Professional Documents
Culture Documents
Contents
A Retrospective Review of Vision Threatening Complications Post Intravitreal Bevacizumab in CRVO.................................................................................... 1033
Dr. Narendra G. Venkata, Dr. Sambasiva Rao Velagapudi
Is Elevated Plasma Homocysteine in Patients With Retinal Veinous Occlusion A Indicator for Severe Macular Edema?....................................................... 1036
Dr. Poninder Kumar Dogra, Dr. Sqn Ldr Avdesh Oli, Dr. Brig Ajay Banarji, Dr. Brig T. S. Ahluwalia
Associations of AMD in Central India. The Central India Eye and Medical Study (CIEMS) ................................................................................................ 1039
Dr. Nangia Vinay Kumar B., Dr. Jost Jonas, Dr. Arshia Matin, Dr. Maithili Kulkarni Dr. Maneesh M. Bapaye, Dr. Meena M. Bapaye, Dr. Charuta M. Bapaye
Recording Posterior Segment Surgery with Handycam............................ 1044 Our 5 Years Experiences with 102 Intravitreal Injections of Avastin as Primary Therapy for ROP............................................................................... 1047
Dr. Rohan Chauhan, Dr. Banker Alay S.
Clinical Features Diagnosis and Management of Choroidal Neovascular Membrane in Pediatric Population............................................................... 1054
Dr. Jyoti Prakash Vyas, Dr. Giridhar A., Dr. Thomas Thachil
Dr. Sucheta Kshirsagar, Dr. Pravin Narwadkar, Col.M.Deshpande, Dr. Nilesh Kakade
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he term choroidal osteoma was coined by Gass in 1978.1 These tumors demonstrate evidence of bone formation in the choroid and are believed to be choristomatous in origin.2 In a follow-up study of 36 patients, the probability of loss of visual acuity (20/200 or worse) was more than 50% over 10 years.3 Choroidal neovascularization (CNVM) is the most frequent cause of visual loss (>50%) in choroidal osteoma.4
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DISCUSSION
LASER photocoagulation was initially used for Choroidal osteoma with extrafoveal secondary CNVM.5 Aylward et. al. found the success rate in such cases to be only 25%.2 Nearly half of Choroidal osteoma related CNVM were subfoveal, which could only be observed. Extrafoveal CNVM too was poorly responsive to laser photocoagulation, probably due to depigmentation of RPE and degenerated RPE/Bruchs membrane complex, resulting in the reduced laser uptake. Surgical removal of subfoveal CNV has been performed successfully; however, the visual result has been poor.6 Reports of PDT for osteoma-related CNVM have been published. However, issues related to cost, risk of vision loss and need for multiple retreatments have been raised.7 TTT has also been tried in this condition but there is lack of visual recovery.8 Bevacizumab has been used successfully for the treatment of CNVM due to neovascular AMD.9 We used intravitreal bevacizumab for the treatment of Choroidal osteoma related CNV and observed rapid regression of CNV with a marked improvement of visual acuity. Marked improvement of visual acuity and rapid regression of CNVM was observed in our patient following 3 intravitreal injections of bevacizumab. However, recurrence was seen two months later which was treated with one more injection after which CNVM got stabilised and patient is maintaining a visual acuity of 6/6. Narayanan R et. al. reported prompt visual recovery and rapid CNVM regression following bevacizumab injection for Choroidal osteoma related CNVM.10 Similar finding were noticed by Ahmadieh H et. al.11 This treatment modality may be superior to previous methods in terms of anatomic and visual results. This dramatic effect may be attributable to the very thinned and degenerated RPE/Bruchs membrane complex, resulting in the better penetration of bevacizumab into the underlying subretinal space. In conclusion: 1. Intravitreal bevacizumab may be an effective treatment modality in management of CNVM secondary to choroidal osteoma. 2. Larger series of such cases need to be studied to further validate our findings.
REFERENCES
1. Gass J D, Guerry RK, Jack RL, Harris G. Choroidal Osteoma. Arch Ophthalmol 1978;96:428-35.
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6. Foster BS, Fernandez-Suntay JP, Dryja TP, Jakobiec FA, DAmico DJ. Clinicopathologic reports, case reports, and small case series: Surgical removal and histopathologic findings of a subfoveal neovascular membrane associated with choroidal osteoma. Arch Ophthalmol 2003;121:273-6. 7. Singh AD, Talbot JF, Rundle PA, Rennie IG. Choroidal neovascularization secondary to choroidal osteoma: successful treatment with photodynamic therapy. Eye (Lond) 2005;19:482-4. 8. Shukla D, Tanawade RG, Ramasamy K. Transpupillary thermotherapy for subfoveal choroidal neovascular membrane in choroidal osteoma. Eye (Lond) 2006;20:845-7. 9. Avery RL, Pieramici DJ, Rabena MD, Castellarin AA, Nasir MA, Giust MJ. Intravitreal bevacizumab (Avastin) for neovascular age-related macular degeneration. Ophthalmology 2006;113:363-72. 10. Narayanan R, Shah VA. Intravitreal bevacizumab in the management of choroidal neovascular membrane secondary to choroidal osteoma. Eur J Ophthalmol 2008;18:466-8. 11. Ahmadieh H, Vafi N. Dramatic response of choroidal neovascularization associated with choroidal osteoma to the intravitreal injection of bevacizumab (Avastin). Graefes Arch Clin Exp Ophthalmol 2007;245:1731-3.
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Dr. V. K. Dhull, Dr. Anugya Agrawal, Dr. Geeta Gathwala, Dr. Manisha Nada
etinopathy of prematurity (ROP) is one of the leading causes of blindness and marked visual impairment among premature and low birth weight neonates. The rate of blindness caused by ROP varies greatly among countries and different regions within countries depending on their level of development, standard of neonatal care, neonatal outcomes and whether effective screening and treatment programs exist. That is why, screening guidelines must not be generalized and must take into account regional differences. As screening criteria differ across different units and time-periods, overall incidence of ROP varies from 20% to 52% with more recent studies reporting lower rates of ROP ranging from 20% to 30%.1-4 An important lesson is learnt from units reporting ROP in different time periods. Initial low incidence of ROP rises with better screening protocols, availability of assisted ventilation services and survival of sicker, smaller neonates. In this phase even sick but relatively mature (late preterm) neonates have been reported to develop ROP. This period is followed by gradual decline in incidence of ROP especially of more severe variety. Different studies have reported various risk factors. Some of them are debatable, but most established among them are low gestation age, low birth weight and unmonitored supplemental oxygen administration. 5-7 Treatment includes cryotherapy/laser photocoagulation of avascular retina and recently intravitreal injections of anti-VEGF agents for threshold disease and vitreoretinal surgery for advanced stages with variable visual outcomes. Considering so much of diversity in incidence, risk factors and treatment outcomes of this disease, we realised that guidelines and screening programs that take into consideration the characteristics of local populations should be designed. So, we decided to conduct a prospective study in our region, in order to design a better and more efficient screening program and analyse risk factors and efficacy of latest treatment modality using anti VEGF agents.
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RESULTS
In total 207 surviving preterm neonates who met inclusion criteria were screened. Subjects were finally divided in two groups. In group I: ROP was present while in group II: ROP was absent. At the completion of follow-up, 44 (21.26%) were diagnosed to have developed some degree of ROP in at least one eye on at least one occasion. Gender was not found to significantly influence the frequency of ROP in the study (p=0.124). The mean birth weight of group I was 1284.66 209.144 grams and of group II was 1396.04 188.237 grams. This difference was statistically significant using independent sample t-test (p =0.001). The mean period of gestation in group I was 31.095 1.856 weeks and of group II was 32.207 1.545 weeks. This was highly significant using independent sample t-test (p< 0.001). Among the 44 ROP patients, 2(4.54%) cases of unilateral and 6(13.62%) cases of bilateral stage 3 with plus disease, extending over > 6 contiguous/ 8 cumulative clock hours were found. Bilateral cases underwent nonconfluent green laser peripheral retinal ablation using
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DISCUSSION
In our study, incidence of ROP (21.26%) is similar to more recent studies... Our incidence of 14.9% in babies with birth weight >1250 gm. is greater than a report from USA (2006) in which Yanovitch et. al. found 4.2% in babies weighing between 12501800 grams.8 Our study has revealed 10 risk factors that portend the development of ROP in preterm babies in our region. This is comparable to other studies.2,9,10 When these significant factors were analysed using multivariate logistic regression, it was found that oxygen exposure (p< 0.001) was the only independent risk factor, which is a well-established risk factor in the development of ROP including severe ROP, in VLBW and LBW babies.7 A recent study in India with similar screening criteria and similar overall incidence (22.3%) found that 33.6 % babies with ROP required treatment.4 This was greater than that found in our study (11.36%). This difference may be explained by better NICU facilities in our institute. Though the incidence of ROP is significantly greater below the 1500 mark but the fact that 8.1% of high risk babies weighing >1500 grams have ROP, cannot be ignored. The need of the hour is to establish sickness criteria so that only those with significant risk factors in the heavy cohort are screened.
REFERENCES
1. Charan R, Dogra MR, Gupta A, Narang A. The incidence of retinopathy of prematurity in a neonatal care unit. Indian J Ophthalmol 1995;43:123-6.
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6. Seiberth V, Linderkamp O. Risk factors in retinopathy of prematurity. A multivariate statistical analysis. Ophthalmologica 2000;214:131-5. 7. 8. Patz A, Hoeck LE, de la Cruz E. Studies on the effect of high oxygen administration in retrolental fibroplasia: I. Nursery observations. Am J Ophthalmol 1952;35:1248-53. Yanovitch TL, Siatkowski RM, McCaffree M, Corff KE. Retinopathy of prematurity in infants with birth weight > or =1250 grams- incidence, severity, and screening guideline cost-analysis. J AAPOS 2006;10:128-34. Charles JB, Ganthier R Jr, Appiah AP. Incidence and characteristic of retinopathy of prematurity in a low income inner city population. Ophthalmology 1991;88:14-7.
9.
10. Jandeck C, Kellner U, Kossel H, Bartsch M, Versmold HT, Foerster MH. Retinopathy of prematurity in infants of birth weight > 2000g after hemorrhagic shock at birth. Br J Ophthalmol 1996;80:728-31.
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REFERENCES
1. Priglinger SG, Wolf AH, Kreutzer TC, Kook D, Hofer A, Strauss RW, et. al. Intravitreal bevacizumab injections for treatment of central retinal vein occlusion: Six-month results of a prospective trial. Retina. 2007;27:100412. 2. Ferrara DC, Koizumi H, Spaide RF. Early bevacizumab treatment of central retinal vein occlusion. Am J Ophthalmol. 2007;144:86471.
3. Retinal vascular events after intravitreal bevacizumab. (Mansour AM Acta Ophthalmol. 2010;88:730-5.
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Is Elevated Plasma Homocysteine in Patients With Retinal Veinous Occlusion A Indicator for Severe Macular Edema?
Dr. Poninder Kumar Dogra, Dr. Sqn Ldr Avdesh Oli, Dr. Brig Ajay Banarji, Dr. Brig T. S. Ahluwalia
etinal vein occlusions can be either central retinal vein occlusions (CRVO), hemi retinal vein occlusions (HCRVO) or branch retinal vein occlusions (BRVO).1,2 It is second only to diabetic retinopathy as a retinal vascular cause of visual loss, and the effect of this condition has on the visual acuity and visionrelated quality of life can be significant.2 Although the pathogenesis is still not fully understood, some of the common factors associated are age, hypertension, atherosclerotic retinal vessel changes, diabetes, hyperhomocystinaemia and open angle glaucoma. CRVO/HCRVO/BRVO seem to have a comparable risk profile.1 In various studies on cardio vascular diseases it has been found that homocysteine (HCy) is an important risk factor for various atherosclerotic related diseases. The exact mechanism of Homocysteine related damage to blood vessels is not known. Homocysteine is a sulfur-containing nonprotein amino acid that is either metabolized to cystathionine by the transsulfuration pathway, requiring B6, or it is converted back to methionine by B12 and folate, requiring transmethylation.3 The accepted normal range of fasting plasma homocysteine ranges between 5-15 micro mol/litre. Hyperhomocysteinemia is an independent risk factor for atherosclerosis in the coronary, cerebral, and peripheral vasculature4 and increased incidence of myocardial infarction is seen in hyperhomocysteinemia.5 Homocysteine causes oxidative injury to the endothelial cells and enhances the peroxidation of low density lipoprotein, thereby promoting the atheromatous process. Despite the existence of studies pointing to mild hyperhomocysteinemia6 as a risk factor for systemic occlusive vascular disease, thrombosis, and stroke, the question as to whether Hcy is responsible for these events or if it is just an atherosclerosis marker remains to be answered. The relationship, if any, with retinal vein occlusion remains unclear. Till date none of the studies have found any correlation between plasma homocysteine levels and macular edema based on central macular thickness.
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RESULTS
A total of 59 patients of retinal vein occlusion were included in the study. Mean age of patients was 61.45 years with a range of 37 to 82 yrs. 54.23 % of patients were males while females were 45.76 %. 28 eyes had CRVO/HCRVO (47.45 %) and 31 had BRVO (52.55%). Right eye was involved in 59.32% and left eye was involved in 40.67%. Out of 59 patients, 42 (71.18%) had raised plasma homocysteine. The mean value of plasma homocysteine was 35.72 mol /l with a range 7.6 to 147.53 mol /l, SD 29.196. Mean CMT at presentation was 651.28 in patients with hyperhomocysteinemia. In patients with normal homocysteine mean CMT was 319.11 with mean homocysteine level of 9.86 mol/l. Elevated homocysteine clinically and statistically correlated with severe macular edema based on CMT( p value <0.001) as in Fig 1. In conclusion increased homocysteine may also augment thrombotic events, as it inhibits the expression of thrombomodulin secreted by the endothelial cells to prevent the activation of protein C. Homocysteine enhances the activity of factors V and VII and the adhesion of platelets to the endothelium. In addition,the toxicity of homocysteine to the vascular endothelium may also
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REFERENCES
1. Hayreh, S.S., Retinal vein occlusion. Indian journal of Ophthalmology, 1994;42:109-32. 2. G.:, C.J., ed. Central retinal vein occlusion. R. SJ. Mosby St Louis. 2001;3:1368-75.
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6. Lattanzio R, S.F., Ramoni A, Fattorini A, Brancato R, DAngelo A. 80. , Moderate hyperhomocysteinemia and early-onset central retinal vein occlusion. Retina, 2006;26:65-70. 7. Brown BA, M.J., Ward TP, Hollifield RD, Dick JS, Brozetti JJ, Howard RS, Thach AB, Homocysteine: a risk factor for retinal venous occlusive disease. Ophthalmology., 2002;109:287-90.
8. J, S., The many facets of hyperhomocysteinemia: studies from the Framingham cohorts. J Nutr., 2006;136:1726S-30S. 9. Tyagi N, S.K., Steed M, Ovechkin AV, Moshal KS., Mechanisms of homocysteineinduced oxidative stress. Am J Physiol, 2005;289:H2649-56.
10. N, W., Mechanisms of increased vascular oxidant stress in hyperhomocysteinemia and its impact on endothelial function. Curr Drug Metab, 2005;6:27-54. 11. Di Crecchio L, P.M., Sanguinetti G, Iacono P, Ravalico G, Hyper homocysteinemia and the methylenetetrahydrofolate reductase 677C-T mutation in patients under 50 years of age affected by central retinal vein occlusion. Ophthalmology. 2004;111:940-5. 12. Chua B, K.A., Wong TY, Mitchell P Homocysteine and retinal emboli the blue mountain eye study. Am J Ophthalmol, 2006;142:322-4. 13. Chau B, K.A., Wong TY, Mitchell P, Homocysteine and retinal vein occlusion: population based study. Am J Ophthalmol. 2005;139:181-2. 14. Angayarkanni Narayanasamy, B.S., Coral Karunakaran,, Hyperhomocysteinemia and Low Methionine Stress Are Risk Factors for Central Retinal Venous Occlusion in an Indian Population. Investigative Ophthalmology and Visual Science, 2007;48:1441-6.
Associations of AMD in Central India. The Central India Eye and Medical Study (CIEMS)
Dr. Nangia Vinay Kumar B., Dr. Jost Jonas, Dr. Arshia Matin, Dr. Maithili Kulkarni
ge-related macular degeneration (AMD) is one of leading causes of visual impairment and blindness in elderly subjects worldwide.1-6 The list of risk factors for AMD include many parameters, such as smoking, family history and ethnic background.7-25 Since these parameters differ between
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RESULTS
Fundus photographs were available for 4542 (96.4%) subjects. Early AMD was present in 215/4542 subjects (4.70.3%), and late AMD was detected in 8/4542 (0.20.03%) subjects. After adjustment for age, prevalence of AMD was significantly associated with hyperopic refractive error (P=0.001), shorter axial length (P=0.01), and higher corneal refractive power (P=0.02). Each diopter increase in hyperopic refraction or each mm decrease in axial length was associated with an 15% (odds ratio (OR):1.15; 95% confidence interval (CI):1.06,1.24) and 19% (OR:0.81; 95%CI:0.69,0.95) increased probability of early AMD, respectively. AMD was not significantly associated with blood pressure, serum concentration of cholesterol, glycosylated haemoglobin Hb1Ac, highdensity lipoproteins and postprandial glucose, gender, level of education, any parameter of smoking, alcohol consumption, psychiatric depression or of daily activities, anterior chamber depth, lens thickness, intraocular pressure, size of the optic disc, neuroretinal rim and parapapillary atrophy, nor amount of nuclear cataract and status after cataract surgery. If the statistical analysis was adjusted for age and refractive error, age-related macular degeneration was marginally significantly associated with a low intake of fruits (P=0.06).
DISCUSSION
The data from this population-based study demonstrated the expected association between age and age-related macular degeneration. After adjustment for age, hyperopic refractive error, and parallel to it, short axial length, was the single most important associated factor for the disease in adult Indians. The findings of previous studies on that topic have been inconsistent and inconclusive so far. The Rotterdam Study,17 the French DMLA Study,26 the Age-Related Eye Disease Study,14 and the Beijing Eye Study21 found a correlation between hyperopia and AMD. In contrast, the Beaver Dam study did not report on an association between refractive errors and either the 5-year.27 In contrast to previous population-based studies in Western countries as well as in South India, age-related macular degeneration in adult Indians living in rural Central India was not associated with any parameter of smoking, and
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REFERENCES
1. Kawasaki R, Yasuda M, Song SJ, et al. The prevalence of age-related macular degeneration in Asians: A systematic review and meta-analysis. Ophthalmology 2010;117:921-7. 2. Mitchell P, Smith W, Attebo K, Wang JJ. Prevalence of age-related maculopathy in Australia: the Blue Mountains Eye Study. Ophthalmology 1995;102:145060. 3. Vingerling JR, Dielemans I, Hofman A, et al. The prevalence of age-related maculopathy in the Rotterdam Study. Ophthalmology 1995;102:20510. 4. Krishnaiah S, Das T, Nirmalan PK, et al. Risk factors for age-related macular degeneration: findings from the Andhra Pradesh eye disease study in South India. Invest Ophthalmol Vis Sci 2005;46:4442-9. 5. Li Y, Xu L, Jonas JB, Yang H, Ma Y, Li J. Prevalence of age-related maculopathy in adult Chinese. The Beijing Eye Study. Am J Ophthalmol 2006;142:788-93. Correction: Am J Ophthalmol 2008;146:329. 6. Gupta SK, Murthy GV, Morrison N, et al.: Prevalence of early and late age-related macular degeneration in a rural population in northern India: the INDEYE feasibility study. Invest Ophthalmol Vis Sci. 2007;48:1007-11. 7. Bker T, Fang T, Steinmetz R. Refractive error and choroidal perfusion characteristics in patients with choroidal neovascularization and age-related macular degeneration. Ger J Ophthalmol 1993;2:1013. 8. Sandberg MA, Tolentino MJ, Miller S, et al. Hyperopia and neovascularization in age-related macular degeneration. Ophthalmology 1993;100:100913. 9. Vingerling JR, Hofman A, Grobbee DE, et al. Age-related macular degeneration and smoking. The Rotterdam Study. Arch Ophthalmol 1996;114:1193-6. 10. Smith W, Mitchell P, Leeder SR. Smoking and age-related maculopathy; the Blue Mountain Eye Study. Arch Ophthalmol 1996;114:151823. 11. Delcourt C, Diaz JL, Ponton-Sanchez A, et al. Smoking and age-related macular degeneration. The POLA Study. Pathologies Oculaires Liees a lAge. Arch Ophthalmol 1998;116:1031-5. 12. Wang JJ, Mitchell P, Smith W. Refractive error and age-related macular degeneration: the Blue Mountains Eye Study. Invest Ophthalmol Vis Sci 1998;39:216771.
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In the OR we use OPMI MDO (Carl Zeiss Inc.) microscope with S5 stand for posterior segment surgery. The microscope has X-Y and zoom functions. Non contact wide angle viewing system Binocular Indirect Ophthalmomicroscope (BIOM IV) (Occulus, GmBH, Germany) is used for posterior segment visualization. For macula work we use Flat lens of Landers lens system with self stabilizing ring. Flexio MotionTM adapter developed by Carl Zeiss Inc is connected to one port of dual port beam splitter. This adapter can be connected to a wide range of handheld digital camcorders commercially available. We use Sony HDR XR-500E HandycamTM. The handycam records videos in Full HD AVCHD format having resolution of 1080i. The camera has hard disc with 120GB capacity. It records videos for approximately 1200 minutes before hard disc is entirely occupied. The camcorder has automatic functions for focussing, adjusting white balance and illumination. These functions can be changed manually if required though we prefer to use autofocus function as we can avoid manual adjustment during critical stages of surgery. Camera zoom can be adjusted separately using camera controls. Once desired level of magnification is achieved, it further varies proportionately with microscope zoom function. The camera comes with video output cable which is connected to external monitor for real-time viewing.
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For editing the video we use Windows movie maker software preloaded with the Windows office. It is possible to precisely edit the video, blend subsequent clips, add voiceover as well as text where required.
DISCUSSION
Video recording using analog CCD cameras had been a preferred mode for past 20 to 25 years. But in last 4 to 5 years, recording of surgical videos directly into digital formats is preferred. Analog video formats have much lesser resolution (230 lines) as compared to digital formats (720 or 1080 lines in HD format). Further it has to be converted to digital format before editing and archiving. Process of conversion causes further loss of resolution.2 The process of conversion into digital format is cumbersome and time consuming. Hence digital formats have become more popular. The video recording system we describe here consists of FlexioMotionTM adapter by Carl Zeiss Inc. attached onto one of the ports of dual port beam splitter. This adapter supports wide range of handheld digital camcorders. We use Sony HandycamTM HDR XR 500E, which has hard disc which can store 120GB of data. This camcorder records videos in Full HD which has resolution of 1080i. It uses AVCHD format which was developed by Sony and Panasonic. AVCHD format compresses video to a great extent without losing quality. Audio format used to compress the audio data supports 8 channel surround sound without loss of quality. During edition if the video this format can be stored in different resolutions without losing video and audio quality. The difficulties that we faced during use of this system were mostly related to autofocus function. As the camcorder is designed to focus at closest object, an air bubble in anterior vitreous leads to loss of focus of posterior structures. In the psedophakic eyes these bubbles can be easily removed with vitrectomy
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REFERENCES
1. Ankur Sinha, Rohit Saxena, H S Sethi, Kiran Turaka. Hand held digital camera for digital video recording of ophthalmic surgery. Indian J Ophthalmol 2006;54:209. 2. Raju B, Raju NSD, Raju AS, Sudhakaran CP, Razak A. Digital video recording and archiving in ophthalmic surgery. Indian J Ophthalmol 2006;54:53-7.
Our 5 Years Experiences with 102 Intravitreal Injections of Avastin as Primary Therapy for ROP
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RESULTS
Retrospective analysis of 102 eyes of 58 patients with severe ROP who received single IB (0.025cc) injection. Baseline characteristics : 102 eyes (58 patients), (OD :49, OS :53), 39 males and 16 females with birth weight and gestational age ranging from 25-36 weeks (Mean 28 weeks) and 820-1900 grams (Mean 1241 grams), respectively, were included in the study. The follow-up ranged from 3 to 5 years, with a mean follow up
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DISCUSSION
Laser or cryotherapy has been the gold standard in treating severe ROP. However even following optimal treatment there are many eyes that have a very poor visual prognosis. Recently, VEGF has been recognized to play a role in the pathogenesis of severe ROP. The safety and efficacy of intravitreal anti-VEGF drugs like bevacizumab (AvastinTM), pegaptanib (MacugenTM) and ranibizumab (LucentisTM) in various retinal vascular diseases have been established. The choice of bevacizumab was deliberate to try to minimize the possibility of systemic complications. The molecular weight of bevacizumab is 149 kd, that of VEGF-trap (investigational) is 110 kd, and that of ranibizumab (Lucentis; Genentech, Inc.) is 48 kd. It is especially undesirable to inject a small molecule that might easily penetrate into the undifferentiated peripheral retina and cause local damage. In addition, a small molecule could potentially traverse the retinal barrier completely and escape into the circulation in amounts more likely to cause systemic complications. Only 1:1,000 of the bevacizumab level in the treated eye has been shown (in rabbits) to be present in the nontreated eye or in the blood. In adults, the intravitreal half-life of bevacizumab is 5.6 days, that of VEGF-trap is 4.4 days, and that of ranibizumab is 3.2 days. Injection of substances into the preterm vitreous, which is very viscous compared with the more liquefied aging vitreous, likely increases this half-life considerably
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REFERENCES
1. Quiroz-Mercado H, Ustariz-Gonzalez O, Martines-Castellanos MA, et al. Our experience after 1765 intravitreal injections of bevacizumab: the importance of being part of a developing story. Semin Ophthalmol. 2007;22:109-25. 2. Sangtam T, Vinekar A, Maheshwar B, Dogra MR, Eong KA. Intravitreal bevacizumab (Avastin) for post-laser photocoagulation anterior segment ischemia in aggressive posterior retinopathy of prematurity. Indian J Ophthalmol 2007;55:317. 3. Shah PK, Narendran V, Tawansy KA, et al. Intravitreal bevacizumab (Avastin) for post laser anterior segment ischemia in aggressive posterior retinopathy of prematurity. Indian J Ophthalmol. 2007;55:75-6. 4. Quiroz-Mercado H, Ustariz-Gonzalez O, Martines-Castellanos MA, et al. Our experience after 1765 intravitreal injections of bevacizumab: the importance of being part of a developing story. Semin Ophthalmol. 2007;22:109-25. 5. Azad R, Chandra P. Intravitreal bevacizumab in aggressive posterior retinopathy of prematurity. Indian J Ophthalmol 2007;55:319.
6. Travassos A, Teixeira S, Ferreira P, Regadas I, Travassos AS, Esperancinha FE, Prieto I, Pires G, van Velze R, Valido A, Machado Mdo C.Intravitreal bevacizumab in aggressive posterior retinopathy of prematurity. Ophthalmic Surg Lasers Imaging. 2007;38:233-7. 7. Lalwani GA, Berrocal AM, Murray TG, Buch M, Cardone S, Hess D, Johnson RA, Puliafito CA. Off-label use of intravitreal bevacizumab (Avastin) for salvage treatment in progressive threshold retinopathy of prematurity. Retina. 2008;28(3 Suppl):S13-8. 8. Mintz-Hittner HA, Kuffel RR Jr. Intravitreal injection of bevacizumab (avastin) for treatment of stage 3 retinopathy of prematurity in zone I or posterior zone II. Retina. 2008;28:831-8. 9. Kusaka S, Shima C, Wada K, Arahori H, Shimojyo H, Sato T, Fujikado T. Efficacy of intravitreal injection of bevacizumab for severe retinopathy of prematurity: a pilot study. Br J Ophthalmol. 2008;92:1450-5. Epub 2008 Jul 11.
10. Jager RD, Aiello LP, Patel SC, Cunningham ET Jr. Risks of intravitreous injection: a comprehensive review. Retina. 2004;24:676-98. 11. International Committee for the Classification of Retinopathy of Prematurity. The International Classification of Retinopathy of Prematurity Revisited [published correction appears in: Arch Ophthalmol. 2006;124(11):1669-1670]. Arch Ophthalmol. 2005;123:991-9. 12. Chung EJ, Kim JH, Ahn HS, Koh HJ. Combination of laser photocoagulation and intravitreal bevacizumab (Avastin) for aggressive zone I retinopathy of prematurity. Graefes Arch Clin Exp Ophthalmol. 2007;245:1727-30. Epub 2007 Aug 10. 13. Honda S, Hirabayashi H, Tsukahara Y, Negi A. Acute contraction of the proliferative
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Clinical Features Diagnosis and Management of Choroidal Neovascular Membrane in Pediatric Population
Dr. Jyoti Prakash Vyas, Dr. Giridhar A., Dr. Thomas Thachil
ubfoveal choroidal neovascularization in children is a rare event, typically occurring as a complication of inflammatory or infectious chorioretinal disease. Visual acuity may be compromised by the subfoveal location of the choroidal neovascular complex, exudative macular detachment, subretinal or subretinal pigment epithelial hemorrhage, and cystoid degenerative changes of the neurosensory retina. Wilson and Mazur and Goshorn et. al. reported that 58% of subretinal neovascular membranes in children and adolescents undergo spontaneous involution, with 29% achieving a final visual acuity of 20/50.The prognosis for subfoveal neovascularization in children is reportedly more favorable than for adult neovascularization from either exudative agerelated macular degeneration (AMD) or presumed ocular histoplasmosis (POHS). Intravitreal injection of anti VEGF agents is the current standard of care treatment in treatment of neovascular age related macular degeneration(AMD). Intravitreal anti-VEGF therapy is also being used increasingly in cases of retinal veno occlusive disease, proliferative diabetic retinopathy and non AMD related CNV from causes like myopia, idiopathic, postinflammatory.
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RESULTS
16 eyes of 16 patients were enrolled of which 14 eyes with adequate follow up were analyzed. The mean age of the patients was 14.5 years (Range 7-18 years) with a mean period of follow up of 27.5 months (Range 6-89 months). The sex distribution was equal. All patients except one had unilateral disease. The patient with the bilateral disease had CNV secondary to Bests disease. The etiologies included post inflammatory in 48.57%, posttraumatic in 7.1%
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Representative Cases
Case No. 1: A 17 year old male developed diminution of vision OD to 6/60 N36. Ocular examination, fundus photography, FA and OCT showed subfoveal active CNV (Fig 1a). Loading dose of Bevacizumab was given at monthly intervals. Repeat FA (Fig 1b) showed residual activity so two additional doses of Bevacizumab were given at monthly intervals. BCVA was 6/9 N6 at 6 months and repeat FA showed scar with staining. (Fig 1c). Case No. 2: A 12year old female developed diminution of vision OS to 6/36 N36. Ocular examination, fundus photography, FA and OCT showed subfoveal active CNV (Fig 1a). Combination therapy with IVTA and thermal laser was done. Repeat FA showed total resolution. BCVA was 6/6 N 8p at 6 months. The BCVA improved to 6/6 N6 at 1 year and she has maintained the same BCVA till her last follow up (38 months).
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1(a) 1(b) 1(c) Figure 1: (a) Shows the pretreatment FA showing a subfoveal predominantly classic CNV and OCT shows a fibrovascular PED with serous macular detachment; (b) Post loading dose of Bevacizumab residual activity of the CNV on FA and minimal serous macular detachment with fibrovascular PED on OCT. (c) Final FA and OCT after 2 additional doses of Bevacizumab, showing RPE window defects and FVPED. OCT shows no residual serous macular detachment. Figure 2: (a) Shows the pre treatment FA showing juxtafoveal classic CNV and the OCT showing a pre RPE fusiform lesion. (b) Post treatment with IVTA with thermal laser, FA showing scarring of the CNV with no residual activity. OCT shows hyperreflectivity in the juxtafoveal region with no residual intraretinal edema or serous macular detachment. 2(a)
2(b)
DISCUSSION
Although the clinical course of subfoveal CNV secondary to AMD is well documented in the literature, sparse information exists on both the natural history and treatment of CNV in the pediatric age group. Due to the rare occurrence of this entity, there are not many published reports in the available literature; it poses challenges in the management. Von Eiken et. al. reported photodynamic therapy to be successful in 1 case of a 5-year-old girl with subfoveal CNVM. The successful use of anti-VEGF therapies in younger patients, most notably in neonates with retinopathy of prematurity, has allowed for application of this treatment to other pediatric conditions. Cakir and colleagues reported two children with choroidal neovascular membrane that regressed following treatment with bevacizumab with documented
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REFERENCES
1. 2. Wilson ME, Mazur DO. Choroidal neovascularization in children: report of five cases and literature review. J Pediatr Ophthalmol Strabismus 1988;25:239. Goshorn EB, Hoover DL, Eller AW, et. al. Subretinal neovascularization in children and adolescents. J Pediatr Ophthalmol Strabismus 1995;32:17882.
3. Surgical Management of Subfoveal Neovascularization in Children J Sears, A Capone, Jr,.T Aaberg, Sr. H Lewis, H Grossniklaus, P Sternberg, Jr,. E DeJuan, Ophthalmology 1999;106:9204 4. Rosenfeld PJ, Brown DM, Heier JS et. al. MARINA Study Group, NEJM 2006; 355:1419-1431,,, Avery RL, Pieramici JD, Rabena MD, Castellarin AA, Nasir MA, Giust MJ, IVA for NVAMD, Ophthalmology; 2006;113:363-72. 5. 6. Buch H, Nielsen NV,Copenhagen City Eye Study, Ophthalmology 2005;112:787-78. Campochiaro PA, Hafiz G, Intravitreal ranibizumab for macular edema due to retinal vascular occlusion, implication of VEGF as a critical stimulator. Mol Ther 2008;16:791-799, Rodriguez- Fontal M IVL for DR Curr Diabetes Rev. 2009;5:47-51
7. von Eiken J, Hoh H, Rehfeldt K. Photodynamic therapy for choroidal neovascularization due to choroidal coloboma in a 512 -year-old child. Klin Monatsbl Augenheilkd 2007;22:140-45. 8. Cakir M, Cekic O, Yilmaz OF. Intravitreal bevacizumab for idiopathic choroidal neovascularization. J AAPOS 2009;13:296-8. 9. Cakir M, Cekic O, Yilmaz OF. Intravitreal bevacizumab and triamcinolone treatment for choroidal neovascularization in Best disease. J AAPOS 2009;13:94-6.
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etinopathy of Prematurity (ROP) is a disease peculiarly occurring in preterm neonates. It is a retinal vascular disease which, if left untreated can lead to irreversible blindness or severe visual impairment in babies. ROP is of particular significance for country like ours due to high number of preterm births .In last decade or two, modern neonatal care has been hugely responsible for survival of extremely premature babies. Currently developing countries like India are facing Third Epidemic of ROP1. Aggressive Posterior ROP (APROP) is a particularly aggressive form of the disease seen extremely preterm babies born before 30 weeks of gestational age or born with less than 1200 grams of birth weight 2. APROP starts earlier and progress very fast to blinding sequelae as compared to classical ROP.
Rationale
There have been very few publications discussing the spectrum of APROP. One study published from North India analyses the spectrum of APROP and outcome after laser treatment.3 Another study by Drenser et. al., analyses the anatomic and functional outcome after treatment of APROP.4 There has been no published data from western India. We conducted this study to find out clinical spectrum, anatomical outcome of treatment and also the correlation of occurrence of APROP with risk factors. To analyses the clinical presentation of aggressive Posterior retinopathy of prematurity cases, there correlation with risk factors and anatomical treatment outcome.
Objective
1. 2.
To study the clinical signs. To study various risk factors present in the neonates.
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RESULT
The mean Birth weight of babies was 1238 grams (Range 750 gm to 1742 gm). The mean gestational age was 30.6 weeks (range 28 weeks to 34 weeks). Six babies were above 1251 gms of birth weight, 4 were between 1000 to 1250 gms of Birth weight, 3 were of < 1000 gms. Other risk factors which were observed in these babies were ventricular support in 7(53.5%) babies, oxygen supplementation 9(69.2%). 14 eyes regressed after laser treatment alone, 8 eyes needed subsequent Inj. Avastin for non regressing ROP, 4 eyes were treated primarily with inj. Avastin; one eye developed stage 4B ROP even after laser and avastin and underwent lens sparing vitrectomy.
DISCUSSION
For our case series it is evident that APROP occurs in more mature and bigger babies in India .We had a baby with birth weight as higher as 1742 gms presenting with APROP. Recent neonatal forum of India (NNFI) guidelines recommend ROP screening of babies with birth weight < 1750 gms.5 We agree with recommendation that babies above this criteria but having strong neonatal course should be referred for ROP screening .
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REFERENCES
1. Gilbert C, Retinopathy of prematurity : A global perspective of the epidemics, population of babies at risk and implications for control, Early Human Development 2008;84:77-82. 2. Jalali S, Anand R, Kumar H, Dogra M R, Azad R, Gopal L, Programme planning and screening strategy in Retinopathy of prematurity. Indian J of Ophthalmol 2003;51:89-97. 3. Sanghi, Gaurav MS*; Dogra , Mangatr. MS*;Das, Pranab MS*; Vinekar, Ananad MS, FRCS*; Gupta, Amod MS*;Dutta, Saurabh MD. Aggressive Posterior Retinopathy of Prematurity in Asian Indain Babies: Spectrum of Disease and Outcome After Laser Treatment.
4. Drenser, Kimberly A. MD, Phd. Trese, Michael T. MD, Capone, Antonio Jr. MD, Aggressive Posterior Retinopathy of Prematurity. 5. Chairperson: Ranjan Kumar Pejaver ; Members: Archana P Bilagi, Anand Vinekar; Reviewers: Ashok K Deorari, Subhadra Jalali :NNF Clinical Practice Guidelines 2010.
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