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EDITORIAL

5 The World beckons......

7 PRESIDENTIAL ADDRESS

RETINA

15 Pseudophakic Retinal Detachment - Management Challenges Deependra Vikram Singh, Yog Raj Sharma, Ajay Pal Singh Jinjha

21 Endogenous Endophthalmitis: Case Series Mallika Goyal, Sridhar A

OCULOPLASTY

29 Ocular Manifestations of Nasopharyngeal Tumors Ruchi Goel, Saurabh Kamal, Smriti Nagpal, Sushil Kumar, Sonam Angmo Bodh

CATARACT

33 Cataract Surgery in Uveitis Mahesh Punjabi

SQUINT

37 Accommodative Esotropia A Practical Approach Arun Samprathi

REFRACTIVE SURGERY

45 Post Lasik Ectasia Ramendra Bakshi

CORNEA

49 Doxycycline- A Corneal Surgeon’s Friend in Need Manisha C. Acharya, Sonia Sharma, Umang Mathur, Jyoti Garg

GLAUCOMA

53 Management of Failing Bleb Amit Porwal

CLINICAL MEETING

57 Clinical Case-1: What next? Managing a case of ARMD Anju Kumari, B.P. Guliani

61 Clinical Case-1: Watch that Squint Meetu Bansal, Archana Gupta Mahajan

65 Clinical Case-2: Amniotic Membrane Graft in Ocular Surface Reconstruction

Mridula Mehta, Sudhank Bharti

MISCELLANEOUS

67 Fugo Plasma Blade - Its role in Ophthalmology Daljit Singh, Seema K. Singh

TEAR SHEET

79 Points to Ponder in Keratorefractive Surgery Reetika Sharma


The World beckons......Respected Seniors & friends,

The Delhi Ophthalmological Society is going places! It is with a feeling of immense pleasure and pride that we wish to announce the � rst DOS International Conference (I-DOS) to be held in Pattaya-Bangkok, Thailand on November 21 to 24, 2012.

DOS embarks to sail offshore for the � rst time; it will be a meeting for the DOS members and their families. This novel attempt ventures to take the DOS academic sessions out of the seasonal sultry humidity of Delhi to Pattaya & Bangkok, off the Gulf of Thailand. The DOS executive beckons you to join us with fun � lled enthusiasm and zest, to travel far from the madding crowd and the daily grind of routine life in an attempt to combine academic and social interaction on a common platform. This will be an excellent opportunity to come together yet again and to socialise, bond and revel in each other’s company in one of Asia’s largest beach resorts and shopping haven, stay in luxurious hotels and enjoy excellent shows, water-sports, beach games, boat rides and an awesome shopping experience. The tranquil surroundings of Pattaya coupled with the splendour of Bangkok promise to form an apt platform to rejoice, rejuvenate and rediscover ophthalmology. In midst of a very enjoyable itinerary are planned three high quality academic interactions that will cover the complete array of ophthalmology and satisfy both the connoisseur and the generalist.

Come and be a part of history as DOS becomes a truly international society. Join in to experience a ‘never before conference’, which promises to be one that you cannot forget. Experience a new way of learning, mixed with ample portions of fun and a world of luxury, experience the feeling of being treated as a king.

A trip to beat all trips: With special rates only for DOS members and their spouses.

Enjoy learning and travelling without the hassle: Leave all the planning to us.

Be there, make history.With best wishes,

Rohit SaxenaSecretary, Delhi Ophthalmological Society


What is the purpose of life? Some may like to do research, achieve greatness, want to leave a legacy or want to be immortal. The biggest achievement recognized globally is the Nobel Prize. Do you remember who got the Nobel Prize this year? I am not trying to belittle their achievements. I salute them for their commitment, perseverance and their sacrifi ces. But for an ordinary individual like me, what’s more important is to enjoy my life to the fullest. We have been working hard through schools, colleges and the early years of settlement in practice. Virtually half of our life is gone. Do we need to continue in the same vein or do we need to pause, relax and relook at our lives? When I analysed this, I realized that I don’t have to be as aggressive and competitive as I was ten years back. I want to chill out, enjoy myself and want to live rich, not die rich. I want to spend time with

my family and friends. I want to have new friends, new responsibilities in various societies and groups and contribute whatever I can without bothering about the fi nancial gains. Believe me, I enjoy every moment of it .The best period of my life was as Secretary DOS. I know that people will not remember what I did, but I feel happy that I did my best and contributed to the society in a big way. My best work was writing a book on phacoemulsifi cation which helped so many people.

There are certain prerequisites and ways to enjoy life. We need to achieve fi nancial security. According to International standards, anyone having one million dollars besides the property which he is using for personal purposes is called a “High Networth individual”, and he does not have to work for life. Another estimate puts this fi gure twenty fi ve times of your present expenditure. You need this when you stop earning altogether, which is not the case. This means that any doctor having his own house plus a secure job or his own clinic, can start enjoying his life. You also need to achieve something in your life fi nancially, academically or contribute to social causes or organizations to feel good about yourself. And fi nally your happiness depends upon how good an understanding you have with your close family and friends .If you achieve something and there is nobody to share, it comes to a naught. Just imagine a scenario – you did record number of surgeries in a day, earned huge amount of money, and come back home…and your partner says “Is this the time to come back home?” Or your family has been waiting for a movie or dinner - you are physically with them, but a tired and retired man. Or your child is going to receive an award, but you are not there to see the expression on his face. What’s the use?

Sometimes inspite of your best efforts, it may not be possible to have the best understanding with your partner.The greatest stress busters in such a situation are your friends and hobbies. Do devote time to cultivate them.

Happiness is better than pleasure, but happiness is elusive. On the other hand pleasures are measurable by materialistic things. I love my pleasures. Keep on striving for happiness but keep enjoying the good things in your life to feel lucky and blessed.

At the end, I would like to say, that if it is the last day of your life, you’ll never regret that you didn’t spend enough of time in the offi ce or made enough of money. If at all, you’ll regret not spending enough time with your family and enjoying your life to the fullest.

Dr. Harbansh LalPresident, DOS

Enjoy Your Life

12 l DOS Times - Vol. 18, No. 3 September, 2012


Pseudophakia is a known risk factor for Rhegmatogenous Retinal Detachment (RRD). RRD after cataract extraction

develops in approximately 0.5% to 1.0% of eyes.1-3 A large population-based retrospective study evaluating 10256 cataract surgery patients found that cumulative probabilities of RD at 1, 5, 10, 15, and 20 years after cataract extraction (CE) were 0.27%, 0.71%, 1.23%, 1.58%, and 1.79% respectively.4 More important � nding was cumulative probability ratio of RD at 20 years after CE remaining 4.0-fold higher than would be expected in a similar group of residents not undergoing CE. Another caser series followed 453 emmetropic eyes subjected to uneventful phacoemulsi� cation with intraocular lens implantation in the capsular bag.5 After a period of 5 years PVD occurred in 107 of 141 (75.88%) eyes without preoperative PVD and total of 14 eyes (3.1%) developed RRD. These all evidences call for a long follow up of pseudophakic patients and meticulous indirect ophthalmoscopy whenever they complain of symptoms of PVD. Figure 1 show fundus picture of large � ap tear in a patient with acute PVD developed 6 weeks after cataract surgery. The treatment of pseudophakic RRD (PPRD) was described � rst by Tassman and Annesley in 1966 using scleral buckling techniques.6 Management of PPRD has undergone signi� cant changes following introduction of vitrectomy techniques. The challenges encountered during PPRD management and the latest advancements in vitreous

Retina

Deependra V. Singh

1Deependra Vikram Singh MD, 2Yog Raj Sharma MD, 3Ajay Pal Singh Jinjha MD1. Eye-Q Superspeciality Eye Hospitals, Gurgaon, Haryana

2. Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, New Delhi, 3. Director Retina Services, Eye Hospital Jaipur

surgery to address these challenges are discussed here. Table 1 shows the common challenges encountered.

Choice of Surgery

Sutureless Pars plana vitrectomy (PPV) with silicone oil or gas injection suits most cases with PPRD.7 Table 2 list advantages of PPV for PPRD. Macula on quadrantic RD with anterior � ap tear in a patient with uncomplicated pseudophakia is an exception where scleral buckling still has a role. (Figure 2) Scleral buckling for such patient should be done as a simpli� ed procedure with <90° buckle. Encirclage alone can also be used for very small anterior breaks.

IOL issues

Uncomplicated Pseudophakia with Acrylic/PMMA IOL in Bag with no PCO/YAG opening poses minimal challenge to Vitreoretinal surgeon. Table 1 lists the challenges from variety of other IOLs. The decision to retain or explants IOL varies from cases to case.

IOL ExplantationAll patients with silicone or subluxated IOLs need detailed preoperative counselling explaining them the need for IOL explantation during surgery. The importance of reattaching retina should take precedence over temptation to retain IOL

Table 1: Challenges encountered during PPRD managementManagement Issues Delayed Detection and presentation

Clinical PicturePPRD more likely to;

IOL IssuesChallenges include

Intraoperative challenges for PPV for PPRD

Postoperative Challenges

Signs and symptoms of PVD* ignored

Have PVR Silicone IOLs No Break RDs Silicone Oil in Anterior Chamber

Confused with CME/CSR/ERM**

Have No Break RDs IOLs in ciliary sulcus with or without subluxation

Vapors on IOL surface/fogging

PVR

Small peripheral breaks dif� cult to be detected.

Giant Retinal Tears Large YAG opening PCO, Air in AC Epi-macular Membrane

Slowly progressing inferior RDs

Total RDs involving Macula

Anterior Chamber or iris � xated IOLs

Poorly dilating pupil

IOL re� exes and PCO hinder examination

Unstable IOLs/absent PC

*PVD; Posterior Vitreous Detachment, **CME; Cystoid Macular Edema, CSR; Central Serous Retinopathy, ERM; Epiretinal Membrane


Figure 2: Macula on quadrantic pseudophakic RD with single anterior � ap tear managed with scleral buckle

and same should be informed to the patient. The fact that a successful reattachment surgery can always be followed by IOL re-implantation in future (if indicated) helps reassuring a sensitive and apprehensive patient. Figure 3 show a subluxated IOL that has to be removed during surgery for PPRD.

IOL retention with inferior PIEyes with large PCR or absent posterior capsule or with anterior chamber IOLs should undergo a large surgical

inferior PI after � uid air exchange and endolaser to prevent silicone oil from entering AC. Described by ANDO for aphakic eyes,8,9 inferior PI is quite useful for eyes with AC IOLs also. (Figure 4) The bimanual approach with vitreous forceps grasping the iris from one port and cutter through the other port for cutting iris ensures a peripheral location without cutting the sphincter. Keeping cutter in suction-only mode to localize the site for PI and then initiating cutting also reduces the chances of sphincter tear.

Figure 1: Large � ap tear in a patient with ocute PVD developed 6 weeks after cataract surgery


Table 2Advantages of Vitrectomy as compared to Scleral Buckling for PPRDLess destructive to conjunctiva and muscles

Less incidence of induced Refractive error and motility problems

More predictable Takes care of vitreous opacities and traction

Also advantageous in cases with complicated pseudophakia

More likely to detect break in “no break” PPRDs

Can treat breaks of all sizes and location

Earlier macular reattachment

ILM peeling possible in vitrectomy only

Easy on VR surgeon’s Back

Intraoperative challenges

No break PPRDsWhile break localization subtotal PPRDs is often assisted by LINCOFF’s rules, same can be challenging in total PPRDs that are not bullous. A stream of sub retinal � uid, different in texture from infusion � uid, entering the vitreous cavity immediately after vitrectomy is initiated can often help us localize the break. The same phenomenon gets enhanced after injecting per� uorocarbon (PFCL) described as Schlieren phenomenon. Indentation along with wide angle viewing systems also allow surgeon to detect the small breaks intraoperatively. The cases where no break can be detected despite all above manoeuvres are helped by 360° endolaser in 2 or 3 rows placed as anterior as possible.

Diffi cult visualization; PCO/FoggingPCO hampering intraoperative visualization can easily be excised with vitrectomy cutter to improve visualization. If vitreous surgery does not require ILM or membrane peeling, PCO removal may not be necessary and should be avoided. Fogging is encountered during � uid-air exchange (FAE) in cases with no posterior capsule or large YAG opening. Normally these vapours on the back surface of IOL can be wiped off with a soft silicone tip to allow completion of FAE. If fogging recurs frequently, the back surface can be coated with little Viscoelastics to enhance visualization. Figure 5 shows intraoperative fogging over YAG opening and its management with soft silicone tip.

Figure 3: Explantation of subluxated IOL during surgery for PPRD

Figure 4: Large inferior PI is a must in post vitrectomy eyes with silicone oil


Air in ACContact wide angle visualization allows unhampered visualization in this situation for almost all cases otherwise switching back to � uid infusion and using PFCL to reattach retina followed by endolaser retinopexy is helpful. All cases where air enters AC are prone to have silicone oil in AC postoperatively so a inferior PI is a must to prevent pupillary block glaucoma.

Poorly dilating pupilPoorly dilating pupil in pseudophakic eyes often results from adhesion of sphincter to rhexis margin. Again, wide angle viewing enables us to complete surgery in such cases. Rarely vitreous surgeon would require iris hooks for managing such cases. Peripheral indentation by trained surgical assistant also helps completing the surgical procedure.

Post operative challenges

Silicone oil in ACDe� cient posterior capsule or absent zonules with IOL subluxation are risk factors for post operative silicone oil migration into AC. A large and patent inferior PI would often prevent this, but not always. Silicone oil occupying less than third of AC volume poses no immediate threat to cornea and can be observed for few months. The decision on when to remove silicone oil is hardly ever in� uenced by presence of silicone oil bubble in AC. However a large silicone oil bubble with pupillary block needs immediate removal with reinjection with either a large PI or IOL explantation.

PVR and Epiretinal membranePVR and epiretinal membrane formation seen in up to 10% cases are known complications of surgery for RRD. Figure 6 show an eye with PPRD developing ERM at macula postoperatively. The detailed discussion on this complication is beyond the scope of this section. All the measures directed towards PVR prevention should be taken while operating patients with PPRD. Some of these measures include minimizing in� ammation, controlling in� ammation with oral and periocular steroids, restricting laser photocoagulation to areas requiring retinopexy only, avoiding cryopexy, avoiding Viscoelastics and prompt control of intraoperative bleeding. We have also found ILM peeling for selected cases with PVR helpful in preventing ERM formation. Brilliant blue dye seems to be very effective in facilitating this surgical manoeuvre.

SummaryAlthough advancements in Vitreoretinal instrumentation and surgical skills have improved the management of PPRD, few challenges still keep troubling vitreous surgeons. Wide angle viewing systems, large inferior PI, brilliant blue dye and intraoperative scleral indentation are key additions to VR surgeon’s armamentarium. Also selecting large optic rigid PMMA IOLs in cases with PCR by anterior segment colleagues is highly recommended.

Figure 5: Intraoperative fogging over YAG opening

Figure 6: PPRD can develop ERM at macula post operative


References1 Javitt JC, Street DA, Tielsch JM, et al. National outcomes of cataract

extraction. Retinal detachment and endophthalmitis after outpatient cataract surgery. Ophthalmology 1994;101: 100–5, discussion 106.

2 Tielsch JM, Legro MW, Cassard SD, et al. Risk factors for retinal detachment after cataract surgery. A population-based case-control study. Ophthalmology 1996;103:1537– 45.

3 Olsen G, Olson RJ. Update on a long-term, prospective study of capsulotomy and retinal detachment rates after cataract surgery. J Cataract Refract Surg 2000;26:1017–21.

4 Erie JC, Raecker MA, Baratz KH, Schleck CD, Burke JP, Robertson DM. Risk of Retinal Detachment after Cataract Extraction, 1980–2004 A Population-Based Study. Ophthalmology. 2006 Nov;113(11):2026-32. Epub 2006 Aug 28.

5 Ripandelli G, Coppé AM, Parisi V, Olzi D, Scassa C, Chiaravalloti A, Stirpe M. Posterior Vitreous Detachment and Retinal Detachment after Cataract Surgery. Ophthalmology 2007;114:692–697.

6 Tassman W, Annesley WH Jr. Retinal detachment in prosthetophakia. Arch Ophthalmol 1966;75:179–88.

7 Sharma YR, Karunanithi S, Azad RV, Vohra R, Pal N, Singh DV, Chandra P. Functional and anatomic outcome of scleral buckling versus primary vitrectomy in pseudophakic retinal detachment. Acta Ophthalmol Scand. 2005 Jun;83(3):293-7

8 Beekhuis WH, Ando F, Zivojnovi� R, Mertens DA, Peperkamp E. Basal iridectomy at 6 o’clock in the aphakic eye treated with silicone oil: prevention of keratopathy and secondary glaucoma. Br J Ophthalmol. 1987 Mar;71(3):197-200.

9 Ando F. Usefulness and limit of silicone in management of complicated retinal detachment. Jpn J Ophthalmol. 1987;31(1):138-46.

10 Friberg TR, Tano Y, Machemer R. Streaks (Schlieren) as a sign of rhegmatogenous detachment in vitreous surgery. Am J Ophthalmol 1979;88:943– 4.


Retina

Mallika Goyal

Mallika Goyal MD, Sridhar A, MSApollo Health City, Jubilee Hills, Hyderabad

Endogenous endophthalmitis (EE) is infection in the globe from hematogenous transmission. It is a sight-threatening

emergency and the aetiology is often multifactorial. Delayed diagnosis may exacerbate the poor visual prognosis. The infection can be bacterial or fungal.

We report a series of interesting cases of endogenous endophthalmitis treated at our Service over the last 3 years, and highlight certain important points with regard to diagnosis and management of this serious disorder.

Case 1

An 8 year old boy on chemotherapy for acute lymphoblastic lymphoma presented with LE irits, and was placed on topical steroids. Seen in the retina service on day 5, there was disc congestion and edema. A diagnosis of ocular lymphoma with involvement of optic nerve was contemplated: MRI optic nerves returned normal.

Day 6 there was a large haemorrhagic macular abscess and a diagnosis of endogenous endophthalmitis was made (Figures 1,2).

Vitreous tap revealed Klebsiella species resistant to all tested drugs except to gati� oxacin.

Day 7 there was hypopyon with panophthalmitis (Figure 3, 4).

Management included intravenous gati� oxacin for 2 weeks

followed by oral gati� oxacin; vitrectomy and several intravitreal injections of gati� oxacin. The infection resolved after 6 weeks with atrophic bulbi.

Figures Case 1 (Figures 1-4)

Case 2

A 26 year old lady with no systemic disease, no history of surgery, delivery, injections or fever in the last one year presented with RE sudden vision drop. A creamy circular retinal lesion superonasal to fovea with trace vitreous cells was seen (Figure 5).

Blood culture, serology for HIV and Toxoplasma were negative. Physician and gynaecological review returned unremarkable.

At day 5 the lesion had enlarged with signi� cant vitreous cells (Figure 6).

Vitreous tap revealed candida on smears, no growth on culture.

Figures 1-4

Fig.1 Fig.2

Fig.3 Fig.4

Fig.5 Fig.6

Fig.7 Fig.8

Fig.9 Fig.10

Figures 5-10


She was placed on intravenous voriconazole 200 mg bid for 2 weeks followed by oral voriconazole 200 mg bid.

RE vitrectomy with intravitreal amphotericin B (5 micrograms) injection was done. Over the next few weeks there was retinal vascular sheathing and worsening of vitreitis (Figures 7, 8). Pupil became rigid and small.

Repeat vitrectomy with intravitreal amphotericin B 5 micrograms & voriconazole 10 micrograms was performed. Over 8 months, several intravitreal injections of this combination at weekly- biweekly intervals were administered with eventual scarring of the lesion and visual acuity 6/24 (Figures 9, 10). Oral voriconazole was used for 12 months. Liver function tests were monitored every month while she was on voriconazole.


Case 3

A 50 year old diabetic gentleman presented with LE sudden drop in vision. Fundus RE was unremarkable except for mild

non-proliferative diabetic retinopathy and an inconspicuous small sub-retinal elevation inferior to macula (Figure 11). LE had disc congestion and peripapillary hypopigmented lesions (Figure 12).

Fundus � uorescein angiography revealed RE distinct hyper� uorescent patch corresponding to the sub-retinal lesion seen clinically, and a patch of retinal vascular leak superior to macula (Figures 13, 15). LE lesions revealed initial blocked choroidal � uorescence with late phase leakage and staining starting from lesion edges (Figures 14, 16). These distinct and extensive � ndings con� rmed the clinical suspicion of EE with both eyes multiple retinal abscesses. Signi� cantly, RE was asymptomatic at this time with no other evidence of in� ammation or infection.

Blood culture and physician check were normal. He complained of toothache: dentist consultation revealed infection of the dental roots, multiple caries and plaque.

Vitreous tap and dental specimen culture revealed no growth. Microchip RNA DNA evaluation of vitreous specimen returned positive for E coli.

Based on the internist’s and dentist’s recommendation, he was treated with intravenous antibiotics, augmentin, ceftazidime and metrogyl for 2 weeks followed by oral o� oxacin. Both eyes intravitreal antibiotics (vancomycin and amikacin) were administered, LE followed by RE. Response was poor with increasing vitreous haze (Figures 17, 18).

Vitrectomy with intravitreal antibiotics (cefazolin with ceftazidime) for the 2 eyes was done on day 5 and day 8 respectively with gradual resolution of infection over 3 weeks (Figures 19, 20). Vision after 6 weeks of therapy was 6/6, N6 each eye.


Case 4

A 42 year old non-diabetic lady presented with both eyes pain and blur, RE > LE. She was treated earlier elsewhere as iritis. She had been hospitalised a month earlier for dengue fever. Both eyes revealed multiple patches of retinal haemorrhages and abscesses with vitreous cells 1+ (Figures 21, 22).

Fundus � uorescein angiography revealed initial blocked choroidal � uorescence over the fundus lesions with hyper� uorescence starting from lesion edges in later phases (Figures 23-27). The angiographic � ndings were more extensive than those seen clinically.

A diagnosis of Dengue retinitis with endogenous endophthalmitis was made.

Vitreous tap did not reveal any growth on culture. Microchip RNA DNA analysis revealed Pseudomonas species. RE had received intravitreal cefazolin and ceftazidime at this time.

She was treated by an internist with intravenous antibiotics (gati� oxacin 400 mg od and dorpenem 500 mg tid) for 2 weeks followed by oral gati� oxacin for 4 weeks.

LE intravitreal cipro� oxacin and ceftazidime were administered. There was gradual resolution of fundus lesions though RE had increasing vitreous haze in the � rst 2 weeks (Figures 28-31).

Complete resolution of in� ammation and lesions occurred over 6 weeks, with � nal visual acuity of RE 4/60, LE 6/12 (from dengue foveolitis, Figures 32, 33).

Fig.11 Fig.12

Fig.13 Fig.14

Fig.15 Fig.16

Fig.17 Fig.18

Fig.19 Fig.20

Figures 11-20


She presented 3 months later with � orid neovascularisation disc with vitreous haemorrhage (Figure 34), likely secondary to the dengue retinitis. The proliferation regressed following panretinal photocoagulation (Figures 35, 36). Proliferative retinopathy following dengue retinitis is not reported earlier.


Case 5

A 29 year old gentleman presented with disseminated systemic blastomycosis and

LE vision drop. A lymph node biopsy had con� rmed the diagnosis of blastomycosis. He had recently returned from South America which is endemic for this infection (transmitted via respiratory system).

LE revealed a large subretinal granuloma superior to the optic disc (Figures 37, 38). This had been treated as sarcoidosis elsewhere with intravenous steroids.

In view of a pre-existing biopsy diagnosis, vitrectomy with intravitreal amphotericin B (5 micrograms) and voriconazole (10 micrograms) was performed. The lesion continued to be active and 2 further intravitreal injections of the combination were administered with gradual resolution of the lesion over 8 weeks (Figures 39-41).

Systemic management included intravenous voriconazole 200 mg bid for 2 weeks followed by oral voriconazole 200 mg bid for 6 months.


Case 6

A 19 year old immunocompetent boy treated a month prior for pyogenic meningitis presented with LE blur. Evaluation revealed both eyes multiple retinal haemorrhages and abscesses with trace vitreous cells (Figures 42-43).

The c.s.f. tap had been negative on microbiological examination. With a presumptive etiological diagnosis of haemophilus in� uenzae or streptococcus pneuminae (commonly associated with meningitis), he was placed on oral levo� oxacin 750 mg daily and LE intravitreal cefazolin and ceftazidime was administered.

2 weeks later both eyes revealed resolving lesions, RE without any ocular intervention (Figures 44, 45). Oral levo� oxacin was continued and at 8 weeks lesions had cleared from both eyes with visual acuity 6/6 each eye (Figures 46, 47).


Case 7

A diabetic 65 year old lady with no systemic infections presented with LE blur for 4 weeks. There were hyopigmented unremarkable appearing elevated lesions nasal to disc (Figure 48). Fluorescein angiogram was characteristic (Figures 49, 50).

She was placed on oral levo� oxacin and underwent vitreous

Fig.21 Fig.22 Fig.23 Fig.24



Fig.33

Figures 21-33


tap with antimicrobials injection. However, over the next 10 days vitreous exudates increased (Figures 51, 52).

She underwent pars plana vitrectomy with repeat intravitreal antimicrobials, and was placed on oral levo� oxacin 750 mg daily for 6 weeks. Infection resolved over 3 weeks with a patch of chorio-retinal atrophy corresponding to the initial abscess (Figure 53).


Case 8

70 year old diabetic gentleman with history of recurrent urinary tract infection with balanoprostatitis (admitted for same 3 months earlier: urine culture positive for enterococcus) complained of rapid onset vision drop both eyes. RE fundus view was faint due to cataract. Fluorescein angiogram was characteristic (Figures 54, 55).

He was placed on intravenous vancomycin in view of recent enetrococcus infection, was treated with intravitreal antimicrobials and infection resolved.

Figures Case 8 (Figures 54, 55)

Summary

Endogenous endophthalmitis needs timely management and may take weeks to months for resolution.

This series highlights the need for very high index of suspicion for infection in any patient presenting with “iritis” even if young and immunocompetent with no history of recent illness or surgery. Dilated-pupil exam to look for retinal/ choroidal involvement in every iritis is key to correct diagnosis.

Index of suspicion has to be even higher in diabetics or those immunosuppressed or with history of recent fever or infection1. Dental infection maybe a common but overlooked septic focus.

Culture of vitreous is negative in upto 40% cases2. RNA-DNA microchip analysis picks up the nucleic acids from live as well as dead organisms, cell bound organisms as well as free � oating nucleic acids. The process involves extraction

Figures 37-41

Fig.34 Fig.35 Fig.36

Figures 34-36

Fig.37 Fig.38

Fig.39 Fig.40

Fig.41

Fig.42 Fig.43

Fig.44 Fig.45

Fig.46 Fig.47

Figures 42-47


of nucleic acids, their modi� ed multiplex ampli� cation and analysis on Syndrome Evaluation System platform. It is not dependant on live organisms for diagnosis, and can yield diagnosis even after treatment has been initiated. Other advantages include high sensitivity and speci� city, short processing time (6-8 hours), need for a relatively small volume of specimen, simultaneous investigation for multiple organisms: bacteria, fungi, viruses and parasites, and rapid availability of result (24-48 hours). This modality can complement the conventional microbiology evaluation, specially when infection is non-responsive to treatment and the initial microbiology investigation has returned negative.

Early clinical diagnosis maybe aided by fundus � uorescein angiography which reveals characteristic changes more dramatic and extensive than the lesions seen clinically.

Fungal endophthalmitis needs aggressive therapy that maybe prolonged (upto 8 months in case 2); systemic antifungals maybe indicated for upto a year. Oral voriconazole has excellent ocular bioavailability3.

Antifungals of different groups may work synergistically, hence combination of intravitreal amphotericin B and voriconazole was used for intravitreal injection in cases 2 (where response to amphotericin B alone was inadequate) and 5. While in some situations they maybe indifferent to each other, there is no evidence of antagonism between different groups of antifungals4-13.

Oral � uoroquinolones (fourth generation: gati� oxacin 400 mg od; third generation: levo� oxacin 750 mg od and o� oxacin 400 mg bid) have excellent bioavailability and wide spectrum of action. These can be an adequate substitute for intravenous antibiotics, and can alleviate the discomfort, adverse effects, costs and hospitalisation associated with intravenous antibiotic administration. In fact, in some cases these may alleviate the need for intravitreal antibiotics as well (Case 6, RE). They also act synergistically with antifungals6.

Systemic gati� oxacin, however, can have several systemic adverse effects including wide blood sugar � uctuations

Figures 48-52

Figure 53

Figure 54

Figure 55

Fig.48 Fig.49

Fig.50 Fig.51

Fig.52


in diabetics, severe gastro-intestinal symptoms, and is contraindicated in children. Systemic gati� oxacin, therefore, is withdrawn from most markets and should be used only if the etiological organism is sensitive to this drug alone as in our case 1.

In summary, endogenous endophthalmitis is a sight-threatening disorder. High index of suspicion, timely and aggressive management in collaboration with an internist is indicated to combat infection, preserve vision and the globe.

References

1 Annamalai T, Fong KC, Choo MM Intravenous Fluconazole for Bilateral Endogenous Candida Endophthalmitis. J Ocul Pharmacol Ther. 2011 Jan 16. [Epub ahead of print].

2 Connell PP, O’Neill EC, Fabinyi D, Islam FM, Buttery R, McCombe M, Essex RW, Roufail E, Clark B, Chiu D, Campbell W, Allen P. Endogenous endophthalmitis: 10-year experience at a tertiary referral centre.Eye (Lond). 2011 Jan;25(1):66-72. Epub 2010 Oct 22.

3 Riddell J 4th, Comer GM, Kauffman CA. Treatment of Endogenous Fungal Endophthalmitis: Focus on New Antifungal Agents. Clin Infect Dis. 2011 Jan 16. [Epub ahead of print]

4 Demchok JP, Meletiadis J, Roilides E, Walsh TJ. Comparative pharmacodynamic interaction analysis of triple combinations of caspofungin and voriconazole or ravuconazole with subinhibitory concentrations of amphotericin B against Aspergillus spp. Mycoses. 2010 May;53(3):239-45. Epub 2009 Mar 7.

5 Nishi I, Sunada A, Toyokawa M, Asari S, Iwatani Y. In vitro antifungal combination effects of micafungin with � uconazole, voriconazole, amphotericin B, and � ucytosine against clinical isolates of Candida species. J Infect Chemother. 2009 Feb;15(1):1-5. Epub 2009 Mar 12.

6 Stergiopoulou T, Meletiadis J, Sein T, Papaioannidou P, Tsiouris I,

Roilides E, Walsh TJ. Comparative pharmacodynamic interaction analysis between cipro� oxacin, moxi� oxacin and levo� oxacin and antifungal agents against Candida albicans and Aspergillus fumigatus. J Antimicrob Chemother. 2009 Feb;63(2):343-8. Epub 2008 Dec 24.

7 Córdoba S, Rodero L, Vivot W, Abrantes R, Davel G, Vitale RG. In vitro interactions of antifungal agents against clinical isolates of Fusarium spp. Int J Antimicrob Agents. 2008 Feb;31(2):171-4. Epub 2007 Dec 3.

8 O’Shaughnessy EM, Meletiadis J, Stergiopoulou T, Demchok JP, Walsh TJ. Antifungal interactions within the triple combination of amphotericin B, caspofungin and voriconazole against Aspergillus species. J Antimicrob Chemother. 2006 Dec;58(6):1168-76. Epub 2006 Oct 27.

9 Kratzer C, Tobudic S, Schmoll M, Graninger W, Georgopoulos A. In vitro activity and synergism of amphotericin B, azoles and cationic antimicrobials against the emerging pathogen Trichoderma spp. J Antimicrob Chemother. 2006 Nov;58(5):1058-61. Epub 2006 Sep 19.

10 Cuenca-Estrella M, Gomez-Lopez A, Buitrago MJ, Mellado E, Garcia-Effron G, Rodriguez-Tudela JL. In vitro activities of 10 combinations of antifungal agents against the multiresistant pathogen Scopulariopsis brevicaulis. Antimicrob Agents Chemother. 2006 Jun;50(6):2248-50.

11 Barchiesi F, Spreghini E, Maracci M, Fothergill AW, Baldassarri I, Rinaldi MG, Scalise G. In vitro activities of voriconazole in combination with three other antifungal agents against Candida glabrata.Antimicrob Agents Chemother. 2004 Sep;48(9):3317-22.

12 Cesaro S, Toffolutti T, Messina C, Calore E, Alaggio R, Cusinato R, Pillon M, Zanesco L. Safety and ef� cacy of caspofungin and liposomal amphotericin B, followed by voriconazole in young patients affected by refractory invasive mycosis. Eur J Haematol. 2004 Jul;73(1):50-5.

13 Shalit I, Shadkchan Y, Mircus G, Osherov N. In vitro synergy of caspofungin with licensed and novel antifungal drugs against clinical isolates of Fusarium spp. Med Mycol. 2009;47(5): 457-62.

Eye Surgeon (MS)For 60 Bedded

Modern Eye HospitalAt Haridwar

Contact/ Send C.V.

1. Two Phaco Machine Along with One Hand Piece Each In Good & Properly Workin Working Condition.

Sale Price Negotiable MAKE – Storz Protege 1. Year- 1997-98 (Started in 2000) Model No.- DP X 100 2. Year – 20052. DCR Laser, Biolitec (Germany).

Purchased In 2007. But Not Used Serial No.- 2354-G.

Sapt Rishi Link Road, Haridwar – 249410 (U.K.)PH. :- 01334- 260190, MOB.- 09412931046Email- [email protected]

Ganga MataCharitable Eye Hospital

Shabu James

Rectangle


Nasopharyngeal masses, though a domain of Ear nose and throat surgeons, occasionally perplex ophthalmologists

with varied presentations because of their close vicinity to the orbit. Nasopharynx marks the junction of oropharynx and nasal cavity. Tumors originating in this space are angio� bromas and carcinomas. Due to their aggressive and destructive nature they are rarely limited to the nasopharynx and usually extend to the nose, paranasal sinuses, pterygomaxillary fossa, infratemporal fossa, temporal fossa, cranium and even neck. Even the benign angio� bromas cause signi� cant structural and functional damage. The tumors may grow to substantial size before the symptoms are attributed to the actual disease.

Boundaries of nasopharynx: It is bounded anteriorly by posterior choanae and posterior part of nasal septum; posteriorly it communicates with oropharynx.; soft palate and part of hard palate form its � oor; basi sphenoid and basi occiput constitute the roof; laterally, pharyngeal end of eustachean tube is seen. Fossa of Rosenmuller is seen above and behind the pharyngeal end of eustachean tube. Nasopharyngeal carcinoma (NPC) commonly arises from fossa of Rosenmuller. Its apex is in close relationship with the carotid canal, and its base is closely related to skull base. Foramen lacerum lies medially.

Ocular involvement occurs in the form of neuroophthalmic manifestation with symptoms such as ocular pain, double vision, loss of vision and eye protrusion and signs such as ophthalmoplegia, exposure keratopathy and proptosis in various combinations1.

Nasopharyngeal angiofi bromas

The benign Juvenile nasopharyngeal angio� broma (JNA) are the most common benign neoplasms of the nasopharynx, with the propensity for aggressive local growth. This highly vascular tumor predominantly occurs in adolescent males. (Figure 1)

The triad of nasal obstruction, nasopharyngeal mass and recurrent epistaxis usually indicates an angio� broma. In a series of 218 JNA cases, 14% had exophthalmos, 5% had decreased visual acuity and 2% had partial ophthalmoplegia. Recognition of ocular involvement in JNA is of the utmost importance, for it is often a manifestation of orbital or intracranial extension or both. Early multidisciplinary diagnostic evaluation (otolaryngological, neurosurgical, and ophthalmological) followed by a team surgical approach to excision is most likely to yield ef� cacious results2.

Oculoplasty

Ruchi Goel

Ruchi Goel MS, DNB, FICS, Saurabh Kamal MS, DNB, Smriti Nagpal MBBS, Sushil Kumar MD, Sonam Angmo Bodh MS, DNB

Gurunanak Eye Center, Maulana Azad Medical College, New Delhi

The goal of treatment is to relieve symptoms and not to totally remove every bit of tumor. The usual indications for treatment are (1) hemorrhage, (2) nasal obstruction, and (3) orbital encroachment. CT and MRI are used to establish the diagnosis, to de� ne the extent of the tumor before biopsy, and to determine whether angiography is needed3.

Figure 1(a): A young boy showing right sided angio� broma 1(b): Fullness seen on

right side of palate


Resection of these tumors is carried out by lateral rhinotomy. The post operative complications themselves can result in nasolacrimal duct obstruction, exotropia and proptosis.(Figure 2)

The other modalities of treatment are radiation and embolization. The disadvantages of radiation therapy are thyroid carcinoma and radiation induced sarcomas; atrophic rhinitis; osteomyelitis; soft tissue necrosis; retardation of growth centers of face.

Nasopharyngeal carcinomas

The clinical manifestations and course of nasopharyngeal malignancies are closely related to the anatomical peculiarities of this region. The marked invasive and metastatic properties of nasopharyngeal carcinomas are responsible for its symptomatology. Most patients present in 5th-7th decade of life. Important avenues of communication exist between the nasopharynx and the posterior choanae, oropharynx, eustachian tubes and the base of the skull. (Figure 3) The tumor arising from nasopharynx may spread in the following directions:

• Anteriorly to nasal cavity, paranasal sinuses, pterygopalatine fossa and orbital apex.

• Posteriorly to the retropharyngeal space and node of Rouviere, destruction of lateral mass of atlas

• Laterally into the parapharyngeal space

• Prestyloid compartment with involvement of mandibular nerve, pterygoid muscles and in� ltration of deep lobe of parotid gland.

• Post styloid compartment causing vascular compression of carotid sheath, invasion of last four cranial nerves and cervical sympathetic nerves

• Superiorly through the body of sphenoid and sinus involving the parasellar structures and optic nerve, petrous apex and foramen lacerum. Cavernous sinus may be involved along with III, IV, V, and VI. The brain may also be affected by direct spread and not by hematogenous spread.

• Inferiorly into the oral cavity and retrotonsillar regions.

• Painless cervical lymphadenopathy because of its tendency for early lymphatic spread. Lateral

retropharyngeal node of Rouviere is the � rst echelon node. The � rst node to become palpable is the jugulodigastric node / apical node under the sternomastoid muscle. These are second echelon nodes. Ipsilateral and bilateral nodal involvement is common.

• Epistaxis: is commonly seen in advanced nasopharyngeal carcinoma with or without skull base erosion. It is not torrential in nature but only seen as blood tinged

Figure 3: CECT of brain, orbit and sinus showing a lobulated mass of nasopharyngeal carcinoma encroaching ethmoid sinus, right nasal cavity, right maxillary sinus, sphenoid

sinus, and orbit. The mass is breaking the � oor of anterior cranial fossa with intracranial extension.

Figure 2(a): CECT showing left nasopharyngeal angio� broma. 2(b): CECT after surgery2(c): Clinical picture of patient with left nasopharyngeal angio� broma showing the

lateral rhinotomy incision


mucous secretion. Nasal obstruction may also be seen in advanced cases. Ozaena may also be a feature of advanced nasopharyngeal carcinoma.

• Audiological symptoms like tinnitus, otalgia and deafness are common symptoms of nasopharyngeal malignancy and are caused by blockage to the nasopharyngeal end of eustachean tube by the tumor mass.

• Neurological symptoms like headache, cranial nerve palsy (any cranial nerve can be involved), and Horner’s syndrome.

• Distant metastasis to bone, lungs and liver.

The early manifestations of nasopharyngeal cancer are vague and, as a result the diagnosis is usually not established for six months or more after onset of symptoms.

Ocular symptoms and signs may be the only initial presentation of recurrent nasopharyngeal carcinoma. One must therefore be aware of possible tumor recurrence in patients with a prior history of nasopharyngeal carcinoma who present with symptoms of tearing or an eyelid mass, as this would enable prompt referral to the oncologist and otorhinolaryngologist4.The three main routes for orbital involvement in NPC patients can be as follows: (a) through cavernous sinus (the skull base) to superior orbital � ssure. (b) through paranasal sinus (particularly the ethmoid sinus). (c) through pterygopalatine fossa to inferior orbital � ssure5.

The most frequently affected nerves are the abducens and the trigeminal. 5-year survival in patients with cranial nerve involvement is 21% as compared to 55% in those without such lesions6. Though ophthalmologic involvement most often consists of sixth nerve palsy, later, complete ophthalmoplegia, epiphora, Horner`s syndrome, or a decreased corneal re� ex may become evident. Trotter`s triad consists of neuralgia of the second division of � fth nerve, ipsilateral palatal paresis, and decreased hearing. Direct tumor invasion of the orbit, with proptosis, is unusual7.

The treatment of primary nasopharyngeal carcinoma is external beam radiation therapy with or without chemotherapy. Both the necks need to be treated because of high incidence of neck disease bilaterally. Irradiation of an entire orbit during radiation therapy for nasopharyngeal carcinoma exposes the patient to severe radiation keratopathy. The mean latency may vary from 4-36 months. Its incidence is increased from 0% after doses less than 59 Gy to 100% after doses greater than 70 Gy8.

Recurrences in the neck when the primary tumor is controlled are treated by standard radical neck dissection without sparing the cranial nerve XI9. Treatment of recurrences at the primary site is treated by repeat radiation or nasopharyngectomy with neck dissection followed by radiation.

Nasopharyngeal tumors can thus present with diverse ocular signs and symptoms. Recurrence of these tumors is known to occur and the patients need a close watch life long. Due to their tendency to spread and cause nasal, otologic, ophthalmoneurologic, and metastatic sympyoms/signs, a multidisciplinary approach is required for management.

References1 Dunmade AD, Ademola-Popoola DS. Neuro-ophthalmic manifestation

of nasopharyngeal carcinoma at Ilorin: a � ve year review. Niger J Clin Pract. 2008 Dec;11(4):376-8.

2 Stern RM, Beauchamp GR, Berlin AJ. Ocular � ndings in juvenile nasopharyngeal angio� broma. Ophthalmic Surg. 1986 Sep;17(9):560-4.

3 McCaffrey TV, Neel HB III. Management of angio� bromas. In:Rhinology and sinus disease. A problem oriented approach edited by Schaefer SD. 1st ed. Mosby, Inc, USA,1998,pp 237-243.

4 Lee KY, Seah LL, Tow S, Cullen JF, Fong KS. Nasopharyngeal carcinoma with orbital involvement. Ophthal Plast Reconstr Surg. 2008 May-Jun;24(3):185-9.

5 Long W, Wang L, Luo X. Clinical and MRI diagnosis of nasopharyngeal carcinoma with orbital spread. Zhonghua Yan Ke Za Zhi. 2001 Jul;37(4):295-7. Chinese.

6 Turgman J, Braham J, Modan B, Goldhammer Y. Neurological complications in patients with malignant tumors of the nasopharynx. Eur Neurol. 1978;17(3):149-54

7 Toomey JM. Cysts and tumors of the pharynx. In: Otolaryngology Head and neck. Edited by Paparella MM, Shumrick DA. Volume 3, 1973, WB Saunders Company, pp 341-371.

8 Kwok SK, Ho PC, Leung SF, Gandhi S, Lee VW, Lam DS, Ngan IC, Ming JL. An analysis of the incidence and risk factors of developing severe keratopathy in eyes after megavoltage external beam irradiation. Ophthalmology. 1998 Nov;105(11):2051-5.

9 Wei WI, Ho CM, Wong MP, et al. Pathological basis of surgery in the management of postradiotherapy cervical metastasis in nasopharyngeal carcinoma. Arch Otolaryngol Head Neck Surg 1992;118:923-929.

Pls contact : Dr. Satyawan Sharma Sharma Eye Clinic &

General Hospital Opp. Civil Hospital, Jind (Haryana) Mobile : 094161 86614

� Phaco Machine Galaxy-1, Appa Swamy,

with two hand piece

� Operating Microscope Guardian Opline

Shabu James

Rectangle


Figure 1

One of the most dif� cult task for an ophthalmic surgeon is the management of Uveitic cataract. Cataract in Uveitis

may develop as a result of the intraocular in� ammation, from chronic corticosteroid usage, or more often from both.

This patient of Uveitis with cataract may have come to you as a referral from one of your colleague for phaco surgery or he is one of your own chronic patient which you are following and treating for recurrent Uveitis for many years, now for cataract operation.

Cataract Surgery in Uveitis

The Uveitis eye poses numerous surgical challenges –

• Small pupil,

• Shallow anterior chamber,

• Posterior synchaie,

• Peripheral anterior synchaie,

• Pupillary membranes and

• Zonulolysis.

Pre operative Ocular Examination & investigationA detailed slit lamp examination prior and after cycloplogic drops. Presence of anterior and posterior , Papillary membrane, operable cataract, KP’s, Intra ocular pressure.

Blood ExaminationSugar, ESR, TLC, DLC & Specially for Toxoplasmosis, Syphilis, TB, Rheumatoid Arthritis, B-Scan Sonography, OCT etc.

Control of Pre Operative in� ammation – Optimal time for cataract surgery is - the eye should have been quiescent for 3-4 months prior to surgery.

Good councelling of Patient prior to surgery is important. Patient and attendant should be well aware of the possible complication during and after the surgery.

Surgical Techniques – Standard phaco emulsi� cation with lens implant or phaco with vitractomy(if needed) for a better visual outcome.

Anaesthesia

• Peribulber

• Parabulber

• lignocaine 2% + Marcaine

Cataract

Mahesh Punjabi

Mahesh Punjabi MSKota Eye Hospital, Kota, Rajasthan

Incision

A scleral or temporal clear corneal/Limbal incision may be used. However, the incision should be of adequate length in order to prevent iris prolapse in eyes with small or stretched pupils.Pupil enlargement & Expansion- • Injecting BSS with adrenaline (1:1000 0.5ml adrenaline in 500ml)• Using Iris Retractor

Figure 2


Figure 3

• Malyugin Ring• High Viscoelastic Rhexis Formation & Removal of any membrane in pupillary area and to break the synaechie. Rhexis formation is the greatest challenge. Use of blue dye helps in making good and optimum rhexis.Removal pupillary membrane with help of high visco elastic & rhexis forceps

Nuclear management

Cataract can be removed with standard phaco technique with in the bag lens implant. Irrigation & aspiration - Remove the iris retractor and visco elastic from anterior chamber. Minimum manipulation will give you a very quite eye next morning.

Types of IOL implant

My choice of lens is always single piece hydrophobic acrylic.Complications that may arise from the problems include an undersized or incomplete capsulorhexis, iris prolapse, increased risk of posterior capsular rent, increased risk of intra operative ocular dehiscence, Hypotony & Hyphaema. With modern day cataract surgical techniques, these complication are very much reduced.

Intra Operative Complications

• Zonulolysis • Retained Nuclear Fragments

Early Post Operative Complications

• Excessive In� ammation• IOP Variations • Recurrent Uveitis

Late Post operative Complications

• PCO• Pupil Capture

Figure 4

Figure 5 Figure 6

Figure 7


Figure 8

eliminate longer use of steroids.

Management of post - operative complications especially in� ammation and glaucoma, earlier rather than later, has also contributed to improved outcomes.

Conclusion

Management of the uveitic cataract requires careful case selection, proper timing of surgery, meticulous surgery and close monitoring with appropriate handling of the postoperative complications that may occur. These eyes can achieve good outcomes with proper management

References

1 Rojas B, Za� rakis P, Foster CS. Cataract surgery in patients with uveitis Curr Opin Ophthalmol 1997;8:6-12.

2 Tabbara KF, Chavis PS. Cataract extraction in patients with chronic posterior uveitis. Int Ophthalmol Clin 1995;35:121-31.

3 Hooper PL, Rao NA, Smith RE. Cataract extraction in uveitis patients. Surv Ophthalmol 1990;35:120-445.

4 Okhravi N, Lightman SL, Towler HM. Assessment of visual outcome after cataract surgery in patients with uveitis. Ophthalmology 1999;106:710-22.

5 Foster CS, Barret F. Cataract development and cataract surgery in patients with juvenile rheumatoid arthritis -associated iridocyclitis. Ophthalmology 1992;100:809-17.

6 Foster CS, Fong LP, Singh G. Cataract surgery and intraocular lens implantation in patients with uveitis. Ophthalmology 1989;96:281-88.

7 Dana MR, Chatzistefanou K, Schaumberg DA, Foster CS.Posterior capsule opaci� cation after cataract surgery in patients with uveitis. Ophthalmology 1997;104:1387-393; Discussion 1393-394.

A careful step-by-step surgical procedure can eliminate all the above possible complications.

One should monitor the IOP variation in early and late post operative period. Persistent high IOP will not allow the eye to become quite for a very long time. Good posterior Capsule polishing will delay the YAG capsulotomy for a very long time which is very important in these cases.

Regime of post operative medicationTopical & Systemic Steroids, Cycloplegics, NSAID Drops, IOP Lowering drops (if needed).

Immunosuppressive agents other than steroids also helps control in� ammation. Long-term use of these agents can

Two - Full time eye surgeons (MS/DNB/DO)

If you are expert in cataract surgery (SICS/PHACO) can maintain OPD and have flair for community service – an attractive salary (Plus Perks) are awaiting for you. Apply in confidence with full biodata with photo to:

A well established fast growing eye hospital with facilities for all types of eye operations (Phaco/SICS/DCR/RD). Future planning for Laser, Perimeter, Fundus Camera etc. to make it a super speciality eye hospital

Dr. J.K. PurangDirector

A-114, Vishal Enclave, Rajouri Garden, New Delhi – 110 027

(M): 9811021192, Email: [email protected]

Eye Surgeon

Swami Bhajnanand Eye Hospital, Mainpuri (U.P.)

Shabu James

Rectangle


Accommodative esotropia is a condition where in excessive effort of accommodation results in an inward

deviation of the eyes. Most often it is caused by uncorrected Hypermetropia.

Acquired Esotropia in a visually immature child is a day time emergency. The consequences are loss of Binocular vision & onset of amblyopia. The interval between the time of onset & the treatment determines the visual outcome.

Classifi cation

Accommodative esotropia can be classi� ed into

• Fully accommodative or Refractive Accommodative Esotropia

• Non- Refractive Accommodative Esotropia due to High AC/A

• Partially Accommodative (Mixed) Esotropia1

Fully accommodative or Refractive Accommodative

Esotropia

Accommodative Esotropia which is fully corrected by optical correction of Hypermetropia is called Refractive Accommodative Esotropia.

These children will initially be normal with straight eyes. Around the age of 18 to 24 months, they try to accommodate to clear the retinal image blur. In the process there is excessive convergence. If the child’s fusional divergence is good, it may result in an Esophoria. On the other hand if the Fusional divergence amplitudes are weak, the child develops Esotropia.

Clinical Features• Onset 2-3 yrs of age; but can occur at any age

• Initially intermittent & variable �

Diplopia�

Within 2-3 days suppression �

Longer duration leads to Anomalous retinal correspondence

• Develop amblyopia if uncorrected

• Normal AC/A ratio

• Hypermetropic refractive error (usually between +2 D to +6 D)

Squint

Arun Samprathi

Arun Samprathi DO, DNB, FRCS EdSamprathi Eye Hospital and Squint Centre, Railway Parallel Road, Kumara Park West, Bangalore

TreatmentFull refractive correction is prescribed, so that binocular vision can be restored6,7. Child should wear the refractive correction at all times. If not, child will not relax the accommodation & vision will be blurred with glasses.

Amount of hyperopic correction depends on the age of the patient.

• In Infants < 6 m with Esotropia

Adopted from Binocular Vision and Ocular Mobility: Theory and Management of Strabismus, Gunter K. Von Noorden2


• Any hyperopia of > 2.0 D needs glasses

• Full cycloplegic readings with an addition of +1.5D is prescribed

• In children from 6 months to 4 yrs with Esotropia

• Hypermetropia of > 1.5 D should be fully corrected

• In children above 4 yrs with Esotropia

• Goal is to achieve esophoria

• Maximal plus lens which provides binocular vision with maximal visual acuity is prescribed (but tropia should be corrected)

If after prescribing full hyperopic correction Esotropia is reduced to < 10PD, child continues with glasses. On the other hand if there is residual Esotropia, then we are dealing with Partially Accommodative Esotropia & residual angle needs surgical correction.

Non-Refractive Accommodative Esotropia

• Esotropia greater at near than distance caused by a high AC/A ratio

• Near point of accommodation is normal

Mechanism is an abnormal synkinesis between Accommodation & accommodative convergence – hence excessive convergence with each diopter of Accommodation.

Clinical Features• Age of onset: 6m to 3 yrs

• Deviation –initially small & intermittent

• Suppression occurs early with ARC

• Hypermetropia, myopia or emmetropia

Differentiating features from refractive accommodative esotropia

• No or small deviation at distance; large ET at near with accommodative target

• High AC/A Ratio

• Nervous & emotional children

Figure 1Figure 2: Accommodative esotropia

–without & with glasses

Figure 3: Distance � xation with hyperopic correction

Figure 4: Near � xation with hypermetropic correction


Treatment

Goal of treatment

• To keep the eyes as straight as possible at all distances during the visually immature years

3 Step treatment

• Maximum plus lens for optimal vision

• Eliminate amblyopia

• Measure deviation at distance with full correction in place & decide on the next step

In patients with fusion potential

• If Esotropia is < 10 PD at distance – Bifocals

• If Esotropia is > 10 PD at distance -

• no chance of developing any fusion unless deviation is reduced to < 10 PD

• Bimedial recession is necessary

In patients without any fusion potential

• No use of prescribing bifocals as they have no fusion at distance & hence left alone

Partially Accommodative Esotropia

Partially accommodative Esotropia is a condition where in the child has Esotropia with Hypermetropia, but there is

Figure 5: With the Bifocals

residual Esotropia despite prescribing the full correction at distance & near.

Treatment involves surgery for the residual angle not corrected with hyperopic correction. Bimedial recession is the most commonly used surgical strategy.

Decision Making in Concomitant Esotropias

In the work up of a Concomitant Esotropia, though all steps of strabismus evaluation has to be done, only the following three points are of paramount importance for management.

• Control of Esotropia for distance � xation

• Prism Bar alternate cover tests with accommodative target for distance & near

• Cycloplegic refraction

References

1 http://www.nei.nih.gov/news/statements/cemas.pdf.2 Binocular Vision and Ocular Mobility: Theory and Management of

Strabismus, Gunter K. Von Noorden, Ed., 5th Edition, Mosby, St. Louis, Mo. 1996

3 Harley’s Pediatric Ophthalmology, Leonard B. Nelson, Ed., 4th Edition, W.B. Saunders, Philadelphia, PA 1998.

4 Management of Strabismus and Amblyopia: A Practical Guide, John Pratt-Johnson and Geraldine Tilson, Thieme Medical Publishers, New York, NY 2000.

5 Rutstein RP. Update on accommodative esotropia. Optometry. Aug 2008;79(8):422-31.

6 Li CH, Chen PL, Chen JT, Fu JJ. Different corrections of hypermetropic errors in the successful treatment of hypermetropic amblyopia in children 3 to 7 years of age. Am J Ophthalmol. Feb 2009;147(2):357-63.[Medline].

7 Cho YA, Yi S, Kim SW. Clinical evaluation of cessation of hyperopia in 123 children with accommodative esotropia treated with glasses for best corrected vision. Acta Ophthalmol. Aug 27 2008.

Decision making in Esotropia

Congratulations to Dr. A.K. Grover on being elected as the President of the Asia Paci� c Society of Oculoplastic & Reconstructive Surgery (APSOPRS), the � rst Indian to be elected to this coveted post.

Congratulations


The greatest ongoing challenge faced by refractive surgeons is identifying patients who are at risk of developing

ectasia after LASIK. Corneal ectasia is a rare but potentially serious complication of refractive surgery and occurs more commonly after laser in situ keratomileusis (LASIK). After LASIK, the cornea is structurally weakened, not only by the laser central stromal ablation but also by the creation of the � ap. The cornea may assume an irregular conical shape, and this leads to a decrease in visual acuity secondary to high irregular astigmatism, as occurs in primary ectatic corneal disorders such as keratoconus. Even though corneal ectasia is infrequent after LASIK, it can have a profoundly negative effect on the refractive properties of the cornea1,2 (Figure 1).

The cause and the biomechanical changes that induce keratectasia after refractive surgery are unknown. The cause of corneal ectasia has not been clearly established, although collagen abnormalities, as seen in keratoconus, have been reported. The disease usually evolves with progressive deterioration in uncorrected distance visual acuity (UDVA) and corrected distance visual acuity (CDVA) caused by the irregular astigmatism. Incidence ranges from 0.04 to 0.6%. Post Lasik Ectasia has both medical and medicolegal implications2.

Risk Factors1,2

• Forme Fruste Keratoconus

• Abnormal pre-op topography

• Low residual stromal bed (RSB)

• Young Age

• Low pre-operative corneal thickness

• High Myopia

Low Residual Stromal Bed (RSB)

Minimum Residual Stromal Bed should be 280 microns. As � ap thickness varies widely with mechanical microkeratome, Intra operative pachmetry is important initially to become familiar with performance of the microkeratome. The RSB should not be < 55% of the thinnest location on the cornea and the ablated amount should be <18% of the thinnest location

Ectasia Risk Score System is a scoring system based on Topography, RSB, Age of patient, Degree of Myopia and corneal thickness. The higher the score the more the risk for ectasia.

Pentacam indices Index of surface variance (ISV), Index of vertical asymmetry (IVA), Keratoconus index (KI), Central

Refractive Surgery

Ramendra Bakshi

Ramendra Bakshi MS, FRCSCornea and Refractive Surgery, Centre for Sight, New Delhi

Keratoconus Index (CKI), Index of height Asymmetry (IHA), Index of height decentration (IHD), Rmin, Aberration coef� cient(ABR) are valuable indices to look out for early evidence of ectasia.

BAD (Belin and Ambrosio’s Enhanced Ectasia Display) This is a keratoconus index, based on pachymetry and elevation. BAD II 5 new terms (D values for standard deviation from the mean) representing the front surface (Df ), back surface (Db), pachymetric progression (Dp), thinnest point (Dt), and thinnest point displacement (Dy). A sixth term (D) is the � nal overall map reading taking each of the � ve parameters into account. The parameter is indicated in YELLOW (suspicious) when it is � 1.6 SD from the mean and turns RED (abnormal) at � 2.6 SD from the mean.

Biomechanics

Tensile strength greatest in the anterior 1/3 rd and lowest in posterior 2/3 rd of cornea. The corneal � ap does not contribute to the tensile strength of cornea. Pre-operative corneal hysteresis (CH) and dynamic corneal imaging may serve to identify patients at risk for ectasia3.

Histopathology

Histologic � ndings suggest that post-LASIK keratectasia results in collagen � bril thinning and decreased inter� bril distance within the residual stromal bed. Overexpression of MMPs in keratoconus, absent in post-lasik ectasia corneas Discrepant results between keratectasia and keratoconus suggest that the pathogenesis of the 2 conditions differ4.

Management

• Rigid gas-permeable contact lenses

• Collagen crosslinking

• Intrastromal corneal ring segment (ICRS)

• Simultaneous CXL with ICRS

• Deep lamellar keratoplasty (DALK)

CXL

Collagen crosslinking has emerged as a promising technique to slow or stop the progression of post-LASIK ectasia. The interaction of ribo� avin and UVA causes the formation of reactive oxygen species, leading to the formation of additional covalent bonds between collagen molecules, with consequent biomechanical stiffening of the cornea. Post Lasik ectatic corneas may not have as robust a response to CXL


as keratoconus corneas. Biomechanical differences caused by the LASIK � ap; possible differences in the ribo� avin diffusion rate in post-LASIK corneas, especially at the � ap interface; and intrinsic pathophysiologic differences between keratoconus and ectasia may all contribute to the different responses to CXL between the 2 groups.

Lasik Xtra

The aim of the procedure is to resore strength to the cornea during a LASIK procedure in high risk cases. After the refractive correction has been made in a standard Lasik procedure, Avedro’s ribo� avin formulation, VibeX Xtra (0.25% Ribo� avin, Saline, Isotonic)

is applied to the exposed stroma and the � ap is replaced. UVA illumination from KXL (accelerated cross linking) is then applied through the intact epithelium for little over a minute.

Lasik Xtra poses no material interruption to the normal speed and � ow of the Lasik procedure and does not increase patient discomfort. Lasik Xtra’s strengthening may be applicable to all current Lasik patients, as well as post-Lasik patients who are suffering from corneal ectasia or who are interested in restoring the strength to their cornea5.

Intracorneal Rings

Composed of 2 clear segments, each having an arc length of 150 degrees. Made of PMMA and available in 11 thickness from 0.210mm - 0.450mm. The determination of which thickness of the INTACS segment to implant depends upon, pre-operative manifest refraction, spherical equivalent,

location of the cone and degree of assymetric astigmatism6,7 (Figure 2).

Pallikaris et al, 2010 have shown that INTACS SK (severe keratoconus or steep “K”) improves visual acuity in patients with post-laser in situ keratomileusis corneal ectasia6.

Pinero et al, 2009 have shown that Intracorneal ring segment implantation is a useful option for the treatment of coma-like aberrations and astigmatism in post-LASIK corneal ectasia8.

Figure 2: Single Intacs Segment for a patient with Post Lasik Ectasia

Figure 1: Pentacam of a patient with Post Lasik ectasia


Pokroy et al, 2004 have shown that Implantation of a single Intacs segment inferiorly appeared to improve progressive myopia and regular and irregular astigmatism in eyes with corneal ectasia after LASIK9.

Sequential or Simultaneous?

ICRS can be combined sequentially or simultaneously with CXL. CXL stops or slows the progression of the ectatic process without signi� cantly changing its shape, whereas, ICRS implantation signi� cantly � attens and regularizes the cornea. A stiffer cornea that has been treated by CXL decreases the � attening effect of ICRS implantation, thus restricting its effect and decreasing the maximum � attening potential.

Coskunseven et al have compared the effect of treatment sequence for ICRS and CXL. They concluded that to achieve the maximum overall effect, ICRS implantation should be performed � rst or simultaneously so the segments can reshape the cornea without restriction. The CXL treatment then can be applied to further � atten the cornea and to stabilize corneal biomechanics10.

Deep Anterior Lamellar Keratoplasty (DALK)

DALK is a good option for patients with advanced post – lasik ectasia.This is an extra ocular procedure and thus avoids possible intraocular damage. No postoperative intraocular complication - anterior synechiae of iris or secondary glaucoma. This also limits postoperative astigmatism and rehabilitation time. In DALK donor endothelium is not a consideration hence, the risk of endothelial rejection is virtually nil eliminated. The technique permits use of large diameter grafts (9.0-11.0 mm.) in which the residual astigmatism is generally low as compared to penetrating keratoplasty. The corticosteroids can be tapered off fast so minimal risk of corticosteroid related complications. The follow up is easier as compared to PK11 (Figure 3).

Conclusion

Corneal ectasia is an infrequent but potentially serious complication of refractive surgery. Careful Patient Selection is extremely important. As we refractive surgeons develop strategies for preventing ectasia, we should also focus on improving our ability to interpret corneal topography. Rigid gas-permeable contact lenses, Collagen crosslinking, intrastromal corneal ring segment (ICRS) implantation and deep lamellar keratoplasty are the various options available.

Figure 3: DALK for Post Lasik Ectasia

References

1 Randleman JB, Woodward M, Lynn MJ, et al. Risk assessment for ectasia after corneal refractive surgery. Ophthalmology. 2008;115:37-50.

2 William B Trattler, Predicting Ectasia After LASIK Cataract and Refractive Surgery Today; August 2008

3 David A Luce, devices for measuring corneal biomechanical properties:Determining in vivo biomechanical properties of the cornea with an ocular response analyzer ; J Cataract Refract Surg 2005; 31:156*16235:2084–2091

4 Meghpara et al, Keratectasia After Laser In Situ Keratomileusis: A Histopathologic and Immunohistochemical Study. Arch Ophthalmol. 2008 December ; 126(12): 1655–1663

5 Celik HU,Accelerated corneal crosslinking concurrent with laser in situ keratomileusis. J Cataract Refract Surg. 2012 Aug;38(8):1424-31.

6 Kymionis GD, Bouzoukis DI, Portaliou DM, Pallikaris IG. New INTACS SK implantation in patients with post-laser in situ keratomileusis corneal ectasia. Cornea. 2010 Feb;29(2):214-6.

7 Kymionis GD et al,Management of post-LASIK corneal ectasia with Intacs inserts: one-year results. Arch Ophthalmol. 2003 Mar;121(3):322-6.

8 Piñero DP, Alio JL, Uceda-Montanes A, El Kady B, Pascual I. Intracorneal ring segment implantation in corneas with post-laser in situ keratomileusis keratectasia.Ophthalmology. 2009 Sep;116(9):1665-74

9 Pokroy R, Levinger S, Hirsh A. Single Intacs segment for post-laser in situ keratomileusis keratectasia. J Cataract Refract Surg. 2004 Aug;30(8):1685-95.

10 Efekan Coskunseven, MD, Effect of treatment sequence in combined intrastromal corneal rings and corneal collagencrosslinking for keratoconus. J Cataract Refract Surg 2009; 35:2084–2091

11 Javadi MA, Feizi S. Deep anterior lamellar keratoplasty using the big-bubble technique for keratectasia after laser in situ keratomileusis. J Cataract Refract Surg. 2010 Jul;36(7):1156-60.

NoticeThis to inform all concerned that the life membership fees for membership of the Delhi Ophthalmological Society has been raised from Rs. 3,100/- to Rs. 5,100/-. This is applicable w.e.f.14th June, 2012.Dr. Harbansh Lal Dr. Rohit SaxenaPresident Secretary


Doxycycline (�-6 deoxy-5-hydroxytetracycline), an orally administered drug, is a metal ion chelator

and a broad spectrum antibiotic. It has shown to possess immunomodulatory properties in addition to its broad-spectrum antimicrobial activity1. Doxycycline is a potent inhibitor of MMP enzymes, particularly MMP-8 and MMP-9 along with IL-1 which is a potent proin� ammatory cytokine.

Doxycycline is shown to have varying degrees of success in treating patients with rheumatoid arthritis.2,3 It is also a recommended treatment for patients with ocular surface diseases, particularly recurrent epithelial cell erosion,4,5 Ocular rosacea,6 and keratoconjunctivitis sicca.7 In the latter cases, success has been attributed to the inhibition of tear � lm MMP and interleukin-1 (IL-1) synthesis.

Mechanism of Action

Doxycycline is composed of a four-ring core with attached side groups (Figure 1). The dimethylamino group at the C4 carbon on the upper half of the molecule is necessary for antimicrobial activity. The oxygen-rich lower half of the molecule is critical for binding to both prokaryotic and eukaryotic targets, and interference with this region reduces or eliminates the effectiveness of the drug. This region is relevant as site for metal ion chelation. It prevents access of acyl t-RNA to the acceptor site on the mRNA-30s ribosomal subunit complex, inhibiting protein synthesis, thus exerting its antibiotic action.

In addition to its established functions as an antibiotic, other properties that have recently been ascribed to doxycycline are:

Cornea

Manisha C. Acharya

Manisha C. Acharya MS, DNB, Sonia Sharma MS, Umang Mathur MS, Jyoti Garg MSDr.Shroff’s Charity Eye Hospital, Daryaganj, New Delhi

• Differential inhibition of the activity of members of the matrix metalloproteinase (MMP) family. The mechanism by which doxycycline inhibits MMPs has not been completely elucidated. It is believed that it exerts its anti-proteolytic effects by both direct inhibition of MMPs and by inhibiting their expression and synthesis. Direct inhibition of MMPs appears to be mediated by an interaction between the doxycycline molecule and Zn2+ ions within the MMP. This causes chelation of these structural and catalytic ions within the enzyme8 (Figure2).

• Inhibition of interleukin-1 synthesis

• Inhibition of activated B cell function

• Inhibition of nitrous oxide (NO) synthesis by lipopolysaccharide (LPS) activated macrophage

Antiinfl ammatory Actions of Doxycycline• Inhibition of MMP (Collagenase)Activity

• Inhibition of MMP synthesis

• Inhibition of interleukin-1 synthesis

• Inhibition of activated B cell function

• Inhibition of nitrous oxide (NO) synthesis by lipopolysaccharide (LPS) activated macrophages.

Role of MMP’ s in Ocular surface injury

The matrix metalloproteinases (MMPs) are a family of zinc and calcium ion dependent enzymes of differing substrate speci� city but similar structure and catalytic mechanism. Physiologically, these enzymes participate in tissue remodelling and, pathologically, they cause disruption or disintegration of extracellular matrices.

The in� ammatory cells mainly neutrophils and macrophages play an essential part in corneal melt which requires the presence of an enzyme that can hydrolyse type I collagen, the main structural component of the corneal stroma.

It has been shown that patients with anterior segment diseases inducing an in� ammatory response in eye like PUK contain MMP’s in the tears as well as in cornea.10 The main source of these enzymes appears to be the granulocyte fraction of white blood cells that accumulate at sites of ocular surface in� ammation. These MMP’s cause major ocular tissue disruption leading to corneal melt. It has also been shown that these in� ammatory cell MMP’s can activate the endogenous MMP synthesis in the keratocytes.9,10

Figure 1: Doxycycline- chemical structure


Uses of Doxycycline in Ocular ConditionsEstablished uses Potential usesPeripheral ulcerative keratitis PterygiumInfective Keratitis Choroidal

neovascularizationChemical Burns KeratoconusMeibomian Gland DiseaseDry EyeRecurrent Corneal Erosions

Use of doxycycline in Ocular Conditions

Peripheral ulcerative keratitisPeripheral ulcerative keratitis (PUK) is a chronic, progressive ocular manifestation of rheumatoid arthritis and other similar systemic diseases. This disorder typically progresses from a gradual thinning and melt of the peripheral corneal stroma to the formation of a perforation prone gutter. Activated matrix metalloproteinase I (MMP-I or collagenase I), the enzyme that exhibits speci� city for type I collagen, the major component of the corneal extracellular matrix, has long been implicated as a causative agent of PUK10. Although treatment for PUK relies heavily upon long term systemic immunosuppressive therapy, still it may not prevent corneal perforation probably because of the continued existence of activated proteases and/or in� ammatory cells within the host corneal matrix. In such cases Doxycycline has a role as it inhibits these proteases decreasing the chances of stromal melting.

Infective keratitisThe treatment of infective keratitis is not only to sterilize the ulcer but also to maintain the integrity of cornea. Ulcerative processes can proceed in some cases, despite the absence of microbes, as a result of remaining corneal and tear � lm MMPs. Combining antibiotic therapy with MMP inhibitors like doxycycline can speed corneal healing, because MMPs play an important role in corneal ulceration and stromal liquefaction.

Chemical injury After a chemical injury pH changes of ocular surface causes in� ammation leading to release of proteolytic enzymes which include MMPs, collagenases which in turn cause ulceration

Figure 2: Mechanism of action of Doxycycline

Figure 3: Peripheral Ulcerative Keratitis

and corneal melting. Oral doxycycline treatment protects cornea from melting by inhibiting these proteases.

Meibomian gland diseaseChronic meibomian gland dysfunction particularly affects the lipid layer of tear � lm, destabilizing the tear � lm and quickening the tear � lm’s evaporation, and ultimately causes many disorders of the external eye, including dry eye syndrome. Most of the times it is more of in� ammation of meibomian glands than infection itself. In order to treat this dysfunction, 100-200 mg twice-daily doxycycline that inhibits collagenase and also has antiin� mmatory effects is given improving patients symptoms by stabilizing the lipid layer of tear � lm.

Dry eyeTear hyperosmolarity is regarded as a central mechanism in dry eye. Hyperosmolarity causes damage to the surface epithelium by activating a cascade of in� ammatory events and the release of in� ammatory mediators like MMP’s, IL-1 and TNF� into the tear � lm which in turn causes corneal epithelial damage involving cell death by apoptosis, a loss of goblet cells, and a reduction in mucus secretion, and leads to tear � lm instability.

Oral Doxycycline has a protective role to ocular surface as it has been demonstrated that it decreases tear� lm MMP

Figure 4: Bacterial keratitis


activity signi� cantly directly and indirectly by inhibiting its production from epithelial cells11.

Recurrent corneal erosionsIt has been observed that oral Doxycycline fastens the healing of recurrent epithelial erosions4 and decreases their frequency as well probably by stabilizing Bowman’s membrane and epithelium adhesions.

Future Potential of Doxycycline

PterygiumPterigia are wing-shaped lesions have a propensity to migrate into Bowman’s layer toward the central cornea and distort or obscure vision. In the initial phases of this disorder, it is believed that altered limbal basal epithelial cells invade onto normal corneal basement membrane over a dissolving Bowman’s layer.

Elevated levels of matrix metalloproteinases such as MMP-1, MMP-2 and MMP-9 have been localized in cells at the base of the cornea (pterygium leading edge) and are most likely responsible for the destruction of Bowman’s layer and the local in� ltration of pterygium cells within adjacent epithelial tissue.

Cox CA etal12 have demonstrated that doxycycline inhibited pterygium cell-derived gelatinolytic activities, migration of pterygium epithelial cells, and pterygium cell-mediated angiogenesis in their pterygium murine model.

Choroidal NeovascularizationCNVM is associated with many ocular conditions like ARMD, ocular histoplasmosis syndrome, high myopia, angioid streaks namely. It has been seen that MMP-2 and MMP-9 localize to Bruch’s membrane in areas of new vessel formation, with MMP-9 having the greatest expression at the margins of CNV membranes. The importance of these enzymes in the progression of CNV is evident from genetic and chemical experiments with animal models.

It has been demonstrated that ablation of the mmp-2, mmp-9 or double mmp-2/mmp-9 genes inhibits formation of CNV complexes induced by breakage of Bruch’s membrane. MMP-2 and MMP-9 can also target pigment epithelium-derived factor (PEDF), a potent anti-angiogenic factor, and abolish its biological actions13.

Doxycycline effectively inhibits the progression of CNV, inhibits the activity of gelatinases MMP-2 and MMP-9,

Figure 5: Meibomian gland disease

Figure 6: Dry Eye (a): Severe (b): Mild

(a)

(b)

and increases the levels of PEDF, all of which participate positively or negatively in CNV development.

KeratoconusThe activation of matrix metalloproteinase-2 (MMP-2) is postulated to be a crucial pathogenic factor behind progressive and chronic diseases in which basement membranes are disrupted including keratoconus. It has been shown that the MMP production is signi� cantly more in keratocytes devied from keratoconic corneas as compared to keratocytes from normal corneas14.

Figure 7: Pterygium


MMP inhibitors like doxycycline may have a role in slowing the progression of keratoconus which should be evaluated in future.

Conclusion

It is very evident that Doxycycline is a drug which is very useful in protecting ocular surface from in� ammation which works wonders in many cases in our daily practice as an ophthalmologist. It has proven its worth to be more than just an antibiotic and a lot more needs to be explored.

References1 SmithVA ,CookSD. Doxycycline—a role in ocular surface repair Br J

Ophthalmol. 2004 May; 88(5): 619–625. 2 Nordstrom D, Lindy O, Lauhio A, et al. Anti-collagenolytic mechanism

of action of action of doxycycline treatment in rheumatoid arthritis. Rheumatol Int 1998;17:175–80.

3 Van der Laan, Molenaar E, Ronday K, et al. Lack of effect of doxycycline on disease activity and joint damage in patients with rheumatoid arthritis. A double blind, placebo controlled trial. J Rheumatol 2001;28:1967–74.

4 Durson D, Kim MC, Solomon A, et al. Treatment of recalcitrant recurrent corneal erosions with inhibitors of matrix metalloproteinase -9, doxycycline and corticosteroids. Am J Ophthalmol 2001;132:8-13.

5 Hope-Ross MW, Chell PB, Kervick GN, et al. Oral tetracycline in the treatment of recurrent corneal erosions. Eye 1994;8:384–8

6 Frucht-Pery J, Sagi E, Hemo I, et al. Ef� cacy of doxycycline and tetracycline in ocular rosacea. Am J Ophthalmol 1993;116:88–92.

7 Culbertson WW, Huang AJ, Mandelbaum SH, et al. Effective treatment of phlyctekeratoconjunctivitis with oral tetracycline. Ophthalmology 1993; 100:1358–66.

8 Grif� n MO, Fricovsky E, Ceballos G, Villarreal F. Tetracyclines: a pleitropic family of compounds with promising therapeutic properties. Review of the literature. Am J Physiol Cell Physiol. 2010 Sep;299(3):C539-48. Epub 2010 Jun 30.

9 V A Smith, H Rishmawi, H Hussein, D L Easty.Tear � lm MMP accumulation and corneal disease Br J Ophthalmol 2001;85:147-153 doi:10.1136/bjo.85.2.147

10 V A Smith, H B Hoh. Role of ocular matrix metalloproteinases in peripheral ulcerative keratitis Br J Ophthalmol 1999; 83:1376-1383 doi:10.1136/bjo.83.12.1376.

11 Lemp AM,Foulks GN. The De� nition & Classi� cation of Dry Eye Disease.Guidelines from the 2007 International Dry Eye Workshop

12 Cox CA etal. Doxycycline’s Effect on Ocular Angiogenesis: an In Vivo Analysis Ophthalmology. 2010 September; 117(9): 1782–1791.

13 Samtani S, Amaral J, Campos MM, Fariss RN, Becerra SPDoxycycline-mediated inhibition of choroidal neovascularization.Invest Ophthalmol Vis Sci. 2009 Nov;50(11):5098-106. Epub 2009 Jun 10.

14 Smith VA, Easty DL. Matrix metalloproteinase-2: Involvement in keratoconus. Eu J Ophthalmol 2000;10:215–26

Venue: Auditorium, PGIMER Building, Dr. RML Hospital, New Delhi Date & Time: 30th September, 2012 (Sunday)

Breakfast & Registration 10:00 a.m.

Clinical Session: 11:00 onwards

Clinical Cases:1. Von Hippel-Lindau Disease : Dr. Piyush Ramavat 10 mins. Discussant : Dr. Mukesh Sharma2. Rare orbital tumour : Dr. Malvika Gupta 10 mins. Discussant : Dr. Rachna Meel

Clinical Talk:Work up of a case of proptosis : Dr. Deepa Sharma 20 mins.

Mini Symposium: Humphrey Visual FieldsChairperson: Prof. Shashi Vashisht, Co-chairperson: Prof. Praveen Malik

1. Getting your basics right : Dr. M.D. Singh 20 mins.2. Interpreting single � eld : Dr. Taru Dewan 20 mins.3. Detecting progression : Dr. Suneeta Dubey 20 mins.

20 Early Bird prizes for members arriving before 11.00 A.M

Lunch: 1:30 p.m. Sponsored by: M/s. Allergan India


Trabeculectomy for glaucoma has recently been found to achieve target intraocular pressure (IOP) and to prevent

progression of visual loss in 80% to 90% of those undergoing surgery. Although the failure rate is low, between 2.1% and 6.2% of the blebs fail in early / late (after a number of years) post operative period.Blebs can be -

Functional Bleb

Have a good IOP control

Failing Bleb / Failed Bleb

Have inadequate IOP control & an impending or established obstruction to aqueous out� ow.

Features of functional and failing bleb

Good & Successful Bleb is the one which is moderately elevated, microcystic, avascular and diffuse (Figure 1&2). Failing or Failed Bleb is the one which has increased vascularity – Cork screw vessels, (Figure 3) high IOP, encapsulated - high dome appearance, (Figure 4) � at - localized, absence of microcystFailing Bleb can be divided as –

Early failure - failing within 1 month

Late failure - adequate IOP control with good Bleb, failed at least a month later following surgery. Causes of bleb failure can be - Intraocular, ocular & extraocular.Rapid wound healing response is the most common cause of bleb failure. It can occur at any stage after the surgery. It usually occurs in the � rst 1 – 6 months after surgery. Previous Scar, topical medications and increased In� ammation are the commonest risk factors for bleb failure.Early Bleb Failure can be due to obstruction of internal ostium by – blood, � brinous clot, Iris or Vitreous, Episcleral � broblastic proliferation or tight scleral suture. Subconjunctival or episcleral � brosis is the most common cause of Late Bleb Failure. Factors in� uencing � brosis are young age, Black race, subconjunctival hemorrhage, excessive in� ammation, reaction to sutures.

Approach to a failing fi ltration

Low bleb associated with high IOP - always do gonioscopy and look for obstruction to aqueous � ow at the sclerotomy

Glaucoma

Amit Porwal

Amit Porwal DO, FASCSGlaucoma Services, Choithram Netralaya, Indore, M.P.

site. Obstruction with � brin and blood is transient and does not need any intervention.

Management options

• Topical steroids • Anti - metabolites• Digital ocular compression• Laser suture lysis• Releasable sutures

Figure 1: Functional bleb

Figure 2: Functional bleb


• Laser internal revision• Tissue Plasminogen activator

Topical Steroids

They increase the success rate of glaucoma � ltering surgery by decreasing the wound healing response and helps in maintaining a patent � stula. They are used over a period of 6-10 weeks postoperatively.

Cycloplegic

Helps in decreasing in� ammation and prevents posterior synechiae formation. It also helps in deepening a shallow anterior chamber.

Laser Internal Revision

This procedure is helpful if the internal ostium is obstructed with – Iris, vitreous incarceration or by dense � brinous membrane.

Method – After instilling topical anesthetic drop, Gonio lens is applied. Using single burst mode, energy in the range of 3 to 7 mj s applied. End point is reached if there is fenestration of membrane / tissue & there is elevation of bleb.

Digital Ocular Compression

It is indicated in early postoperative period, with elevated IOP & � at bleb. Digital ocular compression separates the edges of the scleral � ap, expands the subconjunctival space. It decrease IOP & elevates the bleb. Not effective in blocked � stula.

Technique of digital compression (Figure 5)- Slow steady pressure is applied for 15 seconds with the index � nger to inferior sclera through the lower lid or sclera posterior / adjacent to the bleb through the upper lid. It can also be performed by focal compression with a moistened cotton tip at the edge of the scleral � ap. AC depth, height of bleb & IOP should be noted after digital compression. If successful, then it has to be repeated several times. If IOP remains high, removal of releasable suture or laser suture lysis to be considered.

Releasable suture

It allows tight closure of scleral � ap. Aqueous � ow can be increased postoperatively. The externalized suture can be easily removed (Figure 6). Thick tenons, In� amed / hemorrhagic conjuctiva is no bar. Disadvantages being additional intraoperative manipulation, postoperative

discomfort from externalized suture, corneal epithelial defect, increased risk of intraocular infection.

Argon Laser Suture Lysis

In performing Laser suture lysis timing is very critical. It is effective within � rst 2 wks after surgery without antimetabolites; with antimetabolites it is effective for several months after surgery. A conservative step wise approach is to be adapted. One suture is cut at a time.

Figure 3: Failing Bleb, (cork screw vessels)

Figure 5: Bleb formation after Digital ocular compression

Figure 6: Releasable suture

Figure 4: Encapsulated bleb


Technique: After instilling topical anesthetic drop, Hoskins or Ritch lens is applied. These lenses � atten & blanch the overlying conjuctiva. It can also be performed with the help of central button edge of Zeiss or Sussman lens. Parameters: 50 �m spot size, duration 0.1 sec & power of 200 to 500mW is applied.

Antimetabolites

Mitomycin–C and 5-Fluorouracil are the antimetabolites used in the management of failing blebs. Both of them Inhibits � broblastic proliferation.

Mitomycin –C

MMC is an alkylating agent that cross-links DNA. It interferes with any phase of the cell cycle and affects DNA replication, mitosis, and protein synthesis. MMC also induces apoptosis of � broblasts, thereby contributing to its increased potency compared with 5-FU. It is 100 times more potent than 5 FU - kills all cells.

Intra operative application: Concentration - 0.2mg/ml or 0.4 mg/ml. Exposure - 1 to 4 minutes. Exposure depends on - target IOP, tenons thickness and glaucomatous damage.

Sub conjuctival injections 0.04mg/0.1ml or Topical 0.02% drops 4 times a day for 2 wks can be given to manage a failing bleb.

5-Fluorouracil

5-FU is an antimetabolite that speci� cally antagonizes pyrimidine affecting DNA assembly (S phase of the cell cycle) and, after incorporation into RNA in its ribosylphosphate form, protein synthesis (G2 phase). It inhibits � broblastic proliferation – kills dividing cells (Figure 7).

Subconjunctival injections of 5 FU is given 1800 away from bleb 5mg / 0.1ml to manage a failing bleb using a 30G needle with tuberculin syringe. Total dose 15 to 50 mg viz 3-10 injection in 3 weeks times.

Always watch for bleb features, corneal complication & wound leak when using sub conjuctival injections of 5-FU or MMC. MMC causes corneal endothelial toxicity and 5–FU causes corneal epithelial toxicity.

Needling of Bleb

Bleb revision with needling can be performed in OPD or OT. After instilling topical anesthesia & antibiotic drops a

Figure 7: Bleb was managed by subconjunctival injections of 5-FU

Figure 8: Encapsulated bleb, before needling

27 - 30G needle on tuberculin syringe is introduced in the subconjunctival space 5-10 mm away from the bleb. Once advanced in the bleb, subconjunctival � brosis is cut with a � rm back & forth motion. The needle is then entered below the scleral � ap & into the AC through the internal ostium. Change in the appearance of the bleb is seen during or soon after needling. Post needling antibiotic/steroid drops is applied for 2-3 wks. Digital massage is to be instituted early & continued for long term. Needling can be accompanied with S/C inj of MMC or 5-FU combined with 0.1 ml lidocaine. Blebs with thick scar and quick failure MMC works well, while those that succeeded longer and failed slowly may respond adequately to 5-FU (Figure 8&9).

Tissue Plasminogen Activator

It is a clot speci� c � brinolytic agent. Indicated when blood or � brinous clot is occluding the � stula. Frozen (TPA) - 25 �g/ 0.1ml is diluted with non preserved NaCl. Dose of 3 to 25 �g / 0.1ml is injected with 30 gauge needle under topical anesthesia.

Key to successful postoperative management of bleb is: Early recognition of a failing bleb and correct selection and timing of the various intervention options. The available evidence suggests that trabeculectomy revision has a reasonable success rate (30%-60%) 3 years after the procedure and a serious complication rate of roughly 10% or lower.

Figure 9: Same bleb after needling procedure


Refrences1 Azuara-Blanco A, Katz LJ. Dysfunctional � ltering blebs. Surv

Ophthalmol 1998;43:93-126.2 Skuta GL, Parrish RK 2nd. Wound healing in glaucoma � ltering

surgery. Surv Ophthalmol. 1987;32:149-703 Stewart WC, Shields MB, Miller KN, Blasini M, Sutherland SE.

Early postoperative prognostic indicators following trabeculectomy. Ophthalmic Surg 1991;22:23-26.

4 Mietz H, Krieglstein GK. Postoperative application of mitomycin c improves the complete success rate of primary trabeculectomy: a prospective, randomized trial. Graefes Arch Clin Exp Ophthalmol 2006;244:1429-1436.

5 Mietz H, Jacobi PC, Krieglstein GK. Intraoperative episcleral versus postoperative topical application of mitomycin-C for trabeculectomies. Ophthalmology 2002;109:1343-1349.

6 Velpandian T, Sihota R, Sinha A, Gupta V. Transconjunctival penetration of mitomycin C. Indian J Ophthalmol 2008;56:197-201.

7 Pakravan1 M, Miraftabi A,Yazdani1 S, Koohestani N, Yaseri M. Topical Mitomycin-C versus Subconjunctival 5-Fluorouracil for Management of Bleb Failure J Ophthalmic Vis Res 2011; 6 (2): 78-86.

8 Scott DR, Quigley HA. Medical management of a high bleb phase after trabeculectomies. Ophthalmology 1988;95:1169–73.

9 Broadway D, Bloom PH, Bunce C, Thiagarajan M, Khaw P. Needle revision of failing and failed trabeculectomy blebs with adjunctive 5-� uorouracil. Ophthalmology 2004; 111:665-673

10 Green� eld DS, Miller MP, Suner, IJ, Palmberg, PF. Needle elevation of the scleral � ap for failing � ltration blebs after trabeculectomy with mitomycin C. Am J Ophthalmol. 1996; 122:195-204

11 Marit Fagerli, Kjell T, Lofors T, Elsas. Needling revision of failed � ltering blebs after trabeculectomy: a retrospective study. Acta Ophthalmol. Scand. 2003; 81:577-582

12 Shin DH, Kim YY, Ginde SY, Kim PH, Eliassis-Rad B, Khatana AK, Keole NS. Risk factors for failure of 5-� uorouracil needling revision for failed conjunctival � ltration blebs. Am J Ophthalmol 2001; 132:875-80

13 J Singh, RW D Bell, A Adams, C O’Brien. Enhancement of post trabeculectomy bleb formation by laser suture lysis. British Journal of Ophthalmology 1996;80:624-627

14 Kolker ME, Kass MA, Rait JL. Trabeculectomy with releasable sutures. Arch Ophthalmol 1994;112:62-6.

15 Melamed S, Ashkenazi I, Glovinski J, Blumenthal M. Tight scleral � ap trabeculectomy with post operative laser suture lysis. AmJ Ophthalmol 1990;109:303-9.

16 Haynes WL, Alward WLM, McKinney JK. Low energy argon laser suture lysis after trabeculectomy. Am J Ophthalmol 1994;117:800-1.

17 Jones LS, Shetty RK, Spaeth GL, Trabeculectomy. In: Chen TC (ed.), Surgical Techniques in Ophthalmology: Glaucoma Surgery, Philadelphia, PA: Saunders Elsevier, 2008;1–27.

18 Allingham RR, Damji KF, Freedman S, et al., Filtering Surgery. In: Pine J, Murphy J (eds), Shields’ Textbook of Glaucoma, Philadephia, PA: Lippincott Williams and Wilkins, 2005;568–609.

19 King AJ, Rotchford AP, Alwitry A, Moodie J, Frequency of bleb manipulations after trabeculectomy surgery, Br J Ophthalmol, 2007;91(7):873–7.

20 Feldman RM, Tabet RR, Needle revision of � ltering blebs, J Glaucoma, 2008;17(7):594–600.

21 Hung JW, Bellows AR, Bleb Revision. In: Chen TC (ed.), Surgical Techniques in Ophthalmology: Glaucoma Surgery, Philadelphia, PA: Saunders Elsevier, 2008;43–53.

22 Gutierrez-Ortiz C, Cabarga C, Teus MA, Prospective evaluation of preoperative factors associated with successful mitomycin C needling of failed � ltration blebs, J Glaucoma, 2006;15(2):98–102.

23 Shetty RK, Wartluft L, Moster MR, Slit-lamp needle revision of failed � ltering blebs using high-dose mitomycin C, J Glaucoma, 2005;14(1):52–6.

24 Iwach AG, Delgado MF, Novack GD, et al., Transconjunctival mitomycin-C in needle revisions of failing � ltering blebs, Ophthalmology, 2003;110(4):734–42.

25 Kapasi MS, Birt CM, The ef� cacy of 5-� uorouracil bleb needling performed 1 year or more posttrabeculectomy: a retrospective study, J Glaucoma, 2009;18(2):144–8.

26 Hawkins AS, Flanagan JK, Brown SV, Predictors for success of needle revision of failing � ltration blebs, Ophthalmology, 2002;109(4):781–5.

27 Anand N, Khan A, Long-term Outcomes of Needle Revision of Trabeculectomy Blebs With Mitomycin C and 5-Fluorouracil: A Comparative Safety and Ef� cacy Report, J Glaucoma, 2009;18(7):513–20.

28 Lama PJ, Fechtner RD, Anti� brotics and wound healing in glaucoma surgery, Surv Ophthalmol, 2003;48(3):314–46.

29 Suzuki R, Dickens CJ, Iwach AG, et al. Long-term follow-up of initially successful trabeculectomy with 5-� uorouracil injections. Ophthalmology. 2002;109(10):1921-1924.

30 Henderer JD, Heeg MC, Spaeth GL, et al. A randomized trial of the long-term effects of digital ocular compression in the late postoperative period. J Glaucoma. 2001;10(4):266-270.

Muzaffarpur Eye Hospital, the only eye Hospital in Bihar with 201 Indoor beds, a State of Art Hospital with all facilities Phaco, Oculoplasty, Glaucoma, Corneal Transplantation, VR Surgery equipped with all modern and sophisticated equipments having good community health programme with regular free camps, treating over 2,00,000 outdoor eye patients and performing over 20000 IOL surgeries annually, also started retina clinic with separate OT, requires suitable doctors for the following Posts:-

Muzaffarpur Eye Hospital

1. Chief Medical Offi ce 1 Post (MS/DNB having 10 years experience)

2. Ophthalmologist 1 Post (Retina & Vitreous Specialist)

3. Ophthalmologist 5 Post (MS/DNB/DOMS)These posts carry attractive salary with furnished accommodation and other incentives.Interested candidates should send their resume to:-

The Secretary y

Muzaffarpur Eye HospitalJuran Chhapra, Road No. 2, Muzaffarpur – 842001 Bihar

E-mail: [email protected],Phone No. (0621) 2215149, 2220527, Mob.: 09334910514, 09431238124

Shabu James

Rectangle


Age related macular degeneration is a third major leading cause of blindness worldwide (8.7%)1. It is classi� ed into

dry ARMD and Wet ARMD which account for 85% and 15 % cases respectively2. In India it accounts for 1.84 – 2.7%3 cases and is a concern as it is a cause of irreversible blindness.

Case report

Case 1: The patient is a 79 yrs old male who presented with blurring of vision in Feb. 2011. On evaluation he was diagnosed with bilateral cataract and age related macular degeneration. He underwent cataract surgery in RE in October 2011 but in spite of that his vision did not improve beyond 6/9. In view of the same he was advised vitreoretinal specialist opinion who diagnosed him with choroidal neovascular membrane+ pigment epithelial detachment in RE and multiple drusen’s in LE. The patient was advised to undergo ICG and follow up. The patient received multiple intravitreal Anti-VEGF in RE in the subsequent follow-ups but the situation remained the same in terms of visual outcome.

Case 2: The patient is a 71 yrs male who has been complaining of diminution of vision in both eyes since 3 yrs. He is pseudophakic in BE. On evaluation he was diagnosed with choroidal neovascular membrane BE in 2010.he has received 16 intravitreal Anti-VEGF in BE till date but the situation in terms of his visual complaints remains the same. His BCVA in RE: 6/120 & LE: 6/120 PH- 6/60.The IOP in RE & LE is 16 & 19 mmHg respectively.

Case 3: The patient is a 59 yrs. old female complaining of Diminution of vision since Jun 2011. She has been diagnosed with IPCV RE elsewhere. She has received 2 intravitreal Avastin (Jun, Nov 11), Lucentis (Jul 12) & focal Laser photocoagulation (Jul 11) in RE elsewhere. Post Photocoagulation her vision in RE deteriorated due to RPE rip (Figure 5). She has been advised Photodynamic therapy now. At present her BCVA in RE is 6/36 & LE6/12 with early lenticular changes. The Fundus shows advanced ARMD RE and Early ARMD LE.

Discussion

Age related macular degeneration is a third leading cause of blindness worldwide. The concern is increasing because the risk of advanced AMD in the affected eye is 6% for early AMD, 25% for intermediate AMD and 43% in the fellow eye of an advanced AMD affected eye. The risk of legal blindness in the fellow eye after loss of vision in one eye is 12%.

The various risk factors implicated are4

• Gender: adv 7 times in females

Clinical Meeting: Clinical Case-1

Anju Kumari

Anju Kumari MS, B.P. Guliani MDSafdarjung Hospital & VMMC, New Delhi

• Race: white race has a higher incidence than dark colored races. Melanin considered be a protective factor but not proven

• Cigarrete smoking: reduced antioxidants

• Alcohol: oxidative stress????

• Diet: High fat content diet considered as a contributory factor.

• Hypertension

Figure 1: OCT RE of patient no.1 shows PED with thickened RPE-CC complex suggestive of CNVM

Table 1: Results of studies on Anti-VEGF15 letter loss 15 letter gain

Natural History (TAP control Arm)

60-90% 2%

VISUDYNE (TAP) 33% 6%PEGAPTANIB (VISION)

30-40% 6%

RANIBIZUMAB (ANCHOR)

8% 40%


• Greater BMI- change in lipoprotein pro� le, reduced delivery of lutein & zeaxanthin

• Cataract surgery

Genetic studies have shown the following:

• Twin analysis: 45% heritability

• Candidate gene screening??/: ABCA4 - stargardt; TIMP3 - sorsby fundus dystrophy, peripherin-retinal degeneration; small subset of patients have been studied

• Complement factor H gene: Y402 allele

• Factor B & complement component

• Gene 10q 26 cluster

• APOE

• Toll like receptor 4- responsible for cholesterol ef� ux & photoreceptor phagocytosis

The pharmacotherapy has been a mainstay of treatment in cases of AMD. The various drugs studied and evaluated are

• Antioxidants

• Steroids

• COX-2 Inhibitors

• I-CAM Inhibitors

• Alpha-IFN2A

• Rapamycin

• ANTI-VEGF

• Pegaptanib (Aptamer)

• Monoclonal Antibodies-Ranibizumab/Bevacizumab

• Si RNA (Bevasiranib)

• VEGF Receptor Inhibitor (VEGF TRAP)

• Others:

• Squalamine

• Combrestatin-A-4

• PDT-Visudyne

AREDS advised the following supplementation for the patients of AMD5

• 500 milligrams of vitamin C

• 400 International Units of vitamin E

• 15 milligrams of beta-carotene (often labeled as the equivalent of 25,000 International Units of vitamin A)

• 80 milligrams of zinc as zinc oxide

• 2 milligrams of copper as cupric oxide

Our patients had received multiple anti-VEGF intravitreal

Table 2: Expenditure in cases of AMD in various nations6

CANADA FRANCE GERMANY SPAIN UK INDIAArmd Patients (Expense in Euros)

768 Million 1.5 Billion 3.3 Billion 686 Million 01 Billion 1.2+ Billion

Table 3: expense borne by the patient for the treatment of wet AMDCost per dose(RS) Doses expected Frequency Total cost

PDT 65,000 3 3 Monthly 195,000Macugen 45,000 20 4-6 Weekly 900,000Lucentis 65,000 20 4-6 Weekly 1,300,000Avastin 2,000 20 4-6 Weekly 40,000

Figure 2: OCT LE shows multiple deposits at RPE-Bruch’s membrane suggestive of drusen’s

Figure 3: RE & LE OCT shows thickened RPE-CC complex with multi cystic spaces

in RE suggestive of CNVM


injections. As we all know, the recommended as well as off label use of Anti-VEGF is on a rise. As per PRONTO and PIER studies minimum of 06 intravitreal Anti-VEGF are required in the � rst year of treatment in order to achieve some bene� cial effects in WET AMD. But the risk associated with multiple intravitreal Anti-VEGF is endophthalmitis and retinal detachment which cannot be overlooked.

As the tables depict that the economic burden on the affected individual and the nation are tremendous so we need to rationalize our approach to treatment of wet AMD patients. Thus, a combination therapy may come to our rescue to some extent. The rationale7 behind the combination therapy is to:

• Address oxidative stress

• Block neovascular stimulus

• Inhibit growth of abnormal blood vessels

• Maturation of CNV vessels

• Eliminate edema

• Repair or decrease retinal scarring

• Duplicate the visual acuity gains seen in Ranibizumab trials

• Reduce the number of intravitreal injections

Combination therapy in form of PDT plus Ranibizumab treatment can be considered as it

• Achieve visual results similar to those obtained with Ranibizumab alone

• With the advantage of fewer intravitreous injections and

• Less risk of adverse effects like endophthalmitis, retinal detachment.

Photodynamic therapy has the following actions8,9,10–

• Thrombosis and vessel closure(Advantage)

• Causes acute VEGF production and choroidal damage (Disadvantage).

• Promotes upregulation of Pigment Epithelium Derived Factor levels which promote CNV vessel maturation (Advantage).

If damage to the choroid is minimized, PDT +Effective anti-VEGF

• Expected to decrease the number of anti-VEGF therapy injections needed.

• The anti-VEGF agent might ameliorate the increased VEGF caused by the PDT treatment as well

Figure 4: RE OCT shows PED with multiple cystic spaces

Conclusion

The combination therapy of Photodynamic therapy with an Anti-VEGF appears to be a viable alternative as it is expected to decrease the number of anti-VEGF therapy injections needed and the anti-VEGF agent might ameliorate the increased VEGF caused by the PDT treatment as well. A major limitation of Anti-VEGF drugs is that they require multiple intravitreal injections, every 4 to 6 weeks interval for a minimum period of 2 year. In our experience and as poer the various published articles all available treatments are temporary. We can hope of a new product to be considered by the Pharamceutical industry so that the short term effects of the available treatments can be a thing of past. As treating physician we have to answer patient queries like I want to read, I am fond of reading, depressive looks, when I will be OK, will I be ok with injection, Is it last injection? These cases are representative of many cases which all of us may be facing every day and looking for answers at one stage or other stage.

References

1 WHO fact sheet no.2822 Albert jakobiec’s principles and practice of ophthalmology third edition:

38 ;4133 Nirmalan PK,Katz J, Robin AL,Tielsch JM,Namperumalsamy P,et

al.Prevalence of vitreoretinal disorders in rural population of Southern India:The Aravind comprehensive Eye Survey.arch ophthalmol 2004;122:581-6.

4 Textbook of vitreoretinal diseases and surgery � rst edition: genetics of age related macular degeneration 2009; 1: 2-8.

5 AREDS Research Group:A randomized,placebo-controlled clinical trial of high dose supplementation with vitamins C and E, beta carotene, and zinc for age related macular degeneration and vision loss.Arch Ophthalmol 2001;119:1417-1436

Figure 5: RE OCT shows RPE rip subfoveally


6 Yearly � nancial burden of ARMD patients worldwide report 87 Konerding MA. Ocular angiogenesis: translating preclinical indications

to successful clinical development. Expert Opin Ther Targets. 2004; 8: 255-258.

8 Schmidt-Erfurth UM, Gabel P, Hohman T, for the PROTECT Study Group. Preliminary results froman open-label, multicenter, phase II study assessing the effects of same-day administration ofranibizumab (Lucentis) and vertepor� n PDT (PROTECT Study). Abstract #2960. Presented at theAssociation for Research in Vision and Ophthalmology 2006 Annual Meeting. April 30-May 4, 200 Fort Lauderdale, Fla.

9 Wolf S, Gabel P, Hohman TC, Schmidt-Erfurth U, for the PROTECT

study group. Fluorescein angiographic and OCT results from an open-label, multicenter, phase II study assessing the effects of same-day ranibizumab (Lucentis) and vertepor� n PDT (Visudyne). Abstract #3542. Presented at the Association for Research in Vision and Ophthalmology 2006 Annual Meeting. April 30-May 4, 2006.Fort Lauderdale, Fla..

10 Augustin AJ, Offermann I, Schmidt-Erfurth:. Combination of photodynamic therapy and intravitreal triamcinolone for the treatment of choroidal neovascularization. Report of a large case serieAbstract #3541. Presented at the Association for Research in Vision and Ophthalmology 2006 Annual Meeting. April 30-May 4, 2006. Fort Lauderdale, Fla.

Sunday, 23rd September, 2012at India Habitat Centre, Lodhi Road, New Delhi

Saturday & Sunday 27th & 28th October, 2012 at India Habitat Centre, Lodhi Road, New Delhi

21st November to 24th November, 2012

Saturday & Sunday 16th & 17th February, 2013at Jawaharlal Nehru Auditorium, AIIMS, Ansari Nagar, New Delhi

Friday, Saturday & Sunday 12th, 13th & 14th April, 2013 at Hotel Ashok, Chanakaya Puri, New Delhi


History: A 20 year old male patient presented to Bharti Eye Hospital with chief complaint of inward deviation

of eyes.

Past history: There was a history of Toric ICL surgery both eyes done 1 year back when his refractive status was

• RE= -18.0/-2.25x10; Vn-6/36

• LE= -19.0/-2.75x170; Vn- 6/24

Records show at that time he was diagnosed as pathological myopia with posterior staphyloma OU.

Also there is history of Squint Surgery in early childhood, of which no records were available.

On Examination, general appearance, build and vital parameters were normal. The best corrected visual acuity was 6/18 both eyes; on anterior segment examination, the ICL was in situ, the rest was unremarkable. Fundus shows posterior staphyloma both eyes with periphery and macula normal.

Orthoptic Examination: Hirschberg: 7-10 degrees RET (Figure 1).

However, on Cover tests, it was found to be an exophoria, more for near than for distance, measured to be 8 prism diopters base in prisms for distance and 25 prism diopters for near on Prism Bar Cover Test.Ocular movements were full in all nine gazes (Figure 2).


Archana G. Mahajan

Meetu Bansal MBBS, Archana Gupta Mahajan MBBS, DNBBharti Eye Hospital, Greater Kailash -1, New Delhi

The patient was diagnosed to have Pathological myopia status Post ICL and Post Squint Surgery OU with Exophoria and negative angle kappa.

Discussion

Angle kappa is the angle between the visual axis and the pupillary axis (Figure 3&4).

As a rule, the pupillary axis is slightly nasal and inferior to the fovea- so on � xation therefore the corneal re� ex will not be centered but will be slightly nasal to the center.

A re� ex that is more nasal to the pupillary center will thus cause a positive angle kappa.

A suf� ciently large positive angle kappa may simulate an exodeviation and produce pseudostrabismus.

Positive angle kappa is more common in the general population than the negative angle kappa. Some authors make the erroneous conclusion that the negative angle kappa is always pathological.

Size of angle kappa• Emmetropes- +3.5 to +6.0 degrees (average is 5.082)

• Hypermetropes- +6.0 to +9.0 degrees (average is 7.55)

• Myopes- around +2 degrees or Negative

In case of a positive angle kappa, an existing exodeviation

Figure 1 Figure 2


will look worse than it actually is, or it may mask all or part of an esodeviation.

A large positive angle kappa is seen in High hyperopes, ROP with temporal dragging of the macula, is also present in Aniridia patients, a sign of albinism in patients with congenital nystagmus.

However, if the fovea’s position is nasal to the point at which the optical axis cuts the globe’s posterior pole, the corneal re� ection of a light � xated by that eye will appear to lie on the temporal side of the pupillary center. This is called negative angle kappa.

It may simulate an esodeviation and again produce a pseudostrabismus, may make an existing esotropia look

worse than it actually is, or may mask all or part of an exodeviation.

Pseudoesotropia secondary to nasal displacement of the fovea may be caused by high myopia.

Vertical angle kappa may be seen secondary to retinal scars e.gtoxocaracanis

Clinical Signifi cance of Angle KappaAs angle kappa may simulate/conceal/ or exaggerate a deviation, it must be considered to obtain the best estimate of the actual deviations in whom this determination is made by the corneal re� ection test.

If one were to aim at aligning the visual axes in a patient with large angle kappa to facilitate binocular vision, the relative postoperative position of the eyes might be cosmetic overcorrection or under correction.

Figure 3

Figure 4

Figure 5

worse than iit actually iis or may mask all or part off an

Figure 6


Renewed interest in angle kappaAngles of the eye have, of late, received a renewed interest secondary to the signi� cant role they play in refractive surgery. It is clinically important to the Refractive Surgeon because in patients with large angle kappa, the center of the pupil is no longer the point through which a fovea-centric ray of light passes. Thus, any treatment that is performed centered on the pupil results in a decentered ablation. This effect is more pronounced with corrections for astigmatism and higher-order aberrations if angle kappa is not compensated for.

Angle kappa and multifocal IOLsIn eyes with small anglekappa, a fovea centric ray may passthrough the central ring of themultifocal IOL but in eyes with largeangle kappa, a fovea centric ray mayhit on the edge of the ring, causing edge glare effects and deterioration in quality of vision (Figure 6)

InferenceThis case was presented with a view to highlight the different presentations of strabismus. We reaf� rm the fact that the the corneal re� ex can be misleading in evaluation of the strabismus as in our case it appeared like an esotropia but was actually an exophoria. Cover tests are and should always be the gold standard in diagnosis and measurement of squint. Also, considering the increasing number of refractive procedures and multifocal IOLs being done, pre operative evaluation should include a thorough orthoptic evaluation and checking for angle kappa as well.

References1 Shaterian ET, Weismann IL. An unusual case of pseudostrabismus. Am

Orthop J 1973; 23:68-70.2 Urist MJ.Pseudostrabismus caused by abnormal con� guration of the

upper eyelid margins. Am J Ophthalmol 1973; 75:455-4563 Binocular vision and ocular motility; Theory and Management of

Strabismus; Gunter K. von Noorden4 A study on 16 patients was completed on sep ,2011 by University of

Minnesota.5 Donders FC: on anomalies of accomodation and refraction of the eye, 18646 Giovanni FG, Siracusano B: the angle kappa in ametropia. New trends

Ophthalmol 3:27,1988 7 Kappa Angle Measures of Strabismic and Nonstrabismic Individuals ;

William E. Scott, MD; A. Jane Mash; University Hospitals, Iowa City Arch Ophthalmol. 1973; 89(1):18-20.

8 MC brodsky, Am.j.Ophthal; vol 137, 4:625-629, Apr 200, Negative angle kappa

9 The angle kappa in strabismic individuals; HikmetBasmak, Strabismus vol.15:193-196;2007

10 Horizontal and vertical angle kappa;Strum V, kraft SP; university of Toronto, Epub 2011 Apr

11 Tennent Institute of Ophthalmology, GartnavelGeneral Hospital, Glasgow, ScotlandStone N, Weir CR Strabismus 165-6 17

12 Measurement of angle kappa and centeration in refractive surgery, Park CY, Oh SY, Dongguk University, iilsan hospital, Koyang; CurropinOphthalmo. 2012; Jul23(4): 269-75

13 Adjusting ablation for angle kappa may improve vision quality in hyperopic LASIK; escrs.org

14 Topographic-guided hyperopic and hyperopic astigmatism femtosecond laser-assisted LASIK:AJKanellopoulos; clin Ophthalmol. 2012;6:895-901

Dr. Shroff ’s Charity Eye Hospital Offers

Ms Kalpana GuptaMedical Education Department

Dr. Shroff’s Charity Eye HospitalKedar Nath Road, Daryaganj, New Delhi-110002Email: [email protected] � Website: www.sceh.net (Ph): 011-43528888 (M): 9899195676

Long term fellowship programmes in Ophthalmology for December 2012 sessionSpecialty Fellowships: Vitreoretina, Paediatrics, Cornea, Oculoplasty • Course duration: 18 months • Number of seats available: 1 in each specialty • Eligibility criteria: MS or MD or DNB in ophthalmology

Cataract & Microsurgery Fellowship: • Course duration: One year • Number of seats available: 2-3 • Eligibility criteria: Fresh DO, MS candidates aspiring to improve their cataract management

skillsSession commencement: December 2012 Date of Interview: 17th November 2012, Saturday For application and further information, send your curriculum vitae along with cover letter and passport size photograph to [email protected]

Shabu James

Rectangle


Amniotic membrane or amnion is the innermost layer of placenta. It has a stromal matrix composed of collagen

with thick basement membrane over which lies a single layer of epithelium. Amniotic membrane has become a popular biological bandage owing to its lack of immunogenicity and unique properties that promote rapid epithelialization with reduced pain, in� ammation and scarring. These properties have popularized its use in ocular surface reconstruction. Amniotic membrane has been successfully used in patients with persistent epithelial defects, pterygium, symblepharon, and for ocular surface reconstruction. In this report we describe two cases of chemical injuries with subacute presentation and their clinical course along with our experience with amniotic membrane transplant in these cases.

Cases

Two cases of chemical injury residents of Rawanda presented to us simultaneously after suffering from chemical injury at their workplace where they both together were � xing some pipes containing caustic soda. Both the cases were young males and were 25 years (case 1) and 22 years (case 2) respectively. Both had received emergency care in form of copious washing and treatment in the form of topical eye drops the exact records of which were not available. These cases presented to us 25 days after the accident. Clinical


Mridula Mehta

1Mridula Mehta MS, DNB, 2Sudhank Bharti MS1. Senior Consultant Oculoplasty, Bharti Eye Foundation, East Patel Nagar, New Delhi.

2. Director, Bharti Eye Foundation East Patel Nagar, New Delhi.

characteristics of both the cases are described in Table 1.

These cases were initially treated at our centre with topical antibiotics, lubricants, topical steroids, topical IOP lowering agents, cycloplegics and oral steroids (case 1 RE and case 2 both eyes). Case 1 left eye received topical antibiotic and lubricating drops. Surgical management was performed in case 1 in RE in the form of entropion surgery and amniotic membrane graft (AMG) with overlay technique and a symblepheron ring was placed in the palpebral � ssure (Figure

Table 1:Clinical characteristics of cases 1 and 2 Case 1 Case 2 OD OS OD OSBCVA CFCF 6/6 6/36 6/60Eyelids and adnexa Upper lid entropion and

ptosis. (Figure 1)wnl Upper lid entropion Upper lid entropion

Conjunctival involvement

40% No symblepheron

OK 40%No symblepheron

50%No symblepheron

Limbal ischaemia >270 degrees Not obvious 360 degrees 360 degrees Corneal epithelial defect

Subtotal Super� cial punctate keratitis

Subtotal Subtotal

Stromal involvement Haze + clear Haze+ Haze+AC and iris iridocyclitis clear iridocyclitis iridocyclitisIOP wnl wnl wnl wnlPosterior segment Media hazy

USG-B scan- wnlwnl Media hazy

USG-B scan- wnlMedia hazyUSG-B scan- wnl

Figure 1: Case 1 with grade IV chemical burns in RE along with RE entropion, LE had mild

grade I chemical injury


2). Bilateral AMG was performed for Case 2. The corneal epithelial defects in all the three eyes healed in about two weeks and patients were discharged on topical antibiotics, lubricants, topical steroids, topical IOP lowering agents, cycloplegics and oral steroids on tapering dosages and were managed in their country by ophthalmologists which were in constant contact with us.

At six months follow up case 1 reported disturbed vision in: RE visual acuity was FCCF, and LE: 6/12. Retinoscopy LE showed scissor re� ex and refractive error of -0.75D sph -0.75 D cyl at 140o. The RE eyelid was ptotic but the lashes were normal, with dry ocular surface and with 360 degree conjunctivalization and vascularization of cornea along with conjunctival congestion (Figure 3). There was slight shallowing of fornices RE. IOP was normal digitally. Pentacam revealed keratoconus LE. Case 2: Visual acuity: BE was FCCF, there was upper lid entropion both eyes. Ocular surfaces were dry conjunctiva, with shallowing of the fornices with symblepheron formation in BL upper lid and left lower lids. There was conjunctivalization of cornea with 360 degree vascularization and stromal opaci� cation. IOP: normal digitally. No surgical intervention was done for case 1 and patient was prescribed mild topical steroids RE and lubricating eyedrops both eyes. In case 2 bilateral upperlid entropion surgeries with symblepheron release with overlay AMG was done.

At one year follow up the ocular surface congestion decreased in the three eyes of the case 1 and 2 and ocular surfaces were non-in� ammed with normal looking conjunctival vessels. Entropion in the three eye lids were well corrected and minimal symblephera were was present in case 2.

Discussion

In our small case series AMG was effective in reducing patient’s pain, discomfort and watering. Healing of the epithelial defects with conjunctivalization of cornea occurred over 2 weeks. AMG is effective treatment as an overlay graft for epithelial healing, patch graft in case of symblepheron release and areas of de� cient conjunctiva and as a graft to replace the damaged ocular surface or stromal matrix. Healing properties of AMG have been attributed to presence of various growth factors, provision of a scaffold by the basement membrane component which facilitates migration of epithelial cells, reinforcement of adhesive properties of basal epithelial cells, and probable promotion of epithelial differentiation. AMG has been thought to be of bene� t in restoring the ocular surface in patients with partial limbal stem cell de� ciency. In case of extensive loss of stem cells due to ischaemia the treatment is limbal stem cell transplant

Figure 3: Case 1 follow up at 6 months, clinical photographs in 3(a): primary gaze showing vascularized

cornea with stromal opaci� cation and conjunctivalization. 3(b): Downgaze photograph shows shallowing of upper

fornix. 3(c): Lower fornix was normal

Figure 2: Case 1: Upper lid entropion (tarsal wedge resection with everting sutures) and overlay AMG

covering entire ocular surface with symblepheron ring

(LSCT) along with AMG if stroma is not involved and LSCT and kerotoplasty if stroma is involved.

In acute stage of injury mediators of in� ammation cause collagenases to be activated and may probably cause change in corneal pro� le and in late phases ischaemia is thought to promote apotosis and necrobiosis which can lead to degenerative changes in cornea and lead to development of keratoconus in OD of the case 1.

(a)

(b)

(c)

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DOS Times Traders Index


What is Fugo plasma blade? It is an “electromagnetic plasma” cutting device, developed by an ophthalmic

surgeon, Dr.Richard Fugo. It tool him 17 years to develop. It consists of a console and a hand piece that carries the working tip. There are two variable rotary switches for cut power and intensity. It works on 4 rechargeable battery cells. One charge allows a cutting time of 40 minutes. It produces visible “focussed electromagnetic radiation”/plasma on the tip of a � lament, that has the power to cut. It is the only electromagnetic device for intra-ocular use, approved by FDA. We have been using it for over 12 years. It is an interesting tool,because it cuts in a different way. Its plasma ablates the tissue, just like an excimer laser. The working end of the tool is the blunt tip of a steel wire, varying in size from 100 micron to 600 microns.

How does it work ?

A metal or diamond knife/blade cuts by mechanically disrupting the tissues. When the knife is withdrawn the tissue apposes exactly. Not so with Fugo blade. When the activated tip touches the tissue, the touched part disappears (gets ablated). Obviously, some tissue disappears in the line of incision. Therefore it can not be used to make incisions in the cornea.

What happens is, the plasma energy from the activated working tip is transferred to the molecules of the tissues, by the process of resonance. The tissue molecules absorb

Miscellaneous

Daljit Singh

Daljit Singh M.S., D.Sc., Seema K. SinghDr.Daljit Singh Eye Hospital, Sheranwala Gate, Amritsar, Punjab

the energy, go to higher energy levels, become unstable and explode. The explosion is at molecular level and it thus creates what we see as an incision. Electron microscopy shows that there is no thermal collateral damage of the tissue, exactly the same way as an excimer laser. Small vessels also get removed, therefore the incisions are blood-less, a very desirable feature when doing procedures on vascularized tissues.

Figure 1: Fugo blade console, handle and the tip

Figure 3: Capsulotomy in a pediatric cataract.Any sized capsulotomy can be done in seconds

Figure 2: The activated tip of Fugo blade shows cutting yellow plasma around the � lament.The orange colored

second cover is photonic non-cutting cloud


Fugo plasma blade vs electrolysis and radio-cautery

Fugo blade is a new fundamental energy, the excimer laser like plasma. Electrolysis and radio-cautery do not resemble it even remotely.

Fugo blade applications in ophthalmology

Every � eld of ophthalmology, be it intra-ocular or extra-ocular, has been in� uenced by the introduction of Fugo blade. Let us discuss some of them.

Cataract and related issues

Fugo blade is useful for doing capsulotomy, membranectomy and pupilloplasty. Capsulotomy can be done on any kind of cataract and at any age. The edge of the capsulotomy rim is like a postage stamp, which David Apple has described as ideal. It does not matter if the anterior capsule is thin or thick or of unequal thickness. The thickest any traction on the tissues and without bleeding. Capsule shall be cut, without the slightest tactile sensation to the surgeon. The capsulotomy never runs towards the periphery. It may be done in one pass or multiple passes. The only precaution is to keep the anterior chamber formed with viscoelastic material

during the procedure. Capsulotomy can be done as easily on a dislocated lens (Marfan or trauma) since during the process, there is no traction and the lens does not move.

A � bro-vascular membrane in the pupillary area can be cut as easily as the normal capsule, without any bleeding. Making a pupil by removing a circular or any shaped area of iris is as easy. A thick scar on the front or/and the back of the intraocular lens can be cut with this tool, without injuring the lens itself.

Fugo blade can make femtosecond laser like cuts in the cortex and the nucleus, but that does not materially help in the surgery of phakoemulsi� cation.

Glaucoma

Glaucoma surgery is concerned with the creation of a passage for the aqueous to reach the subconjunctival tissues, from where to get absorbed. All common surgical techniques involve the cutting of the tissues in layers, till an opening is created in to the anterior chamber and then the tissue layers are sutured back. The result of surgery depends upon the size of the internal opening, the sutures on the scleral � ap, healing reactions along the scleral � ap edges and scar

Figure 4(a)&(b): Pupilloplasty and membranectomy can be done without

(a) (b)

Figure 5(a)&(b): Congenital � brovascular cataract with extensive adhesions with ciliary body. The cataract is cut with Fugo blade, after � xing the iris claw lens. Two large iridectomies have been done

with Fugo blade without any bleeding

(a) (b)


formation in the tenon capsule and subconjunctival tissues. The extent of tissue reaction and scarring depends upon the trauma in� icted at the time of surgery. The scar formation is reduced/controlled by the use of anti-mitotics during and after the surgery. It is generally not known that there exist lymphatics in the subconjunctival tissues, the tenon capsule and the sclera. The lymphatic network of lymphatics is responsible for the drainage of the out coming aqueous. Surgical and cautery damage to the lymphatics increases the risk of scarring and ultimate failure of surgery.

The Fugo blade as an additional surgical tool off ers a few new possibilities

A � ltration track can be made without dissecting the tissues in layers. The tissues can be removed very precisely. There is no collateral surgical/thermal damage. Compared to routine procedures, Fugo blade surgery produces a small foot print on the ocular tissues. In case of failure, it is easy to redo surgery in the same or an adjoining area.

The following kinds of surgeries are possible with Fugo blade

Non-perforating glaucoma surgery

The conjunctiva is detached from the limbus and retracted upwards. The limbus and adjoining sclera get exposed NPGS may be done without a scleral � ap. The sclera is ablated with

a 600 micron Fugo blade tip, one mm proximal to the limbus, till the ciliary body is barely visible. The posterior end of the Schlemm canal is situated at that depth, a little distance anteriorly. Fugo blade tip is used to ablate anteriorly. Soon the posterior end of Schlemm canal gets opened and aqueous is seen � owing. The surgery is complete. The conjunctiva is sutured back to the limbus.

Microtrack Filtration

The anterior chamber is drained through a micotrack near the limbus. The surgery is simple. The conjunctiva is pushed or pulled toward the cornea. The limbal tissue is visible under the conjunctiva. An activated 100 micron Fugo blade tip is passed through the pulled down conjunctiva and the limbus, till it reaches the anterior chamber. As it is withdrawn, the aqueous follows. The conjunctiva is allowed to retract. The bleb starts forming. A bandage lens is place over it.

Figure 6: Shows the lucid interval canal and its relationship to the cornea and the

lymphatics at the limbus

Figure 7: Bleb formation in a case of Microtrack Filtration in a case of buphthalmos. Buphthalmos cases sometimes

need multiple operations

Figure 8: Microtrack Filtration in a case of angle recession glaucoma. OCT of the bleb shows the track.

The conjunctival bleb wall is thick and safe

Figure 9: A block block is removed, while saving the marginal strip of the muscle. This prevents misalignment in any kind of strabismus surgery


Transciliary fi ltration

The � ltration is done from the posterior chamber. All the anterior chamber related complications are thus avoided. It may be done after making a fornix based conjunctival � ap or without making a � ap. The Fugo blade tip passes through the sclera and the ciliary body, in to the posterior chamber and the drainage starts.

All three techniques have a small foot print on the sclera and re-surgery is easy in case of failure. Fugo blade techniques are useful in dealing with failed trabeculectomy and glaucoma valve cases, as well as cases of tenon cysts.

Non-dissecting techniques produce healthy thick conjunctival blebs that are least prone to blebitis and bleb infection.

Fugo blade techniques have been done along with collagen matrix and cross-linked sodium hyaluronate. However, we have not found any additional bene� t from them.

The research on Microtrack Filtration continues. The variable factors are minimal. The most important are the diameter and direction of the � ltration track and the use of mitomycin. All the factors concerned with dissecting surgery have been eliminated. The aim of the research to make it possible to offer � ltration surgery as a � rst option for the management of glaucoma, at least for the economically stressed patients. The surgical time with every Fugo blade glaucoma surgery technique is about 3-4 minutes and is practically trauma free.

Extraocular muscle surgery

Because of the peculiar bloodless cutting/ablating characteristics of Fugo blade, new innovations have been introduced in the conduct of extraocular muscle surgery. The most important concern in strabismus surgery is the risk of mis-alignment, when a muscle is completely detached and � nally reattached to the sclera. For this reason, there is great reluctance in doing surgery on cases of troublesome phorias. No more fear with the new techniques. What are the new techniques ?

The surgery is done not with forceps and scissors, but with forceps and Fugo blade. The muscle is approached directly by going through a single incision cutting/ablating the conjunctiva and tenon capsule, in a bloodless manner. As incision is made, cavitation bubbles by Fugo blade keep in� ating the tenon capsule. When the depth is reached, the

tenon capsule is seen separated from the muscle by the same air bubbles. When he cleavage line is found, we have reached the end of our search for the muscle. The muscle is carefully exposed. The whole procedure of going through the depth of the tissues is done carefully, lest sclera gets cut.

The edges of the exposed muscle are de� ned and two muscle hooks are passed underneath. The tenon capsule that is enclosing the muscle is peeled off posteriorly with a forceps to a desired distance. The muscle thus lies exposed. It is stretched between the muscle hooks. An old time lens spatula is introduced under the muscle belly/tendon. This is to protect the sclera when the muscle is cut. Now we go to the actual cutting of the muscle. The muscle is either weakened or it is strengthened. The weakening/ recession is done as follows:

Recession/block removalThe muscle is incised/ablated lengthwise close to both the edges. Make sure that the marginal strips of the muscle are not so thin that they break under stretch. With the lens spatula still under the muscle, the belly of the muscle is cut at the posterior end at a desired point. The central block of the muscle, separated from the marginal strip is now hanging freely. The spatula is removed. The hanging muscle strip is then held with a forceps and cut with Fugo blade. A block of muscle has been removed to weaken/recession the muscle. A couple of sutures are applied to the tenon capsule and the conjunctiva to complete the operation. A recession has been achieved without a suture to the muscle.

Figure 10: This shows doubly everted lid. The levator muscle is caught through conjunctival incisions in the fornix. The

musclei is sutured to the anterior surface of the tarsal plate, 2.5 to 3 mm from he superior edge

Figure 11: Shows before and after punctum formation with Fugo blade


Nobody does recession of superior rectus muscle, because there is the superior oblique lurking underneath. No more a problem if this technique is adopted.

Resection/advancementUp to the muscle exposure, the steps of the operation are the same as before. An anchoring suture is passed through the muscle at the desired point up to which resection is done. A block of muscle is removed as described earlier. Now we are left with a vacant area with a strip of muscle on either side and a suture proximal to the vacant area. This suture is passed through the line of original insertion and tied. I use 80 micron steel suture, but any kind of suture can be used. This is followed by closure of tenon and conjunctiva.

Myomectomy of inferior obliqueThe main problem with every kind of muscle surgery is the bleeding in the operating area. This does not happen with Fugo blade incisions. The inferior oblique muscle belly lies about 14 mm from the limbus. It is covered with thick tenon capsule, inside which it works. A horizontal incision is made in the conjunctiva and tenon capsule close to the muscle till sclera is reached. From here a forceps is introduced and moved posteriorly to catch and pull out the inferior oblique plus its capsule. A careful incision on the tenon capsule shall reveal a red-brown shining muscle belly. The muscle is pulled out, a muscle hook is passed underneath. Fugo blade tip is used to completely incise the muscle belly in a bloodless manner. All that remains are a couple of sutures to the tenon capsule and the conjunctiva.

Fugo blade not only makes the surgery blood-less and simple, it is also highly ef� cient. I takes about 5-6 minutes to do the procedures described above. There is little or no pain or postoperative reaction, which allows the child to go to school after 2 days.

Ptosis surgery through conjunctival route

It was � rst done by Bowman in 1857, was reintroduced by Blaskovics in 1928. However the surgery was dif� cult and there were serious postoperative complications. In 1941.... tried to revive it, but to no avail.

I devised a new ways of levator muscle plication through the fornix, with the help of Fugo blade. In my � rst case in 2004, I was con� dent that if I did not succeed, I shall not do any harm. earlier I had been doing Muller muscle plication for cases of

slight ptosis. I did this in place of Fasanella-servat technique. All that remained to achieve was to extend the process of plication to the levator. It is well known that Muller muscle takes origin from the levator. So if you pull muller muscle you can reach the levator muscle, which can be pulled out of the orbit and advanced to the anterior surface of the tarsal plate. The surgery can is done without sacri� cing any tissue. The surgery can be enhanced or undone if need be.

The steps of operation are as follows:

• The lid is double everted over Desmarre lid rectractor. This brings anterior surface of the tarsal plate to the front.

• Three stout sutures are passed close to the upper edge of the tarsal plate and secured with artery forceps.

• Saline is injected under the conjjunctiva to balloon it up.

• Three conjunctival incisions, Muller muscle deep are made,starting from the fornix side and ending short of the upper edge of tarsal plate. Fugo blade helps to make these incisions blood-less and free from burning and charring.

• The fornix ends of the incisions are undermined towards the orbit.

• The levator muscle is approached as follows. Muller muscle is pulled such that the pearly while tenon capsule on the levator comes in to view. Now two forceps are used to pull out the levator to a desired length.

Figure 12: A clean bloodless excision of a large pterygium has been achieved with Fugo blade

Figure 13: Bloodless cutting of orbital part of the orbicularis to relieve blepharospasm


• An anchoring suture is passed twice to secure the levator. This is repeated at two other exposed sites. Thus we have 3 sutures holding the muscle that are to be advanced on the anterior surface of the tarsal plate.

• The anterior surface of the tarsal late is covered by orbicularis and tendon of levator muscle. They are ablated with a 300 or 600 micron tip, to expose the tarsal plate underneath. Save the tarsal plate from ablation.

• The anchoring sutures are passes through half the thickness of the tarsal plate, starting 3 mm from the edge of the superior tarsal margin and emerging at 1.5 mm. Halfway through the tarsal plate look under the tarsal plate, to make sure there is no full thickness penetration of the needle. This is the only important precaution.The sutures are tied reef-knot.I use 80 micron steel suture for this surgery. Steel sutures are stay sure and do not causing any tissue reaction.

• The stout sutures on the tarsal plate are cut. The lid is allowed to go back to its original place. This is assisted with a spatula.

• I tie the two lids together for one day in the case of adults and two days in children. Very young children who can not cooperated (except by crying) in the postoperative period are not suitable for this surgery.

The results are good to excellent. A natural lid fold gets formed. There is lid lag in the beginning, which goes away as time passes. The � nal result is a near natural lid, which is hard to distinguish from the other un-operated lid. The more the experience of the surgeon the better the results.

Lacrimal system

The utility of Fugo blade lies in opening stenosed/closed/absent puncta and in opening closed/stenosed canaliculi. Just ouch the punctal area with 300 micron activated tip and the tissue disappears to reveal the opened vertical part of the canaliculus. When a blocked canaliculus needs clearing, Fugo blade tip is passed up to the blocked point. It is kept straight and pointed towards the sac and then activated and pushed. The blockage gets cleared and the tip reaches the lacrimal sac in a fraction of a second.

Excision of nodules, cysts etc

Limbal nodules, pigmented or non-pigmented are easy to clear with Fugo blade. Finest tissue removal is achieved. Dermoid of the limbus another dif� cult condition-

the corneal as well as the scleral components need removal/ablation. Conjunctival dermoids and fatty tumours are easy to manage. Cysticercus can be removed complete.Tumours along the lid margin can be removed in a clean manner.

Dermoid of the orbit and lid can be removed as follows. A small incision is made to open the cyst. Its contents are expressed or removed with a spoon. The empty cyst is pulled out and it is separated from the surrounding tissues in a blood less manner with Fugo blade.

Pterygium surgery

The conjunctiva and the subconjunctival tissues are removed with 100 micron tip Fugo blade, without touching the sclera. This possible if conjunctiva is raised with local anaesthetic, before the start of surgery. The apex and the limbal part of the pterygium is peeled off with corneal forceps and a plane forceps.Any raised area at or near the limbus is soothed

with500 micron Fugo blade tip. Fugo blade is helpful in removing a conjunctival graft from another site.

Retina surgery

Fugo blade is the only tool to deal with a vascular tumour of the retina.

Primary Blepharospasm

For the present this disabling condition is being treated by repeated injections of neuromuscular blocking agent. The effect is temporary and there are many side effects. Besides it is a costly treatment. This condition can be treated by myotomy of orbital part of orbicularis oculi muscle. The marginal strip of the orbicularis for about 5-7 mm is left uncut. This allows for normal blinking. The treatment is effective and permanent.

Summary

The plasma energy of Fugo blade is a new fundamental energy tool. It cuts without clinically visible thermal/ cautery tissue damage. There are many unique applications with it that are ef� cient and blood less. The recovery from surgery conducted with Fugo blade is quick and postoperative in� ammation is minimum. The learning curve is nil or small. However,it is important to watch somebody using it and to learn the � ne points of different surgeries.

Reference

1 The Applications of Fugo Blade. Editor Hampton Roy. Lippincots, Williams and Wilkins. 2010.

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Tear sheet

DOS Correspondent

Reetika Sharma MD

Reetika Sharma MD, M. Vanathi MDDr. Rajendra Prasad Centre for Ophthalmic Sciences,

All India Institute of Medical Sciences, Ansari Nagar, New Delhi

Goals of evaluation

1. To identify ideal candidates2. To identify the surgery suitable for the candidate3. To identify the contra-indications4. To assess the expectations of the patient

History taking

I. Ocular history a) contact lens wear /contact lens intolerance b) intermittent squint or diplopia c) dry eye / ocular surface disorders d) previous refractive surgery or any other ocular

surgery e) ocular herpes simplex infectionII. Systemic history a) Pregnancy / lactation b) participation in high risk activities / contact sports c) diabetes mellitus d) auto-immune diseases e) Immuno- compromised statusIII. History of medication intake a) Tretinoin b) Oral antihistamines c) Antidepressants d) Sumatriptan e) Hormonal drugs f) History of other medication intakeIV. Occupation HistoryExamination

a) UCVA and BCVA b) Refraction: Manifest and cycloplegic c) Contrast sensitivity d) Glare acuity e) Keratometry f) Corneal topography g) Pachymetry h) Anterior chamber depth, white to white diameter i) Pupil examination (scotopic size) j) Tear � lm examination k) Slit lamp biomicroscopy with particular attention

to cornea l) Dilated fundus examination (posterior pole and

periphery) m) Tonometry

n) Endothelial evaluation o) Wavefront aberrometry p) Ocular motility and alignmentPatient counselling

a) Expectations of patient on the procedure outcome b) Potential risks, bene� ts and alternatives c) Options of refractive procedure suitable for the

candidate after investigations d) Answer all the queries of patients patiently e) Discuss refractive outcomes / surprises f) Night vision symptoms g) Dry eye symptoms and its managementRemember to

a) Ensure the discontinuation of contact lenses before examination for appropriate duration depending upon the type of contact lens

b) Informed consent c) Prescribe preoperative topical antibiotic

prophylaxisIntra-operative

a) Check and calibrate the machine b) Con� rm the identity of the patient and the eye to

be operated c) Check the refractive parameters before starting the

procedurePostoperative

a) Postoperative slit lamp biomicroscopy ( immediate postoperative and at all follow-up visits)

b) Schedule visits as required c) Ensure compliance to postoperative care/

instructions d) Check intraocular pressure in postoperative visits e) Postoperative refractions and visual acuity f) Emphasize to patient on safe keeping of pre-

operative and postoperative refractive and biometric data for future use

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