity in APL patients. Blood component transfusion is the keystone in reducing bleeding besides prompt administration of induction chemotherapy.

There have been very few studies which correlate the hematological findings of APL with their ocular manifestations and predict a course the eyes may follow.

MATERIALS AND METHODSA prospective study of 72 newly diagnosed consecutive APL patients admitted in the Hematology Dept. between September 2011 to October 2012 was carried out. These patients were followed up for 6 months.

All admitted patients were examined for any evidence of bleeding, regardless of presence of visual complaints. Anterior segment evaluation was done using Slit Lamp and posterior segment evaluation using 90D and Indirect Ophthalmoscopy was done,prior to start of any therapeutic measures.

Hematological parameters like Total WBC count (TLC), Total Platelet Count (TPC), Hemoglobin%(Hb), Prothrombin time (pT INR), Fibrin degradation products (FDP), at the time of diagnosis were noted down.

pT INR value of >2 was considered abnormal. FDP greater than 200 is considered a hematological parameter for ongoing coagulopathy. The patients were divided into 3 categories according to their TLC and TPC counts (Sanz criteria) into High Risk (TLC > 10,000 microlt), Intermediate Risk (TLC <10,000 but TPC >40,000 microLt) and Low Risk (TLC < 10,000 but TPC >40,000). The ocular findings, presence or absence, were co-related. Statistical analysis was preformed using SPSS 20. Chi-Square test was applied for univariate analysis.


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RESULTSPresence of Macular Hemorrhage (n=42) was significantly higher in High risk group (p=0.001) and correlated significantly with thrombocytopenia (p=0.001)and with pT INR(p=0.026) .

Presence of intra Retinal hemorrages (n=39) was significantly higher in high risk group (p=0.001 ) and correlated best with thrombocytopenia (p=0.002 ) and pT (p=0.001).

Patients who had Disc edema (n=10), CRVO (n=10) and White Centred Hemorrhages (n=10) were all present in the high risk category (p=0.001). Disc edema, CRVO, WCH correlated best with high Leukocytosis (Median value 592000 cells/µl) as compared to those who didn’t have these findings (median value of leukocytosis= 7602cells/µl). All these patients had associated macular hemorrhage and intraretinal haemorrhages which correlated well with Thrombocytopenia (p=0.002 ) and pT INR (p=0.001).

DISCUSSIONIn a study by Karesh JW, Goldman EJ et. al.1, 53 AML patients were evaluated for their ocular findings. They found that patients with retinopathy had significantly lower platelet counts than those without retinopathy. Coagualtion profile was not taken into account. They also concluded that in 3 of their patients in whom optic nerve edema was present didn’t develope CNS leukemia.

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In the study by Guyer DR, Schachat 2 AP, they found an association between the presence of intraretinal hemorrhages and thrombocytopenia for all patients 66 Acute Non-lymphocytic leukemia and 51 Acute lymphocytic Leukemia).

In another study by Jackson N, Reddy SC et. al.3,4 63 Acute leukemia patients,there was no association found between retinal findings (IRH, Mac.Hmg, WCH) and the haemoglobin level or the platelet count. There was a higher median WBC in patients with IRH (68 x 10(9)/l) than in those without IRH (15.4 x 10(9)/l), P=0.037. When the acute myeloblastic leukaemia cases were considered separately, an association was also found between higher WBC and the presence of WCH and Cotton wool spots. They also found Macular Hemorrhage to be a significant risk factor for development of Intracranial Hemorrhage.

In another study by Reddy SC, Jackson. N 5 127 Acute Leukemic Patients,Retinal lesions were seen in 62 cases (49%), with intraretinal haemorrhages being the most common lesion (42%). A high white blood cell count was significantly associated with intraretinal haemorrhages (p=0.04) and white-centred haemorrhages (p = 0.001), while a low platelet count was significantly associated with intraretinal haemorrhages (p = 0.03) in acute myeloid leukaemia patients.

In their non-ophthalmic study, Chang H, Kuo 7 MC of 116 APL patients, Patients with bleeding had significantly higher WBC counts (26.73 ± 6.18 vs. 13.03 ± 3.03 per μL, P = 0.026 and more prolonged PT (4.85 ± 0.70 vs. 2.59 ± 0.28s, P=0.002)

In our study we found Macular Hemorrhage to be the most common finding (85.7%) Intraretinal haemorrhages and Macular haemorrhages were found to be significantly associated with low platelet count (p=0.002) as well as high pT INR (p=0.001). White Centred Hemorrhages, CRVO, Disc Edema were significantly correlating with high TLC (p=0.001), low Platlet count (p=0.001) and high FDP (p<0.001).

In our study we didn’t find Cotton wool spots in any of our patients. Also,in the 10 cases who presented with disc edema didn’t report of the development of CNS leukemia over the 6 months follow up. We didn’t find Intracranial haemorrhages in any of our 42 patients who had presented with Macular Hemorrhage over the 6 months follow-up though 1 patient died of respiratory distress after 2 months of induction chemotherapy. Resolution of ocular findings were seen by the end of 6 months in most patients.

Follow-up of APL patients is a recommended, as in our study we got as high as 79% (n=57) who had no visual complains out of which 68%(n=49) showed fundus findings. Bleeding in APL patients is attributed to both procoagulant activity of promyelocyte granules and thrombocytopenia. Either mechanism can dominate or both can occur simultaneously in a patient. High TLC and


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raised FDP are important factor in causing sluggishness of the blood flow to the Optic nerve head as well as Retina leading to Disc Edema and ischemic features like White Centred Hemorrhages or CRVO, respectively. Duane et. al.6 confirmed the observation of the fibrin and platelet thrombus in the White centre of Roth spots in leukaemic patients.

ConclusionOur study was first of its kind,to the best of our knowledge, taking APL patients exclusively into consideration. All factors that are known to cause bleeding in these patients were included. Both significant and non-significant associations between the haematological parameters and their clinical manifestations in the eye were found out. In the process, we also reached to a conclusion that screening and close monitoring of these patients for any kind of visual disturbance is recommended as these patients are under a constant threat of vision-compromising bleeding and intra-ocular seeding of leukemic cells.

REfERENCES1. Karesh JW, Goldman EJ. A prospective ophthalmic evaluation of patients with

acute myeloid leukemia: correlation of ocular and hematologic findings. 2. Guyer DR, Schachat AP. Leukemic retinopathy. Relationship between fundus

lesions and hematologic parameters at diagnosis. 3. Jackson N, Reddy SC. Retinal findings in adult leukaemia: correlation with

leukocytosis. 4. Jackson N, Reddy SC. Macular haemorrhage in adult acute leukaemia patients at

presentation and the risk of subsequent intracranial haemorrhage. 5. Reddy SC, Jackson N. Retinopathy in acute leukaemia at initial diagnosis:

correlation of fundus lesions and haematological parameters. 6. R. Ling and B. James. White-centred retinal haemorrhages (Roth spots).7. Chang H, Kuo MC. Clinical bleeding events and laboratory coagulation profiles in

acute promyelocytic leukemia.

Microbial Contamination of Surface and Needles in Patients Undergoing Intravitreal InjectionDr. Bhushan Ghodke, Dr. Pooja Gupta, Dr. Snehal Bonde Chaurasia, Dr. Preeti Kankrej

Endophthalmitis is defined as an intraocular inflammation which predominantly involves the inner spaces of eye and their contents i.e.

the vitreous and/or anterior chamber. It is usually caused by infection . Noninfectious (sterile) endophthalmitis may result from various causes such

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as retained native lens material after an operation or from toxic agents. The use of intravitreal injections of either triamcinolone acetonide or anti-vascular endothelial growth factors (anti-VEGF) have exponentially increased in frequency within the last years for therapy of macular and other diseases. Intravitreal injections of anti-VEGF agents have been proposed for treating choroidal neovascularization. Most of these injections are office-based procedures and therefore questions and concerns are raised regarding the safety and possible complications. Thus in the present study, we quantify the microbial source of contamination which is responsible for cases of post-intravitreal injection endophthalmitis cases.

Financial Disclosure

This is purely an institutional study and we have no financial interest in conducting this study.

Purpose

To evaluate potential sources of bacterial contamination during intravitreal (IVT) injection procedures.

MATERIALS AND METHODSIt is a prospective, clinical study conducted in a tertiary care centre for a period of 2 years from March 2010 to April 2012. A total of 80 patients presented to our Eye OPD, were enrolled and consent was taken for participation in the study. The patients were diagnosed with different macular and retinal conditions after thorough investigations and were subsequently scheduled for intravitreal injection (IVT). 80 patients were given 80 IVT injections. Standard microbiological techniques were used to quantify bacterial contamination of injection needles and bulbar conjunctiva at the injection site in collaboration with Microbiology department. Cultures were collected from the bulbar conjunctiva at the injection site and at the corresponding location in the fellow eye before povidone preparation. After topical Povidone treatment and immediately before injection, a third culture was obtained at the injection site. Additionally, the injection needle was also cultured after the procedure. Outcomes measured were type and quantity of bacterial isolates. Topical antibiotics and povidone - iodine were used as a form of prophylaxis in every case of injection.

RESULTSThe mean age of the patients was 65.25 ± 9.25 and the Male: Female ratio was 1 : 2. Out of 80 patients 50 were given intravitreal bevacizumab, 24 patients were given preservative free triamcinolone acetonide and 6 were categorized under other drugs. The disease spectrum was as follows: 65 patients were having diabetic retinopathy (DR), 10 were age related macular degeneration (ARMD)


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and 5 were catogorised as Others (O). Less than 1% of 75 needles collected were contaminated with bacteria and prevalence of bacterial contamination of injection site on the bulbar conjunctiva was 38% before prophylaxis on the day of the injection with topical antibiotics and povidone-iodine, with a statistically significant reduction to 10% after prophylaxis (P<0.0001). All the patients presented within 7 days of injection with signs of hypopyon, congestion, and diminition of vision. Coagulase-negative Staphylococcus, the most common bacterium isolated from the ocular surface, was isolated from culture-positive needles.

DISCUSSIONIn our study, the mean age, gender ratio and the microbiological profile correlated with other similar studies. Moshfeghi et. al. reported eight cases of culture-positive, acute postinjection endophthalmitis in a total of 922 injections of triamcinolone acetonide (overall risk of 0.3% endophthalmitis, similar to the risk of endophthalmitis reported for ganciclovir. The duration of presentation and clinical profile also corelated with other standard studies. Jonas et. al. reported an endophthalmitis rate of 1:1000 injections of intravitreal triamcinolone. Gragoudas et. al. reported an endophthalmitis rate of 1.3% for pegaptanib sodium intraocular injections. Also, same organism was isolated from the surface and needle post injection. Thus, the possible route of contamination of needle with subsequent development of endophthalmitis in patients receiving intravitreal injection has been evaluated.

Conclusion IVT injection needles became contaminated with bacteria during the injection procedure. Although the contamination rate was low, our study supports a mechanism of post injection endophthalmitis in which there is direct inoculation of ocular surface flora into the vitreous cavity by the injection needle. This contamination can be effectively minimised by use of pre-injection broad -spectrum antibiotics and use of povidone iodine solution.

REfERENCES1. Ramanjit Sihota and Radhika Tandon - Parsons’ Diseases of the Eye - 21st edition.2. Albert and Jakobiec’s Principles and Practice of Opthalmology – Vol 2 –section 10

–retina and vitreous-Chapter 184.3. Nentwich M, Yactayo-Miranda Y, Weimann S, Froehlich S, Wolf A, Kampik A,

Mino De Kaspar H - Bacterial contamination of needle points after intravitreal injection. Eur J Ophthalmol. 2009;19:268-72.

4. Gines JC, Nentwich MM, Peggy Bedoya AH- Bacterial contamination of needles after intravitreal injection in Paraguay. Ophthalmologe. 2012;109:782-7. doi: 10.1007/s00347-012-2591-2.

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Scleral Contact Lenses in the Management of Pellucid Marginal DegenerationDr. Rathi Varsha Madanlal

Pellucid Marginal degeneration (PMD) is an ectatic disorder of the cornea characterized by peripheral band of thinning of the inferior cornea from

the 4-o’clock position to the 8-o’clock position with 1-2 mm of normal cornea between the limbus and the area of thinning and the central cornea is usually of normal thickness. PMD is seen in patients aged 20-40 years.1 It is usually bilateral but unilateral cases are reported.2

Because of the high against the rule astigmatism, there is progressive diminution of both uncorrected as well as best-corrected visual acuity (BCVA) in these patients.

Spectacle helps in the very early stage of the disease but contact lens plays a major role in visual improvement. The surgical modalities include corneal transplantation, either full thickness or lamellar or crescentic lamellar keratoplasty, wedge excision, banana graft first followed later by optical PK later.1 The surgeries are indicated when the contact lens trial fails either due to no improvement with contact lenses, or failure to obtain an acceptable fitting or due to the presence of scars. It is difficult to fit traditional contact lenses in patients with PMD. Scleral contact lens trials are indicated when the visual acuity does not improve or the fitting is not possible with rigid gas permeable (RGP) contact lenses, customized soft, piggyback contact lenses (PBCL) or hybrid lenses.1,3,4

The aim of this study is to assess visual outcome with Scleral Contact Lenses (Prosthetic replacement of the ocular surface ecosystem, PROSE, Boston Foundation for Sight, USA) in patients with PMD.

MATERIALS AND METHODSThis is a retrospective study conducted for the patients seen in Scleral lens clinic during 2008 to 2012. Of the total 941 patients, 19 patients underwent PROSE trial for PMD. Demographics in the form of age, gender, UCVA, BCVA, the location of PMD, were noted. Also, the lenses with different front surface eccentricities (FSE) that were tried for vision improvement were noted.

We have described the fitting of scleral contact lens earlier.5 The lens use is PROSE ( Prosthetic Replacement of the ocular surface ecosystem, Boston Foundation for Sight, Needham Heights, MA, USA). The same was followed. Initially, we were using 18 mm diameter lenses, but later on we started using the 18.5 mm diameter lenses. These are Custom made computer designed, lathe cut lenses with junction less posterior surface. The main goal of fitting these lenses was visual improvement before and with scleral lens wear.


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RESULTS20 eyes of 12 patients received the lenses. The mean age was 43 years (range, 29-64 years). Visual acuity improved with scleral lens by more than 2 lines in all eyes. The LogMAR acuity before lens wear was 0.45±0.31 and with lens wear 0.05±0.08. The p value was statistically significant. (Student’s paired t test). The average follow up was 7.25 months. The average daily lens wear was 9.30 hours.

8 patients had bilateral PMD and 4 had unilateral PMD. The male to female ration was 9:3. Before fitting scleral lenses, 20% of the patients were not using any correction. The rest of the patients were using habitual correction as follows; glasses 10%, RGP 45%, SCL 20% and PBCL 5% cases. The location of the thinning was inferiorly in 70% and superiorly in 10%, PMD with keratoconus was noted in 20%.

The indication for the scleral lens was lens popping, failure of PBCL and RGP failure.

The average Sim k value on Orbscan IIz for those patients for whom the lenses were ordered was are Sim K minimum 44.13± 7.06 and Sim K maximum 54.66 ± 6.3.

The ordered lens parameters were as follows. The diameter of the lens was r 18mm for 60% and 18.5 for 40%. The average vault of the lens was 5.35. The FSE ordered was 0.6 in 85%, 0.3 in 5% and 0.8 in 10% of lenses.

The patients who did not order the lenses either wanted to decide 3 eyes, continued with the glass wear, one patient, continued RGP wear, one patient and one patient had lens insertion failure.

Three patients (3 eyes) develop corneal hydrops within first three months of lens wear and underwent penetrating keratoplasty later.

DISCUSSIONThe visual acuity in our study improved by more than 2 lines in all patients. In our study 20 eyes of 12 patients ordered the lenses. Baran et. al. in their study showed that 6 eyes of 3 patients ordered the lenses for PMD.6 Rosenthal et. al., had shown in 27 eyes.7 Pullum et. al. had shown improved visual acuity in 7 eyes.8

The main complication in our series was hydrops which occurred in 3 patients and needed keratoplasty. Though we could not attribute the reason for this but we assume that may be the slightly tighter fitting of the lens might have resulted in corneal hydrops. This lead us to fit the lenses with slightly flatter haptic which can reduce vision as more debris may get collected in the fluid.

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As vision improved in 85% patients with 0.6E, the lenses with 0.6 FSE should be the first lens of choice to reduce the chair time.

With scleral contact lenses, the visual acuity improved by more than two lines in all patients.

These are useful when other contact lens options such as RGP, PBCL fails. But as we noted corneal hydrops in three patients, one needs to be careful in fitting these lenses in PMD and should aim for flatter fitting lenses.

REfERENCES1. Jinabhai A, Radhakrishnan H, O’Donnell C. Pellucid corneal marginal

degeneration: A review. Cont Lens Anterior Eye 2011;34:56-63.2. Basak SK, Hazra TK, Bhattacharya D, Sinha TK. Unilateral pellucid marginal

degeneration. Indian J Ophthalmol 2000;48:233-4.3. Kompella VB, Aasuri MK, Rao GN. Management of pellucid marginal corneal

degeneration with rigid gas permeable contact lenses. CLAO J 2002;28:140-5.4. Raizada K, Sridhar MS. Nomogram for spherical RGP contact lens fitting in

patients with pellucid marginal corneal degeneration (PMCD). Eye Contact Lens 2003;29:168-72.

5. Rathi VM, Sudharman Mandathara P, Vaddavalli PK, Dumpati S, Chakrabarti T, Sangwan VS. Fluid-filled scleral contact lenses in vernal keratoconjunctivitis. Eye Contact Lens 2012;38:203-6.

6. Baran I, Bradley JA, Alipour F, Rosenthal P, Le HG, Jacobs DS. PROSE treatment of corneal ectasia. Cont Lens Anterior Eye 2012;35:222-7.

7. Rosenthal P, Croteau A. Fluid-ventilated, gas-permeable scleral contact lens is an effective option for managing severe ocular surface disease and many corneal disorders that would otherwise require penetrating keratoplasty. Eye Contact Lens 2005;31:130-4.

8. Pullum KW, Buckley RJ. A study of 530 patients referred for rigid gas permeable scleral contact lens assessment. Cornea 1997;16:612-22.

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