Jan-March 2008 PDF

DJO VOLUME 14 NUM 7. JAN.
-MARCH 2008
Role of Avastin in Management of Diabetic Retinopathy Cataract Surgery in Patients with Diabetes Mellitus Role of Systemic Acyclovir in Recurrent Cases of Disciform Keratitis" The Science of Spirituality Ocular Tuberculosis: Current Paradigms in Diagnosis and Management Current treatment for Diabetic Macular Oedema Fields in Neuroophthalmology
Editor Dr. Rajpal Insaan
Delhi Journal of Ophthalmology

Editorial Board: DJO
Advisor : Rajvardhan Azad
Associate Editors: Tanuj Dada, Dinesh Talwar Insaan, Sanjay Chaudhary, S. Bharti, Shailesh G.M., Rajesh Sinha, Sonia Bhargav, Mohita Sharma, Ajay Aurora Managing Editors : Pradeep Sharma Insaan, Prashaant Chaudhry, Rohit Saxena, Sanjeev Gupta, Subhash Dadeya, Vishnu Gupta, Sharad Lakhotia, Punita K. Sodhi Deputy Editors: Aditya Insaan, Rajender Khanna, Subrata Mandal, Shibal Bhartiya, Nita Gurha, Anuj Mehta, Manisha Rathi Assistant Editors: Avneesh Gupta Insaan, Rajeev Garg, Tinku Bali Razdan, Neeraj Manchanda, Sarita Beri, S.K. Sahu, G.K.Das, Rakesh Mahajan
Chief Editor : Rajpal Insaan

International Scientific Coordinator: Ashok Garg International advisory board: Samuel J.K. Abraham, NCRM Chennai, India Suresh K. Chandra, USA V.K. Raju, USA Howard Fine ,USA S.M. Betharia ,Muscat Mateen Ahmed ,USA Rasik B. Vajpayee ,Australia Boris Malyugin ,Russia Mark J. Terry ,USA
Senior Executive Editors: S. Bharti, S.C. Lakhotia, Namrata Sharma, Amit Khosla, Sanjay Chaudhary, S K Khokhar, Rishi Mohan, Alkesh Chaudhary, Lalit Verma, Angshuman Goswami, Rajiv Gupta, Sanjeev Gupta,Rajender Prasad, Anita Sethi, Cyrus M. Shroff Contributing Editors : Hemali Sharma Insaan, Umang Mathur, Suneeta Dubey, Prashant Nathani, Shashwat Ray, Shalini Mohan, Rasheena Bansal, Julie Pegu, Abhiyan Kumar, Murlidharan, Thirumalesh, Neeraj Sharma, Punita Sodhi, Siddarth, Sumeet Khanduja, Neha Khanduja, Saurabh Dileep, Zahir Abbas, Sunil, Nagindra Vashist, Ritesh Gupta, Lalit Alok, Munish Dhawan Abstract review editors: Section editors: Cornea Refractive surgery Cataract Glaucoma Retina Ocular Trauma Ocular Psychiatry Oculoplasty Squint and Neuroophthalmolgy Uvea Pediatric Ophthalmology Ocular Genetics Stem Cell Medicolegal advisor Ocular Pharamacology Ocular Microbiology Community Ophtha. Ocular Anaesthesia Ocular Pathology Ritika Sachdeva, Charu Mittal
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Anita Panda, Ritu Arora, Radhika Tandon, Namarta Sharma Rasik B Vajpayee, Mahipal S. Sachdev, J.S. Titiyal, Rajinder Prasad Abhay Vasavada, P.V. Chadha, Anil Tara, Vivek Pal, Sudipto Pakrasi ,A.K.Aggrawal N.N.Sood, H.C.Agarwal, Ramanjit Sihota, Madhu Bhadauria, Usha Raina, Devender Sood J.K.S. Parihar, J.C. Das, Geeta Srinivasan P.N. Nagpal, Atul Kumar , Natarajan, A.K. Singh, R.B. Jain, Amod Gupta, B. Ghose, Y.R. Sharma, Manish Nagpal , M. Dogra, J.S. Guha, Rajpal Insaan Brig.D.P. Vats, Lt. Col. J.K.S. Parihar, Shukla, D.K. Mehta , Mahesh Chandra Ashok Sharma Insaan Ashok Grover, V.P. Gupta, Sushil Kumar, Mandeep Bajaj, Anita Sethi, Neelam Pushkar, Rachana Meel, Archana Sood Vimla Menon, Pradeep Sharma, Kamlesh, P.K Pandey, Gopal Das, Satya Karna, Subhash Dadeya Rajpal Insaan, SP Garg, Vaishali Gupta,Pradeep Venkatesh, Biswas Jyoti May, Virender Sangwan S. Ghose, S Khokhar, Anju Rastogi, Sarita Beri, Jasbir Kaur, Rima Dada Insaan Samuel JK Abraham,RV Azad, Lalit Kumar,Sujata Mohanty Madan Mohan,T.D. Dogra, P.C. Dixit, R.K. Sharma, Rajendra Prashad T. Velpandian, Alok K. Ravi Geeta Satpathy, Niranjan Nayak Rajkumar Gupta Insaan, R. Jose , G.V.S. Murthy, P. Vashisht, Monica Insaan, Punit Maheshwar Insaan, Yogesh Shukla Pandey, Renu Sinha Seema Sen, Seema Kashyap
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Senior Academic Executive Editors:
A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A A S. Ghose, Chief, R.P. Centre, AIIMS, Delhi K.P.S. Malik, HOD, Safdarjung Hospital, New Delhi D. Rammurti, Director, Lasik Centre, Coimbatore B. Ghose, Director Prof., Guru Nanak Eye Centre, Delhi P. D'souza, HOD, Lady Harding Medical College, Delhi V.P. Gupta, HOD, Guru Tegh Bahadur Hospital, Delhi A.K. Khurana, P.G.I.M.S., Rohtak (Haryana) Hari Mohan, Mohan Eye Institute, Delhi S. Vashist, HOD, Ram Manohar Lohia Hospital, Delhi Madan Mohan, Ex. Chief R.P. Centre P.K. Khosla, Ex. Chief R.P. Centre V.K. Dada, Centre for sight, Delhi; Ex. Chief R.P. Centre H.K. Tiwari, Centre for sight, Delhi; Ex. Chief R.P. Centre N.N. Sood, Glaucoma Imaging Center, New Delhi Brig. D. P. Vats, Army hospital (R & R), Delhi Cantt. S.C. Gupta, Medical Director, Venu Eye Institute, Delhi Amod Gupta, HOD, PGI Chandigarh S. Sood, HOD, GMC, Chandigarh Sandeep Mittal, Medical College & Hospital, Meerut Shrikant, HOD (B.H.U) Varanasi Kamal Jeet Singh, Medical College, Allahabad Daljit Singh, Director, Amritsar Eye Hospital, Amritsar Lingam Gopal, Director, Shankar Nethralaya, Chennai Natrajan, Mumbai, Aditya Jyot Foundation, Mumbai Amar Agarwal, Chennai Cyres K Mehta, Mumbai R.B. Jain, Delhi P.S. Sandhu, Principal, G.G.S Med. College, Faridkot, Punjab Dr. G.C. Jain, Prof. & Head, S.P. Medical College, Bikaner Gur Satendra Singh, Prof., GMC, Patiala G.S. Bajwa, Prof. & Head, DMC, Ludhiana Dr. Harpreet Kapoor, CMC, Ludhiana
National advisory board:

S. Sabharwal , Sharad Lakotia, R.K. Bhandari, A.K. Gupta, G. Mukherjee, P.N. Nagpal, Meenakshi Thakkar, B.N. Khanna, V.Menon, R.B. Jain, P.V. Chaddha, A.K. Singh, Om Prakash, Jolly Rohatgi, Uprit Dhaliwal, Gaurav Y. Shah, S.P.S. Grewal, Praveen Arora Regional Editors: A Aditya Insaan, Shah Satnam Ji Speciality Hospital, Sirsa A Neera Agarwal, Neera Eye Centre, Daryaganj, Delhi A Sanjay Khanna, Khanna Eye Hospital, Delhi A N. Shroff, Shroff Eye Centre, Delhi A Puneet Gupta, Sharnam Eye Centre, Ghaziabad A H.C. Agarwal, Max Eye Hospital, Delhi A Sushil Choudhry, Director, Eye Care, Noida A S. Singh, Tirupati Eye Hospital, Noida A Rajkumar Gupta Insaan, Gurusarmodia Hospital,Ganganagar (Rajasthan) A Piyush Kapoor, Ganga Ram Hospital, Delhi A Suneeta Dubey, Shroff Eye Hospital, Delhi A Charu Mittal, Meerut Medical College, Meerut A S. Sood, HOD, GMC Chandigarh A Abhishekh Chandra, BHU, Varanasi A Devindra Sood, Glaucoma Imaging Center, Delhi A M.C. Agarwal, Deen Dayal Upadhyay Hospital, Delhi A Yogesh Gupta, Hindurao Hospital, Delhi A Anil Mehta, ESI Hospital, Basai Darapur A Harpreet Singh Insaan, Jalandhar A P.S. Negi, HOD, Railway Hospital, New Delhi A Arun Singhvi, ASG Eye Hospital, Jodhpur A Karamjeet Singh, GMC Amritsar
Contribution Methodology: Delhi Journal of Ophthalmology (DJO) is a quaterly journal. Author/Authors must have made significant contribution in carrying out the work and it should be original. It should be accompanied by a letter of transmittal. The article can be sent by email to the Editor and the hard copy mailed. Articles received will be sent to reviewers whose comments will be e-mailed to the Author(s) within 4-6 weeks. The identity of the authors and the reviewers will not be revealed to each other by the editorial team. The contributors shall be responsible for statements in his /her/their work including the changes made during editing. Detailed instructions to the contributors and for advertisements are included at the end of the journal. Request for reprints or any queries should be addressed to the Editors office by email or post. Editorial Process: The DJO has Dr. Rajpal Insaan Additional Professor of ophthalmology Vitreo-Retina unit of R.P.centre AIIMS as its Editor who is assisted by a team of renowned ophthalmologists and an illustrious advisory board. The reviewers, who are leaders in their respective fields, form the back bone of the journal by setting standards for the published work. Editorial Office: Dr. Rajpal Insaan, Room No. 480, Dr. R.P. Centre, AIIMS, New Delhi-29, Tel. No. 011-26593180(D), 26588500,700, 26589900, Extn. 3180, 3188. Fax No. 011-26589380, 26588919, Mob. 09818598899,09868398421, e-mail drrajpal2001@yahoo.co.uk, drrajpal_editordjo@yahoo.co.in Published by: Dr. Rajpal Insaan, Editor DJO, on behalf of Delhi Ophthalmological Society, Delhi Printed by: Unique Prints, B 68/1, Narayana Industrial Area Phase-2, New Delhi-28, Mob. 09910169596, 011-25897397,41417889 Page design by: Dr. Rajpal Insaan, Sajan Insaan, Dera Sacha Sauda, Sirsa, Haryana. Secretarial Assistance: Ghanshyam Dass (93121 30365), Mrs. Anju Vohra
From Darkness to Light
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Contents of DJO Editorial Basics in ophthalmology Fields in neuroophthalmology Dr. Swati, Dr. Rohit Saxena, Dr. Vimla Menon Role of Avastin in management of Diabetic Retinopathy Dr. Manisha Agarwal, Dr. S.P. Chaudhary, Dr. Cyrus M.Shroff Cataract Surgery in Patients with Diabetes Mellitus Dr. Jagat Ram , Dr. Jaspreet Sukhija Ocular Tuberculosis: Current Paradigms in Diagnosis and Management Dr. Rajpal Insaan , Dr. Shibal Bhartiya Obesity and Eye Diseases Dr. Rajpal Insaan, Dr. Sonia Bhargav, Dr Shibal Bhartiya Current treatment for diabetic macular oedema Dr. Rajpal Insaan Role of Systemic Acyclovir In Recurrent Cases Of Disciform Keratitis" Dr. Kirti Jain. Dr. A.K. Sood , Dr. Suresh Chandra, Dr. Sandeep Kumar Dr. V. K. Malik, Dr. Sanjiv Kumar, Dr. Charu Jain, Dr. Reny Kamboj Prashaant Chaudhry, Rajpal Insaan, Vidya Nair, Vinod Kochupillai, Dr. S.C. Manchanda, Dr. R.L. Bijlani Hydrocephalus Requiring Shunt Surgery as an Initial Presentation of VogtKoyanagi-Harada Syndrome Dr. Subrata Mandal, Dr. Anusha V, Dr. Rajpal Insaan, Dr. Pradeep Venkatesh, Dr. Satpal Garg A case of giant choroidal tuberculoma misdiagnosed as amelanotic melanoma. Dr. Anusha V, Dr. Rajpal Insaan, Dr. Pradeep Venkatesh, Dr. Satpal Garg, Dr. Subrata Mandal Dr. Shailesh G.M., MD, DNB, Dr. Munish Dhawan, MD Aims of the Journal 27 - 31 Page No. 11 - 16
Major Review
17 - 19
Major Review
20 - 22
Major Review
23 - 26
Major Review
Current Treatment
Original Article
32 - 34
The Science of Spirituality
37 - 42
Case Report
43 -45
Case Reort
46 - 49
Journal Abstract Instructions to Contributor Forthcoming Events Various Eye Bank Training Programme
50 - 51 52 53 54 55
(DHAN DHAN SATGURU TERA HI AASRA) Respected Members of the DOS family I would like to express my humble gratitude to all DOS members who have provided me help. I dedicate this issue of Delhi Journal Ophthalmology to Beparwah Shah Mastana ji who was the founder of Dera Sacha Sauda Sirsa. Mastana ji who dedicated his whole life in removing the cataract and cobwebs of the minds of people. He founded a spiritual organization which is unique in itself as it does not seek or accept donation in any form. Hai ghat main sujhe nahin Laanat aisi jind Tulsi is Sansaar ko Bhayo Motiya Bind. I am thankful to my Guru Hazoor Maharaj Saint Gurmeet Ram Rahim Singh Ji Insan of Dera Sacha Sauda for providing me strength, ability and self confidence in bringing this issue of DJO. For me, my Guru is everything because he has taught me the scientific method of doing practical research which no one has taught me. It is important to do some research within ourselves not only to understand the true meaning of life but also attain peace and harmony in our daily activities. I have tried to introduce article on meditations because directly or indirectly, it has got positive impact on our life. The gene expression of those who practices yoga and meditation in contrast to normal healthy controls was characterized by enhanced immunity, downregulation of cellular metabolism, and alteration of apoptotic genes in favour of a rapid resolution of inflammation. I have tried to highlighted the various eye banks which are doing good work in eye donations. Article by Dr. Manisha Agarwal has discussed the role of Avastin in management of Diabetic Retinopathy. Article by Prof. Vimla Menon at all has discussed Fields in Neuroophthalmology. Article by Dr. Jagat Ram on Cataract surgery in Patients with diabetes mellitus has emphasized the role of preoperative fundus examination to diagnose CSME and proper management before cataract surgery. Dear colleagues, I hope that you find the present issue of the djo both interesting and intriguing. It should serve the basic purpose enhancing your clinical skills as well as provide a basic frame work to incorporate new procedures in your armamentarium. I am thankful to Prof. S. Ghose for providing necessary help for DJO. Special thanks to Prof. L.P. Aggarwal, who was the founder of Dr. R.P. Centre for Ophthalmic Sciences So, enjoy reading-------- and I sincerely look forward to hearing from you! Dr Rajpal Insaan Additional Professor of Ophthalmology Vitreo-Retinal Services R.P. Centre for Ophthalmic Sciences Editor DJO E mail: drrajpal2001@yahoo.co.uk Telephone- 011-26589380, 26589696 Mob. : 9818598899
Editorial
FIELDS IN NEUROOPHTHALMOLOGY
DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008
BASICS IN OPHTHALMOLOGY
Dr Swati, Dr. Rohit saxena, Dr. Vimla menon
The visual field is a three dimensional area which is visible through each eye when fixating at central target. Extension: centered on fixation point Superior 70 degrees u Inferior 70 degrees u Nasal 60 degrees u Temporally 90 degrees There is binocular representation of visual fields for 60 degrees to the right and left common fixation point. Visual pathway: The visual pathway starts with stimulation of photoreceptors of retina and processing in ganglion cell whose axons converge to form optic nerve. The nasal fibres of optic nerve cross each other at chaisma and then continue as optic tract which represents the one half visual field of each eye. The optic tract is relayed in ipsilateral lateral geniculate body where assortment of fibers occurs and optical radiation origin that terminate in visual cortex (area 17) of the occipital lobe. (fig 1) INTERPRETATION OF VISUAL FIELD Terminologies Isopter: is a line joining the retinal points of same sensitivity Constriction: implies that there is generalized decrease in sensitivity of retina and on kinetic perimetry it encloses smaller area than normal Hemianopia: when one half of visual field is involved either in one or both eyes Homonymous: the defects that are persent in the visual fields of both eye and are on the same side of the vertical meridian. Heteronymous: when the defects that are present in the visual fields of both eye but are on the opposite sides of the vertical meridian.
Address for correspondence:Dr. Swati Dr. Rajendra Prasad Centre for Ophthalmic Science All India Institute of Medical Sciences (AIIMS) New Delhi, India.
Temporal half of left retina Optic nerve Optic tract Optic chiasma Nasal halves of retinas Visual field of left eye Visual field of right eye
Never forget that the image on the retina is inverted.
Temporal half of right retina
Geniculocalcarine tract
Lateral geniculate body
The cerebral cortex receives the encoded images of the contralateral visual fields of both eyes.
Primary visual area (= striate cortex)
Based on Kahle W. Frotsoher M: Color Aves and Textbook of Human Anatomy. 5m ed. Stuffgavt. Theme. Vol. 3 p.355. 2003.
Figure 1: Visual Pathway
Scotoma: it is a localized area of decreased sensitivity. It may be absolute, when patient cannot see even the brightest possible stimulus or it may be relative if some stimuli are seen. They can be classified either by their location or by shape. Congruency: the extent to which homonymous field defects in each resembles the other in shape, size depth and slope of margins. More distal a lesion in visual pathway more congruence field defect it produces. For example lesion of occipital lobe will produce more congruent field defect than that by a lesion of optic tract. Retina Anatomy: The light rays from visual field converge and form image on the opposite corresponding retinal area. Thus the light rays coming from the temporal visual field 11
from on the nasal retina. The 140 million photoreceptor cells have function of detecting light, the signal is then conveyed to ganglion cells in the inner retinal layer and the axons on these ganglion cells form nerve fibre layer. The nerve fiber bundles finally converge at optic nerve head and exit as optic nerve. Fields defects: the layer of retina that is affected by the disease process determines the pattern of field defect. Lesions in outer retina have no particular definite boundaries so it can produce field defects of varying shape and shape Optic nerve Anatomy: optic nerve is formed by the axons of retinal ganglion cells those converge in form of nerve fiber bundles. Its about 50 mm in length and can be divided in to four parts: ONH (intraocular part. 1mm), inraorbital part (25mm), intracanalicular part (10mm), intra cranial (15mm). Organization: The nerve fiber bundles converge in specific pattern to form optic nerve head. The papillomacular bundle is formed by macular fibers that enter the temporal aspect the disc. The arcuate nerve fiber bundle contains the axons that arise from the temporal to the fovea and arch superiorly and inferiorly to the fovea to enter the superior and inferior poles of the disc respectively. The axons from the nasal retina enter radially in to the optic nerve head as nasal nerve bundle. Thus the macular fibers are centrally placed while fibers from the upper part of retina lie superiorly and those from lower retina are placed inferiorly in optic nerve. Field defects: lesions affecting the axons produce a field defect corresponding to the particular pattern of the nerve fiber bundle involved. These defects are well demarcated and respect the horizontal meridian and either involve blind spot or point towards it. Papillomacular bundle: involvement of this bundle of nerve fibers results in Central scotoma (fig 2), Centrocecal scotoma or paracentral scotoma Arcuate nerve fiber bundle defects lead to: Bjerrum scotoma, Seidel scotoma, nasal step of Ronne. Involvement nasal fibers bundle leads to wedge shaped defects Altitudinal defects are caused by involvement of axons at the superior or inferior pole of the optic disc. The arrangement of nerve fibers is maintained through out the optic nerve so even the lesion involving the posterior part of optic nerve produce pattern corresponding to the nerve fiber bundle involved. 12
Figure 2: central scotoma in case of optic neuritis
The Chaisma Anatomy: Chaisma is a flat structure formed by the crossing of nasal fibres of each optic nerve. The chaism is approximoately 4mm high 12mm wide and 8mm long. It is located over the diaphragm sella and posteriorly is related to wall of third ventricle. It continues as optic tract. There may be variation in the location of chaisma that may have important clinical significance. In 80% of its located directly over the sella (central) in such cases the pituitary lesions involve chaisma first; in about 10% of normal its located more anteriorly over the tubercullum sellae (prefixed) in such cases the pituitary lesions will involve optic tract first or in rest 10% of cases it's located more posteriorly over the dorsum sella when the pituitary lesions involve optic nerve first. Relations of chaisma: Anteriorly chaisma is related to anterior cerebral arteries and their communicating arteries.posteriorly it's related to hypophyseal stalk, pituitary body. It forms the floor of third ventricle and lies above hypophysis. Laterally its related to internal carotid artery and cavernous sinus. Organization: At chaisma the fibers representing the nasal visual field (temporal fibers) are present in the lateral part. The inferonasal fibres (superior temporal field) cross anteriorly in the chaisma and loop forward in to the contralateral optic nerve forming willbrand's knee and then continue in contralateral optic tract. The nasal macular fibers decussate most posteriorly. The upper nasal fibers (inferior temporal field) cross in the middle. Thus right optic tract constitutes the right nasal field (right temporal axons) and left temporal field (left nasal decussated fibers) representing the right half of visual space.
Clinical features: the patient with chiasmal lesion presents with varying signs and symptoms depending upon the type, size and site of lesions. Pituitary adenoma presents with signs of compression as well as other endocrinological abnormalities. There may be unilateral or bilateral loss of vision as result of compression of optic nerve by a tumour. Relative afferent pupillary defect may be present in unilateral lesions. Lesions of cavernous sinus and large pituitary adenomas compress the motor nerves of the eye leading to ocular motility disorders. See-Saw nystagmus and occilopsia is feature of tumour or trauma. Field defects: The axons in the chaisma are arranged in such a way that they are limited by a vertical meridian which passes through fovea of each eye; thus the lesion of chaisma and distal visual pathway respect the vertical meridian. The lesion at chaisma and posterior to it would always produce the defect in both eyes. The field defect produced by a lesion involving chaisma depends upon the location of chaisma, site of lesion and part of chaisma affected. Bitemporal hemianopia: The lesions that affect the body of chaisma produce bitemporal hemianopia (Figure 3). In most of the cases the chaisma is central although in some cases it may be pre or post fixed. Pituitary tumours, inflammations, apoplexy are the main lesions that can affect the body of chaisma and produce classical bitemporal hemianopia. Inferior bitemporal hemianopia is characteristic of craniopharyngioma. Saccular aneurysm of vessels in circle of Willi can also lead to bitemporal hemianopia. other ophthalmic conditions that can cause similar field defect are bilateral glaucoma and other optic neuropathies, disc anamolies and psychogenic visual loss.
ipsilateral eye) and temporal hemifield defect in contralateral eye (decussating nasal fibers of contralateral eye) (figure 4). Diseases like meningioma that arise form the dura of teberculum sellae and adjacent structure compress the optic nerve as well as chiasma. Depending upon their site and size they may lead asymmetric involvement of both eyes. Craniopharyngiomas can also lead to asymmetric visual field defects. Meningiomas and carniopharyngiomas when small in size, lead to the compression of the posterior part of the optic nerve or anterior part of chiasma, leading to mono-ocular field defect in ipsilateral eye, most commonly in the superotemporal quadrant (inferonasal decussating fibres). A proper and careful field evaluation will expose the subtle involvement of contralateral eye.
Figure 4: Junctional scotoma
Binasal field defects: A large mass lesion compressing one side of the optic chiasma can on further enlargement cause a midline shift of the chiasma with subsequent compression of the other side as well, leading to a binasal field loss presentation. This pattern of field loss can also be seen with empty sella syndrome, arachnoiditis and as a post-operative defect. Homonymous hemianopia: This type of field defect is commonly seen in cases where the chiasma is prefixed. Thus any lesion which affects chiasma can also affect the optic tract leading to homonymous hemianopia. Large pituitary adenomas and craniopharyngiomas are the most common causes. Lesions that affect the posterior part of chaisma cause central bitemporal hemianopia.
Figure 3: Bitemporal hemianopia in a case of pituitary adenoma
Junctional scotoma: is produced when a lesion involves the junction of the optic nerve and chaisma leading to optic nerve defect in ipsilateral eye and superior temporal (involvement of Willebrand's knee) defect in the contralateral eye. A lesion involving hemichaisma would cause total blindness in one eye (optic nerve of 13
OPTIC TRACT AND LATERAL GENICULATE BODY Anatomy: The optic tract runs superiorly and posteriorly from the optic chaisma and curves around brainstem to terminate in lateral geniculate body. Lateral geniculate
body is a part of thalamic body and is situated along the lateral aspect of the midbrain. Each geniculate body consists of six layers of neurons and second order fibers tralvellling though optic tract relay here. Lateral geniculate body has dual blood supply from anterior and lateral choroidal arteries, which nourish the superior and inferior homonymous quadrants of the retina respectively. Relations: Optic tracts lie between the tuber cinereum and anterior perforated substance. Organization: Each optic tract is formed by temporal fibers of the ipsilateral eye while nasal fibres from the contralateral eye. Thus each optic tract represents one half of binocular visual field. The arrangement of axons present in optic nerve takes a 90 degree turn through chaisma in to the optic tract. Thus the axons from lower retina lie in the lateral aspect; the axons from upper lie in the medial aspect while the macular fibers lie in the dorsolateral aspect. The axons from ipsilateral eye are relayed in nuclei layer 2, 3, 5 while axons from contralateral side relay in 1, 4 and 6 nuclei layer. The fibers from upper part of retina occupy the medial half of the anterior one third of the LGB. The lower retinal fibers occupy the lateral half of anterior one third of the LGB, while the macular fibers are relayed in the posterior two third of LGB. Clinical features: The characteristic optic atrophy pattern is seen in longstanding lesions of optic tract and LGB in form of hemianopic atrophy or Bow tie configuration of arophy. The most useful sign of localizing a lesion between optic tract and LGB is involvement of pupil. The optic tract lesions are associated with various pupillary abnormalities in form of Wernicke's hemianopic pupil and Behr's pupil. While in lesions of LGB pupil reactions are spared. Lesions affecting the optic tracts are craniopharyngiomas, meningiomas, and large pituitary adenomas, demyelinating diseases, vascular lesions such as aneurysms, arteriovenous malformations and hamartomas. Lesions affecting lateral geniculate body can be infarctions of both anterior and lateral choroidal arteries, tumors, trauma and inflammatory disorders. Field defects: All retrochiasmal lesions lead to contralateral homonymous macular splitting hemianopia with varying degrees of congruity. The more posterior the lesion, the more likely that defect would be congruous. Complete optic tract disruption on 14
one side leads to macular splitting complete homonymous hemianopia while the partial involvement will cause incongruous field defect. Similarly a defect of one of LGB will produce complete homonymous hemianopia while the partial lesions of LGB cause sectoral field defect. OPTIC RADIATIONS Anatomy: optic radiations are geniculocalcarine pathways that extend from LGB to the visual cortex. They cross the Wernicke's area as optic peduncles and travel in the retrolenticular part of the internal capsule. Organization: The fibers after exiting from the LGB rotate by 90 degrees again to regain their original arrangement. Thus the superior fibers lie in the upper part of radiation, inferior fibers in the lower part and macular fibers lie in the center. Arrangement of fibers in temporal lobe: the inferior fibers from corresponding superior visual fields of both eyes start from anterolateral part of LGB sweep anterior and then laterally along the temporal horn of the lateral horn to form Meyer's loop, then extend posteriorly to end in the area below the calcarine fissure of occipital cortex. Arrangement of fibers in parietal lobe: The superior fibers that carry inferior field travel directly through the lower portions of parietal cortex below the sylvian fissure to occipital lobe area above calcarine fissure. Field defects: Lesions involving the optic radiations produce field defects which are homonymous and more congruous. Features of temporal lobe involvement Temporal lobe lesions produce contralateral superior homonymous field defects since temporal lobe carries inferior fibers which form Meyer's loop. In more extensive lesions the defect may extend inferiorly but the hemianopia will be denser superiorly. The defects are wedge shaped defects of varying sizes that are homonymous, and incongruous. Temporal lobe lesions cause seizures paragnosia, involuntary movement of mouth, visual and auditory hallucinations. Aphasia is characteristic of left temporal lobe lesion. Most common lobe lesion is tumour which includes glioma and metastasis. Surgical resection of tumor (temporal lobe) when more than 8 cm, itself may produce field defects. Anterior choroidal artery infarction may affect the optic radiation in temporal lobe, as well as LGB. In such cases hemianesthesia along with contralateral hemiplegia occurs. Other lesions are trauma, demyelination, and abscess.
Features of parietal lobe involvement Lesions involving parietal lobe cause inferior homonymous field defect that is described as pie on floor. These defects are usually more extensive and more congruous than temporal lobe defect. The homonymous hemianopia of parietal lobe is always associated with macular splitting (fig 5). The involvement of right parietal lobe leads to deficit of spatial orientation of left space, thus the patient may neglect left half of the body. The involvement of left parietal lobe lesions is associated with Grestmann's syndrome, word blindness, and visual agnosia. The two most important localizing signs of parietal lobe lesion are loss of normal optokinetic response and conjugate deviation of the eyes. The differential diagnosis of lesions involving parietal lobe includes infaction, haemorrhage, a-v malformations and tumours.
field in one eye have their corresponding points in other eye thus there's overlapping of visual field of both eyes. In each eye there is an isolated temporal crescent in visual field for which they are no overlapping points in other eye. This temporal crescent perceived by nasal retina is represented in the anterior most portion of calcarine cortex. Clinical features: Occlusion of left posterior cerebral artery leads to the infarction of calcarine cortex along with splenium of the corpus collosum which leads to field defect in the right side and alexia without agraphia. Other signs include headache, visual agnosia, dyschmatopsia which are mainly secondary to the infarction. Tumours lead to isolated visual field defects and palinopsia. The tumours affecting the occipital lobe are gliomas, meningionmas and metastasis. Bilateral occipital disease is usually due to the vascular lesions which include thromboembolism, hemorrhage, hyperviscosity syndromes, vasculititis. Fields defects: occipital lobe lesions produce field defects that are homonymous and highly congruous. Central homonymous: A lesion affecting the tip of occipital lobe would produce a field defect in the macular area which is homonymous. Atleast 5 degrees of central field must be spared in both eyes on the side of hemianopia. Complete homonymous hemianopia sparing macula: The macular area is watershed zone of anastomoses between the middle and posterior cerebral arteries Most of the occipital lobe lesion (ischemia) results in in which central 3 to 5 degrees of the visual field is spared due to its dual blood supply (fig 6)
Figure 5: Right homonymous hemianopia in a case of left parietal lobe granuloma
VISUAL CORTEX Anatomy: the primary visual cortex (area 17) is located on the medial surface of the occipital lobe near the calcarine fissure. Brodmann's area 18 and 19 are associated visual areas which help in further processing of visual information.
Organization: the right visual cortex receives impulses from the left temporal field and right nasal field. The orientation of fibers in optic radiation is maintained in the visual Figure 6: Macular sparing right homonymous hemianopia cortex. The central field is represented in a case of left occipital lobe ischemia at the occipital tip and separated from the representation of peripheral fibers. The superior Quadrantic defects: The lesion of area below calcarine fibers (representing inferior field) are relayed in area fissure would give rise to homonymous superior superior to calcarine fissure while the inferior fibers quadrantic defect. Similarly a lesion involving are above (superior field) are projected to the area inferior to the calcarine fissure would lead to inferior homonymous fissure. The retinal points which represent the visual defect. Because of their anatomical and vascular 15
separation these defects always respect horizontal meridian and they should not be confused with optic nerve related visual field defects. The former are always homonymous and congruous and respect the vertical meridian as well. Involvement of bilateral occipital lobe may lead to bilateral homonymous hemianopia with sparing of central tubular vision. This should be differentiated with other causes of constricted visual field like malingering, glaucoma, retinitis pigmentosa. Lesions involving bilateral occipital tip would cause bilateral central homonymous hemianopia . A checkerboard pattern field defect results from involvement of occipital lobe below the calcarine fissure on one side and above the fissure on opposite side. There could be asymmetry in field defects in cases bilateral occipital lobe involvement. Temporal crescent: The binocular field of vision is formed by superimposition of corresponding visual points of the central 60-deree visual field of both the eyes, but then in each eye there is a peripheral area which has no corresponding points in other eye. This area is perceived by nasal most retina of the eye and is represented in the anterior most portion of the calcarine cortex. Any lesion involving the anterior most part of the calcerine cortex leads to monocular temporal crescentric field defect in the contralateral eye. Special visual field defects Baring of blind spot: when a small degree of field is mapped the isopter may be constricted and any scotoma outside the isopter may be continuous with blind spot causing true baring of blind spot. False baring of the blind spot is seen when the isopter is just outside the blind spot. Pseudobitemporal hemianopia: field defects that do not respect the vertical meridian. Binasal hemianopia: bilateral nasal defects are usually caused by involvement of arcuate fibers of both eyes. Rarely it may be caused by pressure upon the temporal aspect of the optic nerve or temporal portion of chaisma , as in cases of aneurysm, pituitary tumour, vascular infarction.
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16
ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY
MAJOR REVIEW
Role of Avastin in management of Diabetic Retinopathy
Dr. Manisha Agarwal,1 Dr. S.P. Chaudhary, 1 Cyrus M.Shroff1,2
Vascular endothelial growth factor (VEGF) plays a key role in the development of retinal neovascularization. Various studies beyond doubt have proved the correlation between increased VEGF levels in the vitreous specimen and the severity of proliferative diabetic retinopathy (PDR). There has been a significant reduction in the concentrations of VEGF after panretinal photocoagulation for PDR.3 Bevacizumab (Avastin, Genentech) is a humanized monoclonal recombinant antibody that inhibits all the active isoforms of VEGF.1 (Fig-1) VEGF is the main factor responsible for neovasculariztion, increase in capillary permeability, inflammation and is also said to have a neuroprotective role. Avastin by inhibiting all isoforms of VEGF blocks all these actions mediated through VEGF.
1,2
Intravenous Avastin has been approved by the Food and Drug Administration for the treatment of metastatic colorectal cancer.4 Avastin is currently having an off-label use in Ophthalmology, given as an intravitreal injection in the dosage of 1mg/0.04ml, 1.25mg/0.05ml or 2.5mg/0.1ml. Avastin has a beneficial effect in patients of diabetic retinopathy by the following mechanisms of action:1. Diabetic macular edema (DME)
The major cause of vision loss in patients of diabetic retinopathy is macular edema. Diabetic retinopathy study 5 has given guidelines for macular laser photocoagulation for clinically significant macular edema (CSME).We are aware of the importance of good systemic control of blood sugar levels, hypertension, lipid profile, renal functions prior to macular laser photocoagulation.6,7 Patients with persistent diabetic macular edema not responding to laser photocoagulation. Once the causes of DME such as vitreous macular traction and macular ischemia have been ruled out on optical coherence tomography and fundus fluorescein angiography respectively. We can treat these patients with intravitreal injection of avastin. Avastin helps in reducing DME by blocking the increased capillary permeability mediated through VEGF, without the associated side effects of laser photocoagulation such as macular burn, scotoma formation, decreased contrast senstivity ,choroidal neovascular membrane formation etc.
Figure - 1 Institutional Affiliation of authors:1. Dr.Shroff's Charity Eye Hospital 5027-Kedar Nath Road, Daryaganj, New-Delhi-110002. 2. Shroff Eye Centre A-9 Kailash Colony, New-Delhi.
Intravitreal triamcinilone is also effective against DME, however the advantage of avastin is that there is no risk of steroid induced glaucoma which is a very common side effect of triamcinolone.. Many are now considering intravitreal avastin injection as the first line of treatment for diffuse macular edema after a good systemic control. 17
2.
Regression of neovascularization Elsewhere(NVE)
leakage from NVD in 73% eyes and from NVE in 59% of the treated eyes by blocking all isoforms of VEGF and it's angiogenic effect on retinal neovascularization. However intravitreal injection of avastin in one eye caused a milder regression of the neovascularization in the contralateral eye also which signifies the fact that there is systemic absorption of the drug even after intavitreal injection. 3. Regression of Iris neovascularization(NVI) & Neovascular glaucoma (NVG) Many patients of PDR progress to develop iris neovascularization leading to neovascular glaucoma despite maximum laser photocoagulation. They present with corneal edema secondary to raised intraocular pressure (IOP) or hyphema which hampers further laser photocoagulation if not already completed .In such cases Avastin injection has shown a very good regression of NVI after intravitreal and intracameral injection in as short a time as 24 hours ,again by blocking the angiogenic effect of VEGF.(Fig-3)
& neovascularization on disc (NVD) Pan retinal photocoagulation has been the treatment of choice for PDR, as suggested by the Diabetic Retinopathy Study.
5
Laser photocoagulation
remarkably regresses the neovascularization thus preventing severe visual loss in most of the patients. However in a few situations an adjunctive or alternative therapy to laser photocoagulation is required such as Patients of PDR having undergone several sessions of laser photocoagulation with complete ablation of the retina showing persistence and proliferation of new vessels. Unable to perform laser photocoagulation due to a non-dilating pupil or media opacity such as cataract or vitreous hemorrhage. Intravitreal injection of avastin has shown benefit in regressing neovascularization in such situations along with laser photocoagulation. (Fig.2)
A B
Pre-Avastin
Early Phase
Late Phase
Post-Avastin
Fig.2a&2b: Early and late phase fundus fluorescein angiogram of the left eye showing leakage from neovascularization elsewhere (NVE) in the superior quadrant prior to Avastin Fig.2c&2d: Early and late phase fundus fluorescein angiogram of the left eye showing decreased leakage from the same neovascularization elsewhere (NVE) two weeks after intavitreal injection of Avastin.
Early Phase
Late Phase
Figure - 3
The case series of Robert LA et al,8 has shown resolution of leakage from NVI in 82% eyes of PDR patients treated with intravitreal Avastin injection, with recurrence of iris neovascularization in one case 11 weeks after the injection of avastin. 18
In an interventional, consecutive, retrospective case series by Robert LA et al,8 intravitreal injection of Avastin has shown complete resolution of angiographic
4.
Preoperatively in Diabetic vitrectomy
not possible, cases unresponsive to laser photocoagulation and lastly avastin may enhance the effect of laser photocoagulation by reducing the concentration of VEGF thereby reducing the aggressiveness of neovascularization. References: 1. Ferrara N. Vascular endothelial growth factor: basic science and clinical progress. Endocr Rev 2004; 25: 581-611. 2. Adamis AP, Shima DT. The role of vascular endothelial growth factor in ocular health and disease. Retina 2005; 25:111-8. 3. Aiello LP,Avery RL,Arrigg PG,et al. Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders.N Eng J Med 1994;331:1480-7. 4. Hurwitz H, Fehrenbacher L,Novotny W,et al. Bevacizumab plus irinotecan,fluorouracil, and leucovorin for metastatic colorectal cancer. N Engl J Med 2004; 350: 2335-42. 5. Diabetic Retinopathy Study Research Group. Preliminary report on effects of photocoagulation therapy. Am J Ophtahlmol 1976; 81: 383-96. 6. Gupta A, Gupta V, Thapar S, Bhansali. A. Lipid lowering drug Atorvastatin as an adjunct in the management of diabetic macular edema. Am J Ophthalmology 2004;137:675-682. 7. Gupta A, Gupta V, Dogra MR, Pandav SS.Risk factors influencing the treatment outcome in diabetic macular oedema. Indian J Ophthalmol 1996;44: 145-148. 8. Avery RL, Pearlman J, Pieramici DJ, Rabena MD et al. Intravitreal Bevacizumab (Avastin) in the Treatment of Proliferative Diabetic Retinopathy. Ophthalmology 2006;113:1695-1705. 9. Spaide, Richard F, Fisher, Yale L. Intravitreal Bevacizumab (Avastin) treatment of proliferative diabetic retinopathy complicated by vitreous hemorrhage.Retina.26 (3): 275-278, March 2006.
Intravitreal avastin injection given preoperatively about two weeks prior to a vitrectomy surgery in a patient of PDR helps in reducing intraoperative bleeding when fibrovascular proliferation is segmented or delaminated, thus helping in two ways-avoiding the loss of view during the surgery due to recurrent bleed making membrane dissection easier and reducing the need to elevate the bottle height of the infusion bottle for the purpose of hemostasis thereby reducing the risk of optic nerve ischemia in patients with already retinovascular perfusion. 5. Vitreous hemorrhage in PDR PDR patients with vitreous hemorrhage or with recurrent vitreous hemorrhage after vitrectomy surgery due to causes such as fresh bleed from persistent retinal neovascularization, anterior hyaloid proliferation or proliferation within sclerotomy sites. In such patients the vitreous hemorrhage hampers additional laser and thus an intravitreal injection of avastin in such a situation can help to regress the neovascularization and clear the vitreous hemorrhage. In a recent report of two cases by Spaide et al there was partial resolution of vitreous hemorrhage after 1 week and complete regression after 1 month in two patients of PDR with vitreous hemorrhage treated with intravitreal avastin injection. The role of the anti-VEGF avastin in the treatment of diabetic retinopathy is limited by the duration of action of the drug and the need to repeat the injections .It still remains unclear how frequently avastin injections need to be repeated to ensure permanent regression of neovascularization. Laser photocoagulation despite its associated side effects such as limitation of peripheral visual fields, decreased contrast sensitivity etc. still remains an essential intervention for the treatment of PDR. In future a combination of both intravitreal avastin and laser photocoagulation may offer advantages such as reduction in the requirement of multiple sessions of laser photocoagulation, reduction in side effects of laser photocoagulation, treatment in situations when laser is 19
9
impaired
CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS
MAJOR REVIEW
Cataract Surgery in Patients with Diabetes Mellitus
Prof Jagat Ram and Dr Jaspreet Sukhija
Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh Cataract Surgery in Patients with Diabetes Mellitus Prof Jagat Ram and Dr Jaspreet Sukhija Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh. Cataract is a well recognised complication of diabetes and it has been estimated that up to 20% of all cataract surgery is performed on diabetic patients. The overall risk of developing cataract is two to four times higher in patients with diabetes compared with patients without diabetes, 1 and in patients under the age of 40 years, this risk may be 15 to 20 times higher. The risk of developing cataract increases with poor metabolic control and duration of the disease. Although the cataract has been reported to be reversible after metabolic control, by and large the lenticular changes are irreversible. The 1997 guidelines of the Royal College of Ophthalmologists state that all forms of diabetic retinopathy may become more severe following cataract surgery. Various authors have reported retinopathy progression rates15% to 70%. The rate of DR progression after cataract surgery is known to be influenced by the severity of the preoperative DR, the duration of diabetes, and the adequacy of glycaemic control. More than 90% of patients with diabetes without retinopathy attain a final visual acuity of 20/40 or better. Macular edema is as an important cause of poor postoperative visual gain following cataract surgery. It is believed that inflammation consequent to cataract surgery leads to an increased permeability more easily in patients with diabetes, which in turn results in higher incidence of CME. The incidence of surgical complications is same in patients with diabetes without retinopathy and patients without diabetes. Clinically significant macular edema present in diabetic eyes at the time of surgery is unlikely to resolve spontaneously, and the postoperative visual acuity prognosis is not as good as in eyes without edema. Careful selection of cases and frequent follow-up may be needed in patients with preoperative CSME to reduce the progression of diabetic retinopathy and unresolved macular edema after cataract surgery.
Address for correspondence:Prof Jagat Ram and Dr Jaspreet Sukhija Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh.
PROGRESSION OF DIABETIC MACULOPATHY AFTER CATARACT SURGERY The preoperative status of retinopathy may influence its susceptibility to surgical invasion. Diabetic patients with any type of retinopathy should be advised that cataract extraction might increase the level of retinopathy. (Figure 1)
Figure 1. Right eye fundus photograph shows non-proliferative diabetic retinopathy (NPDR) with clinically significant macular edema (CSME). Fundus fluorescein angiography (FFA) shows leaking micro aneurysms (MAs) with late leakage corresponding to MAs.(A) Three weeks post phaco, no prior photocoagulation performed. Fundus photograph shows clear media with NPDR and CSME. FFA showed leaking MAs with late leakage from MAs with diffuse leakage forming cystoid macular edema (CME). (B) (Courtesy: Prof Amod Gupta and Dr Ramandeep Singh)
Diabetic nephropathy and retinopathy are microangiopathic processes. Thus, those who have diabetic nephropathy are more prone to breakdown of the blood- retinal barrier (BRB), which may facilitate the progression of diabetic retinopathy. Preoperative laser photocoagulation decreases the risk of progression of retionopathy after phacoemulsification. (Figure 2 &3). Gupta et al identified that the interval after cataract surgery was the most common risk factor for the occurrence of maculopathy in the aphakic/ pseudophakic eyes, and this had a significant negative correlate, thereby indicating that the macular edema in aphakic eyes tends to progress sooner after surgery than the natural course in the nonoperated fellow eyes.2 20
MANAGEMENT OF MACULAR EDEMA Macular edema tends to progress if caused by diabetes and improve if it is caused by Irvine-Gass Syndrome. There are no clear guidelines however regarding the optimum management of these eyes. Macular oedema that is not typical pseudophakic cystoid macular oedema can settle spontaneously in some patients. The early application of laser treatment for postoperative macula oedema in patients with diabetes would therefore mean over treating some patients. Generally, laser photocoagulation is deferred until 6 months or so to permit the resolution of Irvine-Gass syndrome. The
Figure2. Right eye fundus photograph shows media haze with non-proliferative diabetic retinopathy (NPDR) with clinically significant macular edema (CSME). Fundus fluorescein angiography (FFA) shows leaking micro aneurysms (MAs) with late leakage corresponding to MAs.(A) Six weeks after laser, he underwent uneventful phacoemulsifaction with intraocular lens implantation. Four weeks post phaco, fundus photograph shows clear media with NPDR and CSME. FFA showed reduction in leaking MAs with late leakage from MAs and minimal diffuse leakage in late phase.(B). (Courtesy: Prof Amod Gupta and Dr Ramandeep Singh)
angiographic CME following cataract surgery carries a favorable prognosis and seldom persists for more than a year. It is reasonable to expect a final visual acuity of at least 20/40 in nearly 90% of these eyes. In contrast, clinical CME that develops in eyes with pre-existing retinopathy often persists. Exactly when laser can be applied in the postoperative edema is still not well established. Such focal/grid treatment is best applied within the first 6 weeks after the surgery. In the series by Dowler's et al3 , macular edema secondary to cataract surgery occurred in nearly 50% of non CSME eyes, and it resolved in half of the eyes within 6 months and 75% within 1 year. Such eyes postoperatively do not require laser photocoagulation and may be managed conservatively. Preferably, diabetic retinopathy should be stabilized with appropriate laser treatment before cataract surgery. However, in patients where cataract density prevents appreciation of CSME or application of laser, laser photocoagulation should be applied as soon as the cataract wound is stabilized.
PHACOEMULSIFICATION/TYPE OF IOL/PCO IN PATIENTS WITH DIABETES

Figure 3. Right eye fundus photograph shows media haze with laser marks in macular area. The patient had been photocoagulated for proliferative diabetic retinopathy (PDR) and macular edema in the past in this eye. Fundus fluorescein angiography (FFA) shows transmission fluorescence with no leaking micro aneurysms (MAs) and new vessels.(A) Four weeks post phaco, fundus photograph shows clear media with laser marks. FFA showed transmission fluorescence minimal diffuse leakage in the foveal center.(B) (Courtesy: Prof Amod Gupta and Dr Ramandeep Singh)
The visual results and rate of maculopathy progression are quite similar to those of techniques. Presence of preexisting retinopathy and surgical inexperience are risk factors for progression of retinopathy. Those having ECCE have also been noted to have an increased rate of anterior segment complications including elevated levels of fibrin and the development of posterior
21
synechias.4 Similarly, postoperative aqueous flare is greater in diabetic patients having phacoemulsification and occurs with increased intensity with advancing retinopathy. Dowler and coauthors report a prospective series of 46 patients with diabetes and bilateral cataract in which they compared ECCE and phacoemulsification. They found that postoperative visual acuity improved more after phacoemulsification than after ECCE, especially in eyes with retinopathy. They postulated that this finding may be a result of the lower postoperative inflammation after phacoemulsification. It is beneficial to consider phacoemulsification earlier in diabetic patients before vision-limiting diabetic complications develop. Krepler et al did not find a significant difference in flare values between the acrylic and HSM IOL groups.6 Thus, in terms of postoperative inflammation, the lenses seem equally suitable for cataract patients with diabetic retinopathy. Variables other than surgical trauma and IOL type that may influence flare after cataract surgery include the grade of diabetic retinopathy and the presence of CSME. However PCO rates have been shown to be least with Acylic hydrophobic IOL. Silicon IOl's should be avoided in diabetics. Hayashi et al showed that diabetics developed greater PCO than nondiabetic patients after cataract surgery.7 PCO in diabetic patients progressed in the late postoperative period. The incidence of Nd:YAG laser capsulotomy was also higher in diabetic patients than in nondiabetic patients. There was no significant correlation between PCO and stage of diabetic retinopathy. Since blood-aqueous barrier breakdown is more severe in eyes with more advanced retinopathy, some chemical mediators that stimulate the proliferation of lens epithelial cells must be present abundantly in eyes with advanced diabetic retinopathy, which may subsequently lead to extensive PCO. However, opacification in the peripheral posterior capsule most certainly precludes visualization of the fundus. Therefore, it is important to keep the entire posterior capsule transparent in the patients with diabetes, not only for visual acuity, but also for laser photocoagulation of the retina. 22
3 5
References 1. Ederer F, Hiller R, Tayler HR: Senile lens changes and diabetes in the population studies. Am J Ophthalmol 1981;91:381-395. 2. Gupta A, Bansal RK, Goel RC: Risk factors for asymmetric diabetic retinopathy following cataract surgery. Annals Ophthalmol 1996 ; 28:311-316 3. Dowler JGF, Sehmi KS, Hykin PG, Hamilton AMP: The natural history of macular edema after cataract surgery in diabetes. Ophthalmology 1999; 106:663668. 4. Krupsky S, Zalish M, Oliver M, Pollack A. Anterior segment complications in diabetic patients following extracapsular cataract extraction and posterior chamber intraocular lens implantation. Ophthalmic Surg 1991; 22: 526-530. 5. Zaczek A, Zetterstrom C. Aqueous flare intensity after phacoemulsification in patients with diabetes mellitus. J Cataract Refract Surg 1998; 24:1099-1104 6. Krepler K , Ries E , Derbolav A, Nepp J, Wedrich A . Inflammation after phacoemulsification in diabetic retinopathy: Foldable acrylic versus heparinsurface-modified poly (methyl methacrylate) intraocular lenses. J Cataract Refract Surg2001;27: 233-238. 7. Hayashi k, hayashi H, Nakao F, Hayashi F. Posterior Capsule Opacification after Cataract Surgery in Patients with Diabetes Mellitus. Am J Ophthalmol 2002;134:10-16.
OCULAR TUBERCULOSIS
MAJOR REVIEW
Ocular Tuberculosis: Current Paradigms in Diagnosis and Management
Dr Rajpal Insaan , Dr Shibal Bhartiya, Dr Sonia Bhargav
In spite of advancement in various tests in diagnosis of intraocular tuberculosis clinical suspicious is the main in diagnosis of the same. We in our centre have not emphasized the various laboratory tests. Therapeutic trial on suspected lesions is very effective The diagnosis of intraocular tuberculosis is difficult because of the large variations in clinical presentation and the lack of uniformity in diagnostic criteria .In most cases diagnosis depends more on corroborative evidence, such as a positive PPD and chest x-ray, and the exclusion of other causes. Direct evidence for the presence of the infectious agent in the ocular cavity and/or ocular tissue is ideal for establishing the diagnosis, this could consist of the demonstration of acid-fast organisms under the microscope or the detection of bacterial genome by nucleic acid amplification procedures. CLINICAL MANIFESTATIONS The varied manifestations of the disease have complicated efforts to name the clinical indicators that would suggest a diagnosis of intraocular tuberculosis. Miliary tubercles have a distinct clinical appearance but tuberculomas can be confused with other diseases, such as syphilis, sarcoidosis, or brucellosis, and neoplasia such as as retinoblastoma, malignant melanoma, lymphomas, or metastatic tumors. In the focal or diffuse forms of choroiditis, other conditions, such as toxoplasmosis, histoplasmosis, multifocal choroiditis with pan uveitis, or autoimmune serpiginous choroiditis, are included in the differential diagnosis. In vasculitis with associated inflammation, snowball vitreous opacities, and neuroretinitis are possible clues to a diagnosis of tubercular etiology. An intractable disease course with multiple recurrences on nonspecific treatment is a clue suggesting a possible tubercular etiology. Such patients should be investigated for tuberculosis.
Address for Correspondence :Dr. Shibal Bhartiya Senior Research Officer Dr. R.P. Centre for Ophthalmic Sciences AIIMS, New Delhi
CORROBORATIVE EVIDENCE 1. Purified Protein Derivative/Mantoux Skin Test The Mantoux test is commonly obtained in patients suspected of ocular tuberculosis. The standard Mantoux test consists of an intradermal injection of 5 tuberculin units (TU) of PPD to raise a wheal of 6-10 mm. The extent of induration is read at 48-72 hours. An induration of less than 5 mm is considered a negative result; an induration of 5-10 mm is considered positive in persons with HIV infection, in those who are in close contact with a patient with infectious tuberculosis, and in those who have healed tuberculosis lesions on chest radiograph. A test result of more than 10 mm is reported as positive for those patients living in high incidence areas, for employees of highrisk congregate settings (e.g., health care workers), and for residents of long-term facilities. Any result > 15 mm is considered a positive result. Mantoux skin test results can be negative in patients with severe tuberculous infection and in very moribund states. In addition the dosage of tuberculo-proteins injected is important, as small doses might fail to incite a reaction. Vaccination with BCG poses a potential source of crossreactions and false-positive results are attributed mostly to prior BCG vaccination. The probability that the reaction in PPD skin test is from the Mycobacterium tuberculosis antigen and not due to BCG increases a) with increase in size of reaction, b) with a patient who has been in contact with a person who has TB, c) with family history of TB or patient's country of origin has a high incidence or prevalence of TB, and d) with an increasing interval between vaccination and skin testing. 2. Interferon-gamma release assays (IGRA) This test is based on the in vitro assays that measure interferon-gamma released by sensitized T cells after stimulation by Mycobacterium tuberculosis antigens. The newer versions of the test use antigens that are very specific to Mycobacterium tuberculosis and include early secreted antigen target (ESAT)6, culture filtrate 23
OCULAR TUBERCULOSIS
protein (CFP)-IO, that are encoded by genes that are present in the region of difference segment of Mycobacetrium tuberculosis. These are much more specific than the earlier versions of this test where purified protein derivative (PPD) was being used as a stimulating antigen. The newer antigens being more specific are not shared with BCG vaccine strains or other species of Mycobacterium.ll Two kits are available commercially: T-SPOT.TB test (Oxford Immunotec Ltd, Oxford, UK) and the QuantiFERON -TB GOLD (QFTG:Cellestis Ltd, Carnegie, Australia). The CDC has updated its guidelines suggesting that QFT-G can be used in place of tuberculin skin test for infection control and survillence and conversion, that is, latent to manifest infection. The UK National Institute for Health and Clinical Excellence has recommended a two-step strategy for diagnosing latent tuberculosis, in which the tuberculin skin test is done first and those who are positive or in whom the test is unrealiable, should be further considered for IGRA. However, there are no published studies yet on the IGRA and ocular tuberculosis. 3. Chest Radiography and Tomography
DIRECT EVIDENCE 1. Examination of Smear and Staining for Acid-Fast Organisms
Examination of smears of infected tissue or fluid after acid-fast staining is the most specific procedure for diagnosing tuberculosis. It has been estimated that at least 106 organisms/ml of sputum are required for detection on a smear. Because the yield of organisms from intraocular fluids is low, direct microscopy of the smears is not often helpful in the diagnosis of intraocular tuberculosis. 2. Culture of Intraocular Fluid/Tissue
Cultures of M. tuberculosis on Lowenstein Jenson medium must be incubated for 8 weeks and the visible colonies are identified by Ziehl-Neelsen stain. The process is prolonged and cumbersome, and may not provide positive results because of the low yield of organisms from intraocular fluids. 3. Polymerase Chain Reaction
Although ocular tuberculosis may occur without evidence of pulmonary disease, the chest radiograph can still provide evidence of active or healed/primary or reactivated tuberculosis. Computerized tomography of the chest and skeleton and cerebral MRI may be undertaken if there is a high index of clinical suspicion as these are more sensitive than radiograph 4. Serodiagnosis
PCR is a sensitive and highly specific technique that works on the principle of amplification of mycobacteial DNA several-fold for easy detection. This is especially useful for intraocular fluids, because PCR can be performed with very small sample sizes. Samples can be either aqueous, vitreous humor, subretinal fluid, or rarely, tissue obtained by chorioretinal biopsy. The reported PCR-positivity for M. tuberculosis is 33.3% of cases in retinal vasculitis and 66.6% in granulomatous panuveits.. Use of real-time PCR technology can differentiate commensals and contaminants from infecting microbes, but so far its use has not been reported in the diagnosis of ocular tuberculosis. Sensitivity may also be improved by dot-blot hybridization of the PCR product by 32Plabeled specific probes. Gene sequencing of the PCR DNA product has confirmed the presence of the H37Rv strain of M. tuberculosis in ocular specimens obtained from intraocular tuberculosis patients using primers targeting the IS 6110 sequence. The reliability of PCR depends on the sensitivity and specificity of a particular assay. These measures are difficult to establish in tuberculosis as the culture that is the gold standard for comparison itself has a poor yield from intraocular specimen and histopathology is mostly not available 24
Serodiagnosis for detection of antibodies or antigens has been used for both pulmonary and ocular tuberculosis. The Middlebrook-Dubos test is a hemagglutinin reaction between sheep red blood cells treated with polysaccharide from M. tuberculosis extract and sera from tuberculosis patients. A positive reaction from the serum in a dilution of 1:8 is thought to be specific for tuberculous infection. ELISA using purified cord factor as the antigen has been found to be helpful for the diagnosis of ocular tuberculosis. The anti LAM-B antibody consists of a nonprotein antigen of mycobacteria that becomes positive when a patient develops tuberculosis. Serodiagnostic tests are currently not preferred because of their low sensitivity and the high number of false-positive test results.
OCULAR TUBERCULOSIS
GUIDELINES FOR DIAGNOSIS Based on laboratory investigations and clinical parameters, follow-up examinations and therapeutic response to ATT, the following guidelines for the diagnosis of intraocular tuberculosis enable the clinician to determine when to initiate ATT. Although these criteria are based on clinical and laboratory investigations, cases can be divided into two groups, confirmed cases and presumed intraocular tuberculosis. Anyone or more of the clinical signs in combination with any of the positive tests could be considered a confirmed (definitive) case of intraocular tuberculosis. Anyone or more of the clinical signs listed in combination with any of the positive tests or a positive therapeutic trial in combination with exclusion of other uveitis entities could be considered presumed ocular tuberculosis and referred to a TB specialist to initiate a full course of ATT. 1. Clinical Signs : Granulomatous Non granulomatous Iris nodules Ciliary body granuloma 1 . Anterior uveitis
4.
Exclusion of Other Uveitis Entities
In the geographic regions where tuberculosis is low in incidence, other causes of uveitis must be excluded by various laboratory investigations inclduing serology for syphilis, toxoplasmosism and others. 5. Therapeutic trial A positive response to 4-drug ATT (isoniazid, rifampicin, ethambutol, and pyrazinamide) over a period of 4 to 6 weeks (under supervision of a TB expert, therapeutic response to ATT in the eye evaluated by ophthalmologist) TREATMENT MEDICAL MANAGEMENT 1. Drug Regimen It is imperative to obtain the opinion of an infectious disease expert/pulmonologist/internistand to comanage the case as the treatment of tuberculosis is complex even more so in the case of drug-resistant tuberculosis. Drug regimens for ocular tuberculosis are similar to those for pulmonary or extrapulmonary tuberculosis. For the treatment of ocular tuberculosis, a few studies have described a course of chemotherapy consisting of isoniazid and rifampicin for 9 months. The J66'C recommends the use of all four drugs (isoniazid, rifampicin, pyrazinamide, and ethambutol) for an initial 2month period followed by a choice of different options over next 4 to 7 months for treatment of tuberculosis. In patients from those regions where the incidence of primary resistance to isoniazid is more than 4%, and in those who come from regions with higher multidrug resistant strains, the use of a four-drug regimen should be followed by consultation with an internist who has expertise in the treatment of drug-resistant tuberculosis. 2. Duration of Treatment The exact duration of treatment and the endpoint for stopping treatment for ocular tuberculosis is not known. Various authos have recommended four-drug therapy for between 6 and 15 months, nearly 95% of patients responding to treatment with the resolution of their intraocular inflammation. The initial regimen consists of isoniazid, rifampicin, ethambutol, and pyrazinamide for 2 to 3 months and treatment with isoniazid and rifampin continued for 9 to 12 months. Response to treatment is usually evident within 4 to 6 weeks. The CDC recommends prolonged therapy for tuberculosis of any site that is slow to respond and thus the patients with intraocular TB may require prolonged therapy. 25
2. Intermediate uveitis : Granulomatous Non granulomatous with organizing exudates 3. Posterior and pan uveitis: Choroidal tubercle Choroidal tuberculoma Subretinal abscess Serpiginous like choroiditis 4. Retinitis and retinal vasculitis 5. Neuroretinitis and optic neuropathy 6. Endophthalmitis and panophthalmitis 7. Eale's disease 2. Ocular Investigations a. Demonstration of AFB by microscope or culture of M. tuberculosis from the ocular fluids. b. Positive polymerase chain reaction from ocular fluids for IS 6110 or other conserved sequences in M. tuberculosis genome. 3. Systemic Investigations a. Positive Mantoux reaction. b. Evidence of healed or active tubercular lesion on radiography of the chest. c. Evidence of confirmed active extrapulmonary tuberculosis (either by microscopic examination or by culture of the affected tissue for M. tuberculosis).
OCULAR TUBERCULOSIS
3.
Immunosuppressive Agents
6.
Ocular Side Effects of Anti-Tubercular Drugs
Low-dose systemic corticosteroids used for 4 to 6 weeks, along with multidrug ATT, may limit damage to ocular tissues caused from delayed type hypersensitivity. Corticosteroids without concomitant ATT must be avoided as they may promote multiplication of bacilli, leading to panophthalmitis or cause activation of latent systemic tuberculosis. 4. Immunomodulatory Agents in Uveitis Patient with Positive PPD
The positive tuberculin skin test indicates past (latent) or present mycobacterial infection. A number of studies have shown a high prevalence of Mantoux positivity in uveitis patients whose uveitis is unrelated to tuberculosis. The anti TNF biological treatment for uveitis or other autoimmune disorders can result in flare-ups of the latent tuberculosis infection. The proposed treatment regimens for latent tuberculosis (patients with positive PPD) are: 1) isoniazid 300 mg/ day for 9 months,1 2) isoniazid twice weekly at a dose of 15 mg/kg where daily treatment is not possible, 3) rifampicin daily for 4 months where isoniazid cannot be used, and 4) rifampicin with pyrazinamide daily for 2 months in situations where treatment period must be confined to 2 months. All these patients, irrespective of age, need treatment if the reaction to 5 tuberculin units of PPD is > 10 mm or 2-5 mm in patients who are HIV positive, who have recent contact with an infected person, or show evidence of old tuberculosis on chest xray.However, the treatment regimens for latent TB may vary in geographical location and local physician should be consulted for the treatment. 5. Drug-Resistant Tuberculosis There has been a decrease in the incidence of primary resistanct tuberculosis, but an increased occurrence of acquired resistance. Numerous factors, including poor compliance, improper drug regimen, physician error in directing treatment or natural mutations, and often a combination of these factors may playa role in the development of drug-resistant tuberculosis. Use of multiple agents, with a minimum of three or four additional antituberculosis agents for a duration of 18 to 24 months, is recommended. The additional agents include rifabutin, fluoroquinolones, interferon-y, and linezolid; all of these agents have been tried for the treatment of drug resistant tuberculosis. Recently the CDC has published that during 2000-2004, of 17,690 TB isolates, 20% were multidrug resistant and 2% were extensively drug resistant (XDR) that were resistant virtually to all second-line drugs, thus documenting the existence of XDR TB as a emerging public health issue. 26
The ethambutol toxicity is dose-related and is rare if the daily dose does not exceed 15 mg/kg. Of the patients receiving daily dose of 25 mg/kg or more, 1-2% experience ocular toxicity.It l is known to cause optic neuritis, acquired red-green dyschromatopsia , central scotomas, disk edema, disk hyperemia, peripapillary splinter hemorrhages, optic atrophy and rarely, retinal edema and foveal pigmentary changes. The optic neuritis is abrupt in onset and is generally seen at 3-6 months of the onset of treatment .All patients should have a baseline ophthalmic examination including visual acuity, visual field, and color vision, If the dose administered is more than 15 mg/kg/day, patients with drug-resistant TB or TB requiring prolonged course of ethambutol should remain under ophthalmic supervision. These patients should be examined every 2 to 4 weeks, whereas for lower doses, follow-up every 3-6 months is adequate. In case of any ocular side effect, the drug should be stopped immediately; following which the vision usually improves. In cases where vision does not improve following discontinuation of therapy, parenteral hydroxycobalamine, 40 mg/ day over a 10- to 28-week period should be considered. Majority of symptoms resolve over a period of 3-12 months, although permanent visual loss is also known to occur. Isoniazid has been reported as a cause of optic neuritis and optic atrophy,albiet rarely. Recently rifampicin has been reported to induce neurodegredation in the optic nerve transection model. Rifabutin, a spiropiperidyl derivative of rifamycin, is more effective than rifampicin against slow-growing mycobacteria, including M. avium-intracellulare, and has been extensively used in HIV-infected patients. This agent, especially when combined with clarithramycin or fluconazole, can cause severe acute anterior uveitis, including hypopyon uveitis, corneal endothelial deposits, and inflammatory vitreous exudates and opacities. However, the druginduced intraocular inflammation responds well to topical corticosteroids. B. SURGICAL MANAGEMENT Tubercular granulomas are quite amenable to medical management, provided it is initiated in timely manner. If necessary local resection ,in case of anterior lesions ,and pars plana vitrectomy have proven to be efficacious in non responsive lesions. Almighty first appeared as a mass radiant Every living being is his descendent We are all His flesh and blood, So how come some one is bad or good. Sant Kabeer Das
OBESITY AND EYE DISEASES
MAJOR REVIEW
Obesity and Eye Diseases
Dr. Rajpal Insaan, Dr. Sonia Bhargav, Dr Shibal Bhartiya
Obesity is a major public health problem, with prevalence increasing at staggering rates in many countries. The World Health Organization (WHO) defines obesity as a body mass index (BMI) of 30 kg / m1 or greater, and overweight as individuals whose BMI falls between 25 kg / m 1 and 29.9 kg/m1 . Different classification are used for some specific populations, such as Asian & children. In Asian populations, it has been proposed that a BMI of 25 kg/ m 1 or greater should be classified as obesity 1. The Current International Obesity Task Force estimates suggest at least 1.1 billion people are over weight world wide, and 312 million of these are obese. The impact of obesity on health is widespread. Among different eye diseases, obesity has been associated cataract 2,3,4, age related maculopathy, diabetic retinopathy & glaucoma. Obesity and Cataract :Obesity has been proposed to be risk factor for cataract development, though the exact underlying mechanisms are unclear. Many studies have reported that over all obesity, measured as BMI and abdominal adiposity, measured as waist to hip ratio (WHR) as independent risk factor for cataract2,3,4. It was found that at any level of BMI, a two unit higher level predicted a 12% increase risk of cataract2. Cortical and posterior subcapsular cataracts have been most consistently associated with obesity 5 , 6 , 8 . Several plausible pathophysiological mechanisms have been proposed to explain the association of obesity and cataract. One theory suggests that leptin, a 16- kDa pleiotropic cytokine expressed and secreted mainly by adipocytes 8, is involved in the molecular mechanisms underlying cataract formation.7. Individual with obesity exhibit hyperleptinemia and leptin resistance9,10. The exact mechanist by which leptin contributes in the process of cataractogenesis is still unclear. In Non-white population, lower BMI is also associated with cataract formation 11,12,13. Obesity and Glaucoma: Several studies have provided evidence in support of a positive association between obesity and intra ocular pressure, the strongest risk factor for glaucomatous optic neuropathy (GON) 14, 15. The Beaver Dam Eye Study
Address for Correspondence :Dr. Rajpal Insaan Additional Professor of Ophthalmology Vitreoretina Unit Dr. R.P. Centre for Ophthalmic Sciences AIIMS, New Delhi
reported a significantly positive association of IOP with several factors including BMI 1 6 . A clear pathophysiological explanation for the association of obesity with IOP and glaucoma is currently lacking. Both the 'mechanical' and 'vascular' etiology theories of glaucoma may be related to obesity. With regards to the mechanical theory, obesity has been postulated to exert an effect on IOP by causing excessive intra orbital adipose tissue, increased blood viscosity, increased episcleral venous pressure and impairment of aqueous outflow facility 17,18,19. On the other hand, the vascular theory suggests that eyes with inherently poor vascular supply to the optic nerve head are more predisposed to damage by elevated or normal IOP 21. Increased oxidative DNA damage was found in the trabecular meshwork of glaucoma patients 22 and oxidative stress has been postulated to cause proteasome failure and induce trabecular meshwork degeneration leading to impairment of the ability of the tissue to modulate outflow resistance 23. Obesity and Age-Related Maculopathy: Age-Related Maculopathy remains the major blinding condition in the elderly, despite the introduction of several new treatment modalities including photodynamic therapy, non - pharmacological approaches to inhibit angiogenesis 24,25,26 and the use of antioxidant supplement 27. The AREDS has reported cross-sectional association between higher BMI and more advanced ARM, as documented from fundus photographs 28. Obesity may increase systemic oxidative stress secondary to hyperleptinemia9,29,30. Oxidative damage to lipids in the Bruch's membrane appears to be important in the etiology of choroidal neovascular ARM31. In response to oxidative stress, the RPE cells may detach and migrate into the subretinal space or outer retina and secrete excessive vascular endothelial growth factor (VEGF), eliciting invasion of neovascularization in Bruch's membrane 31. Plasma fibrinogen and C-reactive protein are elevated in obese persons and may therefore be a potential link between obesity and ARM 32. Obesity and Diabetic Retinopathy: Obesity (BMI > 31.0 kg/m1 for men and 32.1 kg/m1 for women) is found to be associated with progression and severity of retinopathy in patients with type II DM 33. The concentration of VEGF has been found to be higher in the vitreous of eyes with proliferative diabetic retinopathy 34. Serum VEGF and leptin levels has been found to be elevated in obese persons 35. 27
OBESITY AND EYE DISEASES
Obesity and other Eye Diseases: Various other ocular diseases associated with obesity are central retinal vein occlusion, hypercoagulability disorders, oculomotor nerve palsy, floppy eyelid syndrome. BIH, obstructive sleep apnea. References:
1. 2. James PT, Leach R, Kalamara E, et al: The worldwide obesity epidemic. Obes Res 9(Suppl 4):228S-33S, 2001. Glynn RJ, Christen WG, Manson JE, et al: Body mass index. An independent predictor of cataract. Arch Ophthalmol 113:1131-7, 1995. Hiller R, Podgor MJ, Sperduto RD, et al: A longitudinal study of body mass index and lens opacities. The Framingham Studies. Ophthalmology 105:1244-50, 1998. Jahn CE, Janke M, Winowski H, et al: Identification of metabolic risk factors for posterior subcapsular cataract. Ophthalmic Res 18:112-6, 1986. Kuang TM, Tsai SY, Hsu WM, et al: Body mass index and age-related cataract: the Shihpai Eye Study. Arch Ophthalmol 123:1109-14, 2005. Leske MC, Wu SY, Hennis A, et al: Diabetes, hypertension, and central obesity as cataract risk factors in a black population. The Bardados Eye Study. Ophthalmology 106:35-41, 1999. Gomez-Ambrosi J, Salvador J, Fruhbeck G: Is hyperleptinemia involved in the development of agerelated lens opacities? Am J Clin Nutr 79:888-9, author reply 889, 2004 8. Bengtsson B, Heijl A: A long-term prospective study of factors for glaucomatous visual field loss in patients ocular hypertension. J Glaucoma 14:135-8, 2005. Haynes WG: Role of leptin in obesity-related hypertension. Exp Physiol 90:683-8, 2005.
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10. Narin F, Atabek ME, Karakukcu M, et al: The association of plasma homocystenine levels with serum leptin and apolipoprotein B levels in childhood obesity. Ann Saudi Med 25:209-14, 2005. 11. Leske MC, Chylack LT, Wu SY: The Lens Opacities Case-Control Study, Risk factors for cataract. Arch Ophthalmol 109:244-51, 1991. 12. Chatterjee A, Milton RC, Thyle S: Prevalence and aetiology of cataract in Punjab. Br J Ophthalmol 66:3542, 19 13. Mohan M, Sperduto RD, Angra SK, et al: India-US case-control study of age-related cataracts. India-US Case-Control Study Group. Arch Ophthalmol 107:670-6, 1989. 14. Jonas JB, Grundler AE, Gonzales-Cortes J, et al: Pressure-dependent neuroretinal rim loss in normalpressure glaucoma. Am J Ophthalmol 125:137-44, 1988. 15. Leske MC, Wu SY, Hennis A, et al: Risk factors for open-angle glaucoma. The Barbados Eye Study. Arch Ophthalmol 113:918-24, 1995. 16. Klein BE, Klein R, Linton KL: Intraocular pressure in an American community. The Beaver Dam Eye Study. Invest Ophthalmol Vis Sci 33:2224-8, 1992. 17. Bulpitt CJ, Hodes C, Everitt MG: Intraocular pressure systemic blood pressure in the elderly. Br J Ophthalmol 717-20, 1975.
18. Shiose Y: The aging effect on intraocular pressure in an apparently normal population. Arch Ophthalmol 102:883-7, 1984. 19. Shiose Y, Kawase Y: A new approach to stratified normal intraocular pressure in a general population. Am J Ophthalmol 101:714-21, 1986. 20. Halpern DL, Grosskreutz CL: Glaucomatous optic neuropathy: mechanisms of disease. Ophthalmol Clin North Am 15:61-8, 2002. 21. Caulfield LE, West SK, Barron Y, et al: Anthropo status and cataract: the Salisbury Eye Evaluation. Am J Clin Nutr 69:237-42, 1999. 22. Izzotti A, Sacca SC, Cartiglia C, et al: Oxidative deoxyribonucleic acid damage in the eyes of glaucoma patients. Am J Med 114:638-46, 2003. 23. Caballero M, Liton PB, Epstein DL, et al: Protease inhibition by chronic oxidative stress in human trabecular meshwork cells. Biochem Biophys Res Commun 308 52, 2003. 24. D' Amico DJ, Goldberg MF, Hudson H, et al: Anecortave acetate as monotherapy for treatment of subfoveal neo-vascularization in age-related macular degeneration: twelve-month clinical outcomes. Ophthalmology 110:2372-83, discussion 2384-5, 2003. 25. Ferris FL: A new treatment for ocular neovascularization. N Engl J Med 351:2863-5, 2004. 26. Gragoudas ES, Adamis AP, Cunningham ET, et al: Pegaptanib for neovascular age-related macular degeneration. N Engl J Med 351:2805-16, 2004. 27. Hogg R, Chakravarthy U: AMD and micronutrient antioxidants. Curr Eye Res 29:387-401, 2004. 28. Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3, Ophthalmology 107:2224-32, 2000. 29. Bouloumie A, Marumo T, Lafontan M, et al: Leptin induced oxidative stress in human endothelial cells. FASEB 1231-8, 1999. 30. Schorr U, Blaschke K, Turan S, et al: Relationship between angiotensinogen, leptin and blood pressure levels in young normotensive men. J Hypertens 16:1475-80, 1998. 31. Spaide RF, Armstrong D, Browne R: Continuing medical education review: choroidal neovascularization in age-related macular degeneration-what is the cause? Retina 23:595-614, 2003. 32. Valle V, Martos R, Gascon F, et al: Low-grade systemic inflammation, hypoadiponectinemia and a high concentration of leptin are present in very young obese children and correlate with metabolic syndrome. Diabetes Metab 3155-62, 2005. 33. Klein R, Klein BE, Moss SE: Is obesity related to microvascular and macrovascular complications in diabetes? The Wisconsin Epidemiologic Study of Diabetic Retinopathy. Arch Intern Med 157:650-6, 1997. 34. Aiello LP, Arrigg PG, et al: Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders. N Engl J Med 331:1480-7, 1994. 35. Uckaya G, Ozata M, Sonmez A, et al: Is leptin associated with hypertensive retinopathy? J Clin Endocrinol Metab 85: 683-7, 2000.
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CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA
CURRENT TREATMENT
Current Treatment for Diabetic Macular Oedema (DME)
Dr. Rajpal Insaan
Abstract : Diabetic Retinopathy is an important cause of blindness in India and Indeed, the rest of the world.It is important to diagnose Diabetes Mellitus early so that early and proper control of blood sugar and other systemic factors can be done which will decrease the complications related to DM .Inspite of advances in both pharmacological and surgical treatments of DR , it continues to remain a threat to vision in epidemic proportions..Management should include lifestyle changes (yoga and meditation ) ,dietary change ,in addition to drugs and lasers . Introduction: Macular oedema is the most common cause of moderate visual loss in diabetic patients. Blindness due to diabetic retinopathy can be avoided if treated early. Frequency of DME is high in the diabetic population. According to the Wisconsin Epidemiological Study of Diabetic Retinopathy, the four-year incidences of clinically significant DME are 4.3 % for the younger onset group, 2.9% for the older onset and 5.1% for those taking insulin. Pathophysiology: Pathophysiology of DME is not known exactly ,although there are several hypothesis.Electrolyte imbalance caused by the high aldose reductase levels leads to cell death ,especially retinal pericytes which causes microaneurysm formation.Thickening of capillary basement membrane and increased deposition of exracellular matrix also results in abnormal retinal hemodynamics.Breakdown of the inner blood-retinal barrier results in acumulation of exreacellular fluid ,which manifests as DME. There has been various factors like VEGF which have been implicated in inducing neovascularisation. Clinically significant DME (CSME) requires combined evaluation and management by the Endocrinologist and
Address for correspondence Dr. Rajpal Insan Additional professor of Ophthalmology Vitreoretina Unit. Dr. R.P. Centre for Ophthalmic Sciences AIIMS, New Delhi E-mail: drrajpal2001@yahoo.co.uk
the Ophthalmologist. The Early Treatment Diabetes Retinopathy Study (ETDRS) defined CSME as the following: 1. 2. Thickening of the retina at or within 500m of the centre of the macula. Hard exudates at or within 500m of the centre of the macula, associated with thickening of the retina, any part of which is within 500m of the centre of the macula. (residual lipid exudates after disappearance of retinal thickening is not CSME). Zone or zones of retinal thickening 1 disc diameter (DD) or larger, any part of which is within IDD of the center of the macula. Complete management of DME involves thorough evalution, medical and ocular management. EVALUTION Systemic Evalution It should be a routine practice to contact an endocrinologist. Blood glucose, serum lipids, blood pressure and HbA1C should be checked.Evaluation of kidney function is also essential because presence of gross protienuria at baseline has been reported to be associated with 95% increased risk of developing DME among Type I patients in the WESDR . Ocular Evalution Stereoscopic examination of the macular region at the slit lamp with a contact lens, Fluorescein angiography and OCT are a must to evaluate a diabetic macular oedema patient. Diagnosis of DME is clinical, based on stereoscopic examination of the macula. Fluorescein angiography helps to differentiate focal from diffuse macular oedema and rule out macular ischemia. It is however not required for making the diagnosis. OCT rules out or demonstrates macular traction and allows anatomic and objective evaluation of changes following therapy. Correct evaluation of DME is not possible without an OCT examination. Best corrected visual acuity should be recorded in each visit. Medical Treatment It should be our routine practice to contact an endocrinologist to request optimization of the glycemic 29
3.
control and start local treatment of CSME only when the HbA1C is 7.5% or less. A) Blood glucose control- Optimum glycemic control is fundamental1 in the management of DME. In Diabetes Control and Complications Trial (DCCT), intensive management of hyperglycemia decreased the risk of DME .Studies have also shown that persons with type 2 diabetes and CSME refractory to treatment have higher HbA1C than patients who respond to the laser therapy. B) Serum lipids. In the ETDRS, elevated serum lipids were associated with higher prevalence of retinal hard exudates. Serum lipids should be checked and the patient should be referred in case of hyperlipidemia. Treatment of dyslipidemia provides cardiovascular benefits in patients with diabetes, but whether it provides vision benefits remains to be determined. C) Blood pressure. The United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that the intensive treatment of arterial hypertension reduced the deterioration of visual acuity in 47% patients, mainly because the incidence of DME was lower in the intensive treatment group. This beneficial effect was independent of the glycemic control. D) Aspirin therapy and smoking cessation also are recommended by some. Ocular management Based on binocular biomicroscopic examination, fluorescein angiography, OCT and best corrected visual acuity, DME can be classified in various categories for treatment planning: Type 1. DME with focal leakage on fluorescein Macular edema is the most common cause of moderate visual loss in patients and is the second cause of severe vision loss in patients with diabetes. Frequency of DME is high in the diabetic population. According to the Wisconsin Epidemiological Study of Diabetic Retinopathy, the four-year incidences of clinically significant DME are 4.3 % for the younger onset group, 2.9% for the older onset and 5.1% for those taking insulin. Clinically significant DME (CSME) requires combined evaluation and management by the Endocrinologist and the Ophthalmologist .The Early Treatment Diabetes Retinopathy Study (ETDRS) defined CSME as the following: 1. 2. Thickening of the retina at or within 500m of the centre of the macula. Hard exudates at or within 500m of the centre of 30
the macula, associated with thickening of the retina, any part of which is within 500m of the centre of the macula. (residual lipid exudates after disappearance of retinal thickening is not CSME). 3. Zone or zones of retinal thickening 1 disc diameter (DD) or larger, any part of which is within IDD of the center of the macula. Complete management of DME involves thorough evalution, medical and ocular management. EVALUTION Systemic Evalution It should be a routine practice to contact an endocrinologist. Blood glucose, serum lipids, blood pressure and HbA1C should be checked.Evaluaion of kidney function is essential as gross protienuria is associated with a 95% prevalance of DME in Type I patients in the WESDR.In WESDR ,hiher serum cholesterol has been associated with increased risk of hard exudates.Lending further support to this is Gupta et al's observation that redution in edema,subfoveal lipid migration and severity of hard exudates following use of lipid lowering drug atorvastatin as an adjuvant to macular photocoagulation. Ocular Evalution Stereoscopic examination of the macular region at the slit lamp with a contact lens, Fluorescein angiography and OCT are a must to evaluate a diabetic macular oedema patient. Diagnosis of DME is clinical, based on stereoscopic examination of the macula. Fluorescein angiography helps to differentiate focal from diffuse macular oedema and rule out macular ischemia. It is however not required for making the diagnosis. OCT rules out or demonstrates macular traction and allows anatomic and objective evaluation of changes following therapy. Correct evaluation of DME is not possible without an OCT examination. Best corrected visual acuity should be recorded in each visit. Medical Treatment It should be our routine practice to contact an endocrinologist to request optimization of the glycemic control and start local treatment of CSME only when the HbA1C is 7.5% or less. A) Blood glucose control- Optimum glycemic control is fundamental1 in the management of DME. In Diabetes Control and Complications Trial (DCCT), intensive management of hyperglycemia decreased the risk of DME. Studies have also shown that persons with type 2 diabetes and CSME refractory to treatment have higher HbA1C than patients who respond to the laser therapy.
B) Serum lipids. In the ETDRS, elevated serum lipids were associated with higher prevalence of retinal hard exudates. Serum lipids should be checked and the patient should be referred in case of hyperlipidemia. Treatment of dyslipidemia provides cardiovascular benefits in patients with diabetes, but whether it provides vision benefits remains to be determined. C) Blood pressure. The United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that the intensive treatment of arterial hypertension reduced the deterioration of visual acuity in 47% patients, mainly because the incidence of DME was lower in the intensive treatment group. This beneficial effect was independent of the glycemic control. D) Aspirin therapy and smoking cessation also are recommended by some. Ocular management Based on binocular biomicroscopic examination, fluorescein angiography, OCT and best corrected visual acuity, DME can be classified in various categories for treatment planning: Type 1. DME with focal leakage on fluorescein angiography and without vitreous traction on OCT. These patient usually show hard exudates organized in the form of circinate ring that involves or threatens the centre of the macula, with visible microaneurysms that leak on fluorescein angiography. These patients are treated with focal laser photocoagulation according to the guidelines recommended by the Early Treatment Diabetes Retinopathy Study (ETDRS). Type 2. Diffuse DME without vitreous traction on OCT. FA demonstrates diffuse leakage and may show a cystic pattern. The retina may be markedly thickened. Hard exudates may be absent and, if present, do not show a circinate pattern. Although the ETDRS recommended laser treatment for any type of clinically significant DME, most clinicians now believe and consider other treatments for these patients. Macular edema is the most common cause of moderate visual loss in patients and is the second cause of severe vision loss in patients with diabetes. Frequency of DME is high in the diabetic population. According to the Wisconsin Epidemiological Study of Diabetic Retinopathy, the four-year incidences of clinically significant DME are 4.3 % for the younger onset group, 2.9% for the older onset and 5.1% for those taking insulin. 31
Clinically significant DME (CSME) requires combined evaluation and management by the Endocrinologist and the Ophthalmologist .The Early Treatment Diabetes Retinopathy Study (ETDRS) defined CSME as the following: 1. 2. Thickening of the retina at or within 500m of the centre of the macula. Hard exudates at or within 500m of the centre of the macula, associated with thickening of the retina, any part of which is within 500m of the centre of the macula. (residual lipid exudates after disappearance of retinal thickening is not CSME). Zone or zones of retinal thickening 1 disc diameter (DD) or larger, any part of which is within IDD of the center of the macula. Complete management of DME involves thorough evalution, medical and ocular management. EVALUTION Systemic Evalution It should be a routine practice to contact an endocrinologist. Blood glucose, serum lipids, blood pressure and HbA1C should be checked. Ocular Evalution Stereoscopic examination of the macular region at the slit lamp with a contact lens, Fluorescein angiography and OCT are a must to evaluate a diabetic macular edema patient. Diagnosis of DME is clinical, based on stereoscopic examination of the macula. Fluorescein angiography helps to differentiate focal from diffuse macular edema and rule out macular ischemia. It is however not required for making the diagnosis. OCT rules out or demonstrates macular traction and allows anatomic and objective evaluation of changes following therapy. Correct evaluation of DME is not possible without an OCT examination. Best corrected visual acuity should be recorded in each visit. Medical Treatment It should be our routine practice to contact an endocrinologist to request optimization of the glycemic control and start local treatment of CSME only when the HbA1C is 7.5% or less. A) Blood glucose control- Optimum glycemic control is fundamental1 in the management of DME. In Diabetes Control and Complications Trial (DCCT), intensive management of hyperglycemia decreased the risk of DME .Studies have also shown that persons with type 2 diabetes and CSME refractory to
3.
treatment have higher HbA1C than patients who respond to the laser therapy. B) Serum lipids. In the ETDRS, elevated serum lipids were associated with higher prevalence of retinal hard exudates. Serum lipids should be checked and the patient should be referred in case of hyperlipidemia. Treatment of dyslipidemia provides cardiovascular benefits in patients with diabetes, but whether it provides vision benefits remains to be determined. C) Blood pressure. The United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that the intensive treatment of arterial hypertension reduced the deterioration of visual acuity in 47% patients, mainly because the incidence of DME was lower in the intensive treatment group. This beneficial effect was independent of the glycemic control. D) Aspirin therapy and smoking cessation also are recommended by some. Ocular management Based on binocular biomicroscopic examination, fluorescein angiography, OCT and best corrected visual acuity, DME can be classified in various categories for treatment planning: Type 1. DME with focal leakage on fluorescein angiography and without vitreous traction on OCT. These patient usually show hard exudates organized in the form of circinate ring that involves or threatens the centre of the macula, with visible microaneurysms that leak on fluorescein angiography. These patients are treated with focal laser photocoagulation according to the guidelines recommended by the Early Treatment Diabetes Retinopathy Study (ETDRS). Type 2. Diffuse DME without vitreous traction on OCT. FA demonstrates diffuse leakage and may show a cystic pattern. The retina may be markedly thickened. Hard exudates may be absent and, if present, do not show a circinate pattern. Although the ETDRS recommended laser treatment for any type of clinically significant DME, most clinicians now believe and consider other treatments for these patients. Optimization of the glycemic control, treatment of hypertension and lipid abnormalities are of most important in these patients. Therapeutic options(other than laser photocoagulation) for these patients are a) Intravitreal injection of 4mg of Triamcinolone b) Subtenon triamcinolone injections 32
c) Intravitreal injection of anti-VEGF agents d) Vitrectomy-controversial Type 3. Tractional diabetic macular edema. The OCT will show anomalies at the vitreoretinal interphase, with vitreous traction ( anteroposterior or tangential). Treatment for this type of DME is surgical (vitrectomy with removal of the posterior hyaloid membrane, with or without peeling of the internal limiting membrane). Type 4 . Ischemic macular edema. This is an angiographic diagnosis. Fluorescein angiography will show an irregular broadening of the foveal avascular zone. Late leakage of dye from the floor of the avascular zone may be observed in some cases, probably generated at the level of the retinal pigment epithelium. Some authors recommend laser photocoagulation for these eyes. The treatment however remains controversial. Intravitreal injection of 4mg of Triamcinolone 2,3,4 Intravitreal injection of 4mg of Triamcinolone (IVTA) is effective in reducing DME in approximately 60% of cases, usually with improvement in visual acuity. Its action may be the result of inhibition of the arachidonic acid pathway and down regulation of the production of vascular endothelial growth factor. However, the beneficial effect of IVTA on vision and macular thickness is transitory and rarely persists beyond 3 months. It has been demonstrated that measurable concentrations of triamcinolone last no more than 3 months in non vitrectomized eyes. Furthermore, is not without complications, mainly raised intraocular pressure and cataract. In the majority of cases, ocular hypertension can be managed with topical medication, but some patients particularly the younger ones are refractory to glaucoma medication and may require trabeculectomy. IVTA may be repeated, reproducing the initial beneficial effect on vision and macular thickness, but with lesser efficacy. A small pilot study5 suggests that intravitreal injection of the solution of prednisolone sodium succinate may be a good alternative in eyes with macular edema without intraocular pressure rise. Subtenon triamcinolone injections6 Subtenon triamcinolone injections are used by many for the treatment of CSME. Although complications are lower than those observed with intravitreal injection, its effectiveness is also lower, since the intravitreal injections provide a higher concentration of the drug at the retina.
Intravitreal Bevacizumed (avastin)7,8 It is an humanized monoclonal antibody against VEGF. Avastin has been used with good and sometimes spectacular results, in choroidal neovascularitization associated with age-related macular degeneration and macular edema secondary to retinal vein thrombosis. Avastin has been used also in DME. Avastin could be considered as initial treatment for diffuse diabetic macular edema. Vitrectomy.9,10 The role of vitrectomy in eyes with diffuse DME and no detectable anomalies at the vitreomacular interphase in OCT is controversial and should only be considered as a last resort in cases that did not respond to any of the therapeutic modalities mentioned previously. Surgery can be affective even in eyes with posterior vitreous detachment, but this indication is controversial. It is known that eyes with apparent total posterior vitreous detachment may have remnants of vitreous cortex adherent to the internal limiting membrane. ILM peeling is being considered recently in vitrectomy for diabetic macular edema. Future options Several therapies, currently under investigation, may have role in treatment of DME in the future. A) PORSUDEX (Allergan). This small device can be easily implanted as an office procedure. The device provides extended release of dexamethasone, a glucocorticoid steroid several times more potent than triamcinolone. IT has shown promising results in refractory DME. B) Anti VEGF drugs for intravitreal administration LUCENTIS (Genetech) and MACUGEN (pfizer). C) Inhibitor of protein Kinase C-B Ruboxistaurin. Oral ingestion has demonstrated effective in limiting the progression of macular edema towards the center, in comparison with controls. It is not cosualized as an effectiveness method for treatment established diffuse DME. DME results from a series of biochemical and cellular changes, causing progressive leakage and exudation. Focal and grid photocoagulation remains the standard care for diabetic maculopathy. However, the availability of new agents raises the possibility of improvements, if significant benefits can be validated in randomized clinical trials. Posterior vitreous attachments play a critical role through several mechanical or physiological mechanisms. Vitrectomy without ILM removal seems to be effective in reducing the retinal thickness and improving visual acuity. A combination of laser, pharmacological and surgical treatment modalities may be necessary to maintain central vision in eyes with DME. 33
REFERENCES 1. Furlani BA, Meyer CH, Rodrigues EB, Maia M, Farah ME, Penha FM, Holz FG.Emerging pharmacotherapies for diabetic macular edema.Expert Opin Emerg Drugs. 2007 Nov;12(4):591-603. Review. Nicol M, Nasciuti F, Lai S, Ghiglione D, Borgia L, Calabria Intravitreal triamcinolone acetonide as primary treatment for diffuse diabetic macular edema: a prospective noncomparative interventional case series.Eur J Ophthalmol. 2006 Jan-Feb;16(1):129-33 Audren F, Lecleire-Collet A, Erginay A, Haouchine B, Benosman R, Bergmann JF, Gaudric A, Massin P.Intravitreal triamcinolone acetonide for diffuse diabetic macular edema: phase 2 trial comparing 4 mg vs 2 mg.Am J Ophthalmol. 2006 Nov;142(5):79499. Longo A.Intravitreal triamcinolone for diffuse diabetic macular oedema.Br J Ophthalmol. 2006 Sep;90(9):1079-80. La Heij EC, Lundqvist IJ, Berendschot TT, Hardy E, Liem AT, Hendrikse F.Intravitreal prednisolone sodium succinate reduces diabetic macular edema without intraocular pressure rise. Am J Ophthalmol. 2007 Jan; 143(1):176-8. Toda J, Fukushima H, Kato S.Injection of triamcinolone acetonide into the posterior sub-tenon capsule for treatment of diabetic macular edema.Retina. 2007 Jul-Aug;27(6):764-9. Kumar A, Sinha S.Intravitreal bevacizumab (Avastin) treatment of diffuse diabetic macular edema in an Indian population.Indian J Ophthalmol. 2007 Nov-Dec;55(6):451-5. Haritoglou C, Kook D, Neubauer A, Wolf A, Priglinger S, Strauss R, Gandorfer A, Ulbig M, Kampik A. Intravitreal bevacizumab (Avastin) therapy for persistent diffuse diabetic macular edema.Retina. 2006 Nov-Dec;26(9):999-1005. Yanyali A, Horozoglu F, Celik E, Nohutcu AF.Longterm outcomes of pars plana vitrectomy with internal limiting membrane removal in diabetic macular edema.Retina. 2007 Jun; 27(5):557-66.
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10. Helbig H. Surgery for diabetic retinopathy. Ophthalmologica. 2007; 221(2):103-11. Review. Bloomgarden ZT Screening for and managing diabetic retinopathy: current approaches.Am J Health Syst Pharm. 2007 Sep 1; 64(17 Suppl 12):S8-14.
ROLE OF SYSTEMIC ACYCLOVIR IN RECURRENT
ORIGINAL ARTICLE
THE ROLE OF SYSTEMIC ACYCLOVIR IN RECURRENT CASES OF DISCIFORM KERATITIS
Dr. Kirti Jain, Dr. A.K. Sood, Dr. Suresh Chandra, Dr. Sandeep Kumar, Dr. V. K. Malik, Dr. Sanjiv Kumar, Dr. Charu Jain, Dr. Reny Kamboj
Subharti Institute of Medical Sciences, Delhi Haridwar by Pass Road, N.H. 58 Meerut (U.P)
Abstract Background & Objectives: The role of systemic acyclovir, if any, in recurrent cases of Disciform Keratitis, in addition to topical steroids and antiviral was assessed in this study. Material & Methods: We examined the recurrence rate of herpetic disciform keratitis in 15 patients (group A) treated prophylactically with long-term systemic acyclovir (400 mg twice a day) for a period of one year and compared it with that of 15 patients with no prophylactic therapy (group B). These groups of patients were followed up for a further period of 1 year after stopping treatment for any evidence of recurrence. Results: Patients of Group A, who were kept on systemic acyclovir therapy 400 mg twice a day for a period of 1 year, only one patient experienced a single recurrent episode of disciform keratitis while other remained clinically asymptomatic. However, recurrence rate increases to 4 (26.66%) during follow up period of 1 year in the same group of patient. In striking contrast 5 recurrences (30%) occurred in the 15 patients of group B receiving placebo therapy; which increases to 10 (66.66 %) recurrences during follow up period of 1 year. Discussion & Conclusion: The long-term use of oral acyclovir may be of benefit in the prevention of recurrences, and hence may reduce the blinding complications of this disease. Systemic acyclovir therapy has a potential role in the management of recurrent cases of disciform keratitis. A study with a larger sample size is needed to validate the above results. Key words: acyclovir, dexamethasone, Disciform Keratitis, Herpes simplex virus.
Introduction: Recurrent corneal infection by the herpes simplex virus (HSV) is a leading cause of corneal blindness, not only in the developed countries but also in the developing world1, 2. The prevalence of HSV keratitis, reported by Pramod et al2 in south India is 7.8%.Dendritic keratitis (68%) was the commonest presentation followed by disciform keratitis (28%). Often, the primary herpetic lesions disappear, leaving the cornea clear. The virus lies
Address for Correspondence :Dr. Kirti Jain Department of Ophthalmology Subharti Institute of Medical Sciences Delhi Haridwar By Pass Road, N.H. 58, Meerut (U.P) E-mail:jainmanish45@yahoocom
dormant in the trigeminal ganglion and the other ganglion, until unknown triggers reactivates it, causing a recurrence of epithelial, stromal or lid disease. To assess whether antiviral treatment can prevent recurrences of disciform keratitis, we conducted a randomized clinical trial in which oral acyclovir, 400 mg twice daily for 1 year, was compared with placebo in immunocompetent individuals who had a history of an episode of HSV disciform keratitis. Material and method: In medical record of 30 consecutive patients referred to eye OPD of Subharti Medical College, Meerut, between January 2004 to Dec 2006 and subsequently diagnosed as recurrent disciform keratitis; on the basis of prior 34
episode of herpetic disciform keratitis within the preceding year; were analyzed. The diagnosis is made clinically by the presence of characteristic disc like or diffuse stromal edema, folds in descemet's membrane with or without keratic precipitates (KPs) or loss of corneal sensation and the absence of other causes of stromal keratitis. Patients were treated with topical corticosteroids (Dexamethasone 0.1%) eye drops four times daily and acyclovir eye ointment 5% five times daily. All these patients who had an episode of active herpetic disciform keratitis within a year after the primary episode were divided into two group's .Group A patients received oral acyclovir, 400 mg twice a day for one year versus placebo therapy for group B. These groups of patients were followed up for a further period of 1 year after stopping treatment for any evidence of recurrence. Result: 30 patients were diagnosed with recurrent disciform keratitis during the study period. There were 22 males (73.33 %) and mean age of the entire group was 34 yrs (15-60 yrs) , thus majority of patient were young, adult males. In our study there was no clear seasonal pattern. The male female ratio being 2.7:1. 70 % of patients give history of fever malaise followed by gradual diminutions of vision .The clinical features was typically stromal oedema, epithelial oedema, and descemet's membrane folds. As the intense stromal oedema can mask KPs they were observed only in 10 eyes. Patients of Group A who were kept on systemic acyclovir therapy for a period of 1 year, only one patient experienced a single recurrent episode of disciform keratitis while on 400 mg twice a day of acyclovir therapy, while other remained clinically asymptomatic during the period of systemic antiviral therapy. However, total 4 (26.66%) recurrences noted during follow up period of 1 year in patients of group A. While group B patient's show 5 recurrences (30%) within a period of 1 year after the initial episode and 10 recurrences (66.66%) during follow up period of 1 year..Table 1 35
Table 1. Recurrence of Stromal Keratitis Within Patient Subgroups During 12-Month Treatment Period Among Patients With History of Stromal Keratitis Subgroup Acyclovir group No. Sex: Male Female Age: 15 - 24 25 - 34 35 - 44 45 - 54 > 55 2 5 5 2 1 0 1 0 0 0 1 4 5 3 2 0 2 2 1 0 9 6 0 1 8 7 3 2 Placebo group Total no. of Recurrence
Total no. of Recurrence No.
Table 1. Recurrence of Stromal Keratitis Within Patient Subgroups During Follow-up Period of 1 year Among Patients With History of Stromal Keratitis Subgroup Acyclovir group No. Sex: Male Female Age: 15 - 24 25 - 34 35 - 44 45 - 54 > 55 2 5 5 2 1 0 2 1 1 0 1 4 5 3 2 0 4 5 1 0 9 6 2 2 8 7 6 4 Placebo group Total no. of Recurrence
Total no. of Recurrence No.
By applying z- test for proportion, significant difference (p<0.5) was observed for each age group treatment period and follow up period of 1 year. Discussion: Recurrent herpes simplex viral infection of the eye is an between acyclovir group and placebo group during 12 months
important cause of ocular morbidity. The diagnosis of HSV disciform keratitis is purely clinical3. In routine clinical practice virological investigations like polymerase chain reaction are not easily available or feasible to the patient. The exact pathogenesis of HSV disciform keratitis is debatable but it is believed to result from either a direct infection of the endothelial cells or because of a delayed hypersensitivity reaction to HSV antigen expressed on endothelial cells4. The management of HSV disciform keratitis is with topical Corticosteroids and antiviral agents. Corticosteroids prevent the immunological destruction of endothelial cells while acyclovir prevents reactivation of epithelial cells. Power et al5 demonstrated a faster healing with a combination of acyclovir (3%) eye ointment and betamethasone (0.01%) eye drop, compare to acyclovir and a placebo in herpetic disciform keratitis. In adult recurrence rate of herpetic keratitis are about 25% within a year and 33% within 2 years 6. saini et al7 demonstrated recurrence rate of herpetic keratitis 37.5% at one year after first episode and 50% at 2 years. In the present series recurrence rate of disciform keratitis in acyclovir treated patients (6.66%) versus placebo (30%) within one year. However, total 4 (26.66%) recurrences noted during follow up period of 1 year in acyclovir group and 10 recurrences (66.66%) in placebo group. This was comparable with other study. Rodrequez et al8 showed prevention of recurrence on long term use of acyclovir 600-800 mg/ day. Herpetic eye disease study acyclovir. A pilot study to assess the role of systemic acyclovir in recurrent cases of disciform keratitis prevention trial9, demonstrated oral acyclovir twice daily for a period of 1 year or longer reduces the rate of recurrence of stromal keratitis by about 50%. This trial of 30 patients demonstrated that oral acyclovir safely and effectively suppresses recurrences of HSV eye disease during a 12-month treatment period and during follow up period of 1 year. In summary, patients who have had stromal keratitis may have the greatest opportunity for benefit. These individuals are at the greatest risk for 36
developing recurrent attack of disciform keratitis, the form of herpetic eye disease associated with loss of visual acuity. The clear benefit of oral acyclovir in preventing disciform keratitis among patients with a history of prior stromal. The role of systemic acyclovir in recurrent cases of disciform keratitis keratitis identifies these patients as an important target population for suppressive therapy. Thus, although preventive antiviral therapy could be offered to all patients who are at risk of a recurrence, targeting younger people with prior stromal disease might be the most cost-effective way to reduce the national and global burden of visual loss caused by HSV disciform keratitis. REFERENCES: 1. Liesegang, TJ.Classification of herpes simplex virus keratitis and anterior 43. 2. Pramod NP, Rajendran P, kannan KA. Herpes simplex keratiris in South India.Aclinico-virological correlation.jp J Ophthalmology 1999:43:303-7. 3. Pepose JS. Herpes Simplex keratitis: role of viral infection versus immune response.Surv Ophthalmol 1991; 35:345-52. 4. Leibowitz HM, Koleini B.Herpes Simplex keratitis.Clinical diagnosis and management.Ed Leibowitz HM Waring GO 111.Philadelphia 1998:662. 5. 6. Power WJ, Hilleri MP, Benedict-Smith A, Column LM. Br J Ophthalmology.1992 Dec; 76 (12):711-3. klein RJ. Pathogenetic mechanisms of recurrent herpes simplex virus infection.Arch Virol 1976; 51:13. 7. Saini JS, Agarwala R. Clinical pattern of recurrent herpes simplex keratitis. Indian J Ophthalmol 1999; 47:11-14. 8. Herpetic Eye Disease Study Group. Acyclovir for the prevention of recurrent herpes simplex virus eye disease. N Engl J Med. 1998; 339:300-306. 9. Rodriguez A, Power WJ, Neves RA, Foster CS. Doc ophthalmology.1995; 90 (4):331- 40. uveitis.Cornea 1999;18:127-
THE SCIENCE OF SPIRITUALITY

The Science of Spirituality
Dr Prashaant Chaudhry , Dr Rajpal Insaan , Dr Vidya Nair , Dr Vinod Kochupillai , 3 4 Dr S C Manchanda , Dr R L Bijlani
1
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS 2Ex Chief IRCH, AIIMS 3 4 Ex HOD, Cardiology Dept., AIIM Ex HOD, Dept of Physiology, AIIMS the relaxation response may reduce adrenergic endorgan responsiveness. The mechanism for such a change in this responsiveness is not clearly identified. These data are consistent with an earlier study suggesting that subjects eliciting the relaxation response may be less responsive to stress. A landmark research on the physiological correlates of a Meditation technique was published in Science in 1972. This research found that the Transcendental Meditation technique produces a physiological state of restful alertness. During the technique the physiology becomes deeply rested, as indicated by significant reductions in respiration, minute ventilation, tidal volume, and blood lactate, and significant increases in basal skin resistance (an index of relaxation). At the same time the physiology is alert rather than asleep, as indicated by an increased abundance of alpha waves in the EEG. These findings led researcher Dr. Keith Wallace to conclude that restful alertness is a fourth major state of consciousness, termed transcendental consciousness, which is physiologically distinct from ordinary waking, dreaming, and deep sleep. EEG patterns obtained in practitioners of Sudarshan Kriya recorded a significant increase in beta activity in the left frontal, occipital and midline regions. These findings are indications of heightened alertness.
Beta 1 (12.5 18 Hz.)
India has a large heritage of spirituality of which we are all proud. The past decade has seen a rapid spread of spirituality, yoga and its healing effects into our living rooms. More and more people, especially youngsters, are taking to spirituality to deal with an increasingly stressful lifestyle. But have these techniques stood the test of the rigorous scientific research done on them? We aim to shed more light on this debate and present some of the published scientific data that has been researched at renowned institutions on this topic. Overview: How these practices differ from sleep or simply closing eyes and relaxing A frequently asked question is "how are the spiritual practices (yoga, meditation etc) different from our usual forms of 'relaxing'?" The state attained by these practices has been referred to as the "relaxation response"; defined by a set of integrated physiological changes that are elicited when a subject assumes a relaxed position in a quiet environment, closes his or her eyes, engages in a repetitive mental action, and passively ignores distracting thoughts , , , . These behaviors are associated with physiological changes that include decreased oxygen consumption, heart rate (HR), arterial blood pressure (BP), respiratory rate, and arterial blood lactate , . In addition, there are slight increases in skeletal muscle blood flow. All of these changes are different from those reported during sleep or quiet sitting. Physiological changes associated with the relaxation response In subjects eliciting the relaxation response more norepinephrine is required to produce the normal compensatory increases in HR and BP. The elicitation of
Address for correspondence:Dr Prashaant Chaudhry Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences (AIIMS), New Delhi - 110029
Mean Spectral Power in Various
Bands in Control group
Beta 2 (18.5 30 Hz.)
Bands in Control group
Sudarshan Kriya Practitioners
38
Research has also been conducted to study the effect of practice of a yoga technique on Gene expression. Himani Sharma et al investigated the effect of regular practice of Sudarshan Kriya and Pranayam (SK&P- a type of Pranayama) on antioxidant enzymes, genes involved in oxidative stress, DNA damage, cell cycle control, aging, and apoptosis. Their results are summarized in the table below. Table -1 Parameter Glutathione (antioxidant) GSH-Peroxidase Superoxide Dismutase Glutathione S-transferase Expression of antioxidant Cu-Zn SOD, Mn SOD, glutathione peroxidase, and catalase genes Antiapoptotic Cox-2 and HSP-70 Life span of lymphocytes Controls (Mean S.E.M) (n=19) 76.74.06 nmol/ml 5516415 U/l 173.67.6 U/ml Practitioners (Mean S.E.M) (n=23). 96.54.41 6923382.3 U/l 214.712.2 U/ml Higher (P=.034) Significantly higher
Significantly higher (P=.035) and (P=.044) Prolonged by up-regulation of antiapoptotic genes Plasma cortisol is a stress hormone. A study showed that plasma cortisol decreased during Transcendental Meditation, whereas it did not change significantly in control subjects during ordinary relaxation. (Figure 2) EFFECT ON SYSTEMIC ILLNESSES Hypertension and Cardiovascular Disease As our lives become more stressful, we have seen an abrupt increase in diabetes, hypertension and coronary artery disease. A number of researchers have studied the effect of the relaxation response on established systemic diseases. Manchanda SC et al conducted a randomized, controlled trial of yoga (yoga, control of risk factors, diet control and moderate aerobic exercise) versus conventional methods (i.e. risk factor control and American Heart Association step I diet) in 42 angiographically proven coronary artery disease male patients. At one year, the yoga groups showed significant reduction in number of anginal episodes per week, improved exercise capacity and decrease in body weight. Serum total cholesterol, LDL cholesterol and triglyceride levels also showed greater reductions as compared with control group. Revascularisation procedures (coronary angioplasty or bypass surgery) were less frequently required in the yoga group (one 39
This study provided evidence suggesting that SK practice may exert effects on immunity, aging, cell death, and stress regulation through transcriptional regulation. Similarly, Li QZ et al studied the gene expression and gene regulation by mind-body interaction in Asian Qigong practitioners (pilot study). The gene expression of practitioners in contrast to normal healthy controls was characterized by enhanced immunity, downregulation of cellular metabolism, and alteration of apoptotic genes in favor of a rapid resolution of inflammation. Correlating with enhanced immunity reflected by microarray data, neutrophil phagocytosis was significantly increased in Qigong practitioners. Cortisol levels
6.0
Plasma Cortisol (mog/dl)
Eyes-Closed Rest
5.5 5.0 4.5 4.0 3.5 3.0
TM
Before
During
p < .01
After
(Figure 2)
versus eight patients; relative risk = 5.45; P = 0.01). Coronary angiography repeated at one year showed that significantly more lesions regressed (20% versus 2%) and less lesions progressed (5% versus 37%) in the yoga group (chi-square = 24.9; P < 0.0001). Yogendra J et al also noted similar reductions in the LDL cholesterol and triglyceride levels and increase in the HDL cholesterol levels, again in patients with angiographically proven coronary artery disease. They too noted regression of coronary lesions and improvement in myocardial function. These findings have been confirmed by various other authors , . Another study done by Chandra Patel el al on 194 patients with two or more risk factors (BP > 140/90 mm Hg, plasma cholesterol > 243 6 mg/100 ml and smoking >10 cigarettes/day) attempted to see the effect of the relaxation response in preventing cardiovascular disease. They were randomly allocated to a group for modification of behaviour or to serve as controls. The treatment group had group sessions of one hour a week for eight weeks in which they were taught breathing exercises, relaxation, and meditation and about managing stress. After eight weeks and eight months, there was a significantly greater reduction in both systolic and diastolic blood pressures in the group taught to relax compared with the control group, which was maintained at four years follow up. Plasma cholesterol concentration and the number of cigarettes smoked were lower in the treatment group at eight weeks and eight months, but not at the four year follow up. At four years, more subjects in the control group reported having had angina and treatment for hypertension and its complications. Incidence of ischaemic heart disease, fatal myocardial infarction, or electrocardiographic evidence of ischaemia was significantly greater in the control group, thus establishing the beneficial effect of the intervention. Patel C et al compared the plasma rennin, plasma angiotensin levels and blood pressure in untreated hypertensives between a group receiving biofeedback (relaxation and stress management techniques) and a control group. Both the biochemical parameters showed a greater reduction in the biofeedback compared with the control group at eight weeks follow-up. The greater reduction in blood pressure in the subjects in the biofeedback group compared with the control group (11.0 mm Hg systolic and 8.8 mm Hg diastolic), persisting eight months after the training, suggests that relaxation-based behavioral methods might be offered as a first-time treatment to patients with mild hypertension. 40
Aivazyan TA et al in a randomized study on mild essential hypertension showed the treatment group to have a significant reduction in systolic and diastolic blood pressures, peripheral vascular resistance, and hypertensive response to emotional stress, and an improvement in psychological adaptation, quality of life, and capacity for work. There have however been a few studies that have not shown a benefit. Van Montfrans GA et al reported 8 weeks of relaxation therapy (one hour per week training in muscle relaxation, yoga exercises, and stress management) as being an ineffective method of lowering 24 hour blood pressure, being no more beneficial than non-specific advice, support, and reassurance--themselves ineffective as a treatment for hypertension. This may have been due to a sub-optimal intervention (only 1hr/week) failing to elicit the relaxation response adequately. DIABETES Yoga asanas for 30-40 minutes a day were found to have a beneficial effect on glycaemic control and improve nerve function in mild to moderate Type 2 diabetes with sub-clinical neuropathy by Malhotra V et al . Right hand and left hand median nerve conduction velocity increased significantly in the treatment group while the nerve function parameters deteriorated in control group over the period of study. Studies on stress and psychiatric illnesses Nearly half of the world's population has some kind of sleep disorder, with insomnia being the most common. Worry, anxiety, unconscious tensions and major or minor health problems can all affect the quality of sleep. Sat Bir S Khalsa in his study of 'Treatment of Chronic Insomnia with Yoga' found a statistically significant improvement in the sleep parameters (Sleep efficiency (SE), total sleep time (TST), total wake time (TWT), sleep onset latency (SOL), wake time after sleep onset (WASO), number of awakenings, and sleep quality measures were derived from sleep wake diary entries) with yoga, comparable to that seen with somatic or cognitive relaxation techniques. In India, people are known to turn to religion and prayer when disturbed or depressed. The efficacy of Sudarshan Kriya (SK&Y) in melancholic depression was studied in a randomized fashion by N. Janakiramaiah et al . They hospitalized 45 patients and treated them with ECT, Imipramine or SKY. Remission
rates at the end of the trial were 93, 73 and 67% in the ECT, IMN and SKY groups, respectively. Within the limitations of the design (lack of double blind conditions), it was concluded that, although inferior to ECT, SKY was as efficacious as drugs in melancholia and was an alternative as a first line treatment. In an attempt to demonstrate the effect of the relaxation response in depression at a molecular level, Nai-Ling Pan measured the serum cortisol, Brain-derived neurotrophic factor (BDNF) levels and the Beck Depression Inventory (BDI) scores in patients before and after a 6 day course during which they practiced Sudarshan Kriya (SKY). BDNF is a key molecule in the neurotrophic hypothesis of depression in the recent decade. Increase of BDNF levels in the brain and serum seems to relate to antidepressive treatments in animal models and human subjects. Results revealed that BDI scores significantly decreased after the 6-day SKY courses, and the decrease maintained for 12 weeks. The percent changes of serum BDNF levels after the courses were negatively correlated with serum BDNF levels before the course, indicating the normalization effects of the SKY courses. One episode of SKY group practice was found to increase serum BDNF levels but decrease serum cortisol levels. Increase of serum BDNF levels sustained for at least 4 weeks and was not due to the circadian rhythm. It concluded that the intervention of SKY courses and practices has profound antidepressant effects and the effects are highly correlated with its function in normalization of serum BDNF levels. Post Traumatic Stress Disorder This is a state in which one is extremely over-whelmed by circumstances such as wars or natural calamities. The Victim Services Center of Miami (VSCM) and the National Institute of Mental Health and Neuroscience conducted a collaborative study on the effects of Sudharshan Kriya, on post-traumatic stress as applied to survivors of the December 2004 Tsunami at a refugee camp in Nagapattinam, India. All the yoga users experienced a huge drop in scores for posttraumatic stress disorder and depression after just four days with no change in the control group. Counseling provided had no added benefits over the yoga training alone . An Australian Psychiatrist, Dr Janis Carter, studied the benefits of yoga on PTSD in 8 Australian Vietnam war veterans , aged between 50-60yrs old. At the beginning, the veterans were extremely stressed, and most could not sleep for more than a few hours at a time. They had 41
severe anxiety attacks as well as suffering from depression. Many of them were using alcohol as a form of self medication, and were suffering from hypertension, diabetes, fatigue, anger, frustration and confusion. There was a highly significant drop in the Center for Epidemiology- Depression Scale (CED-S) scores were seen in all the participants. It was concluded that yoga provides a cheap, safe treatment, can be self administered, and provides a sense of self mastery, and the benefits are broader than most areas tested. The comorbidites of depression and alcohol dependence are also addressed. Alcohol dependence A Vedamurthachar et al of NIMHANS studied the effect of Sudarshan Kriya and Yoga (SKY) on alcoholics after a week of detoxification management. The patients and controls both completed the Beck Depression Inventory and their plasma ACTH and cortisol (stress hormones) were measured before and at the end of 2 weeks. In both groups, reductions in BDI scores occurred but significantly more so in SKY group. Likewise, in both groups plasma cortisol as well as ACTH fell after two weeks but significantly more so in SKY group. Reduction in BDI scores correlated with that in cortisol in SKY but not in control group. Reduction in stress-hormone levels (cortisol and ACTH) along with BDI reductions were thought to possibly support a biological mechanism of SKY in producing beneficial effects. Tobacco deaddiction In a study on tobacco de-addiction by Kochupillai V et al , 82 tobacco users were taught SK and P and advised to practice regularly. Complete cessation of tobacco use was achieved in 17 of the 34 individuals who could be followed up to 6 months of practice. CANCER It is believed that stress, a psychophysiological process, acts through the immune-neuroendocrine axis and affects cellular processes of body and immune functions, leading to disease states including cancer. Cancer patients who had completed their standard therapy performed Sudarshan Kriya and Pranayam (SK&P). SK and P increased natural killer (NK) cells significantly (P <0.001) at 12 and 24 weeks of the practice compared to baselinexxvi. Increase in NK cells at 24 weeks was significant (P <0.05) compared to controls. The authors feel that when confirmed in large and randomized studies, this result could mean that the regular practice of SK and P might reduce the incidence and progression of cancer.
OPHTHALMOLOGY The head-stand (shirshasana) has been shown to cause a transient and highly significant rise (doubling) of the Intra Ocular Pressure (IOP). However, Mani Baskaran et al could not demonstrate a higher prevalence of ocular hypertensives in yoga practitioners regularly practicing the head-stand, nor did the risk factors contributing to glaucoma show any correlation with magnitude of IOP raise during the posture. On the other hand, Dimiter Robert Bertschinger et al in a case report, showed progression of glaucoma in a 46 year old lady with Juvenile Open Angle Glaucoma (JOAG) who had recently started doing the headstand. This reversed on cessation of the yoga asana. Glaucoma has been accepted by Yoga therapists as a contraindication to head-stand and they do not recommend this asana in these patients. The effect of meditation and relaxation on glaucoma has not been well established. Stuart Brody et al demonstrated and increase of 1.3 mmHg of IOP with psychological stressors. Since meditation and relaxation have been shown do decrease the stress response and also increase the anti-oxidant levels, it was postulated that meditation practices may be beneficial in glaucoma. Gert Kaluza et al studied the effect of a practice which involved special exercises in ocular relaxation and imagination of aqueous humor drainage in 23 patients of Primary Open Angle Glaucoma. They detected a significant decrease in IOP. Twenty-four-hour profiles as well as the water drinking test also showed significant reductions of IOP across time. Medication dosage decreased for 56% of the initially treated patients. The findings suggest that relaxation and visual imagery techniques can be beneficial in reducing elevated IOP levels in patients with open angle glaucoma. Yoga exercises for the eye improved the symptoms of dry eye significantly in computer users in a study by Shirley Telles et al within 60 days of intervention. Yoga exercises were done for an hour, 5 days a week in subjects and included yoga postures (asanas, 15 minutes), regulated breathing (pranayamas, 10 minutes), exercises for the joints (sithilikarana vyayama, 10 minutes), visual cleansing exercises (trataka, 10 minutes), and guided relaxation (15 minutes). The controls noted a worsening of symptoms in the same period. SUMMARY To summarize, the beneficial effects of yoga, pranayam and meditation has been demonstrated at a molecular level and it has been found to be useful in many diseases believed to have a psychosomatic component including 42
hypertension, coronary heart disease, diabetes mellitus, cerebrovascular disease, obesity, psychiatric illnesses like PTSD, insomnia, anxiety, depression and possibly in cancer. These benefits have been shown both clinically and at a genetic level. It has been described by the practitioners to give an experience of joy, enthusiasm, love, belongingness and fulfillment. In addition, they feel better able to cope with stress and have an increased concentration. These may be difficult to demonstrate in a randomized controlled fashion due to its more subjective nature, but is arguably just as important in attaining the WHO definition of health (a state of physical, mental, social and spiritual well-being). The claims made by people who perform spiritual practices and the wealth of data presented above put a strong case for adopting these practices in our lives. Many of these results, you may agree, are almost too good to be true. Maybe this is why our ancient yogi's and learned ones put so much emphasis on adopting such a lifestyle. It seems like we are making a full circle and the way forward may indeed be by returning to our roots! Reference: 1. 2. 3. 4. 5. 6. 7. H. Benson, J. F. Beary, M. P. Carol, Psychiatry 37, 37 (1974). H. Benson, The Relaxation Response (Morrow, New York, 1975). R. K. Wallace and H. Benson, Sci. Am. 226, 84 (February 1972). A. F. Wilson, Am. J. Physiol. 221, 795 (1971). R. K. Peters, H. Benson, J. M. Peters, Am. J.Public Health 67, 954 (1977). H. Benson, N. Engl. J. Med. 296, 1152 (1977). Wallace, R. K. Physiological effects of Transcendental Meditation.Science 167: 1751-1754, 1970. M. Bhatia et al. Electrophysiologic evaluation of sudarshan kriya : an EEG, BAER, P300 study. Indian J Physiol Pharmacol 2003; 157 - 163. Himani Sharma et al. Gene expression profiling in practitioners of Sudarshan Kriya. Journal of Psychosomatic Research 64 (2008) 213-218.
8.
9.
10. Jevning, R.et al. Adrenocortical activity during meditation, Hormones and Behavior 10(1): 54-60, 1978.
11. Manchanda SC et al. Retardation of coronary atherosclerosis with yoga lifestyle intervention. J Assoc Physicians India. 2000 Jul;48(7):687-94. Yogendra J et al. Beneficial effects of yoga lifestyle on reversibility of ischaemic heart disease: caring heart project of International Board of Yoga. 12. Mahajan AS et al. Lipid profile of coronary risk subjects following yogic lifestyle intervention. Indian Heart J. 1999 Jan-Feb;51(1):37-40. 13. Bijlani RL et al. A brief but comprehensive lifestyle education program based on yoga reduces risk factors for cardiovascular disease and diabetes mellitus. J Altern Complementary Med. 2005 Apr;11(2):267-74. 14. Chandra Patel et alTrial of relaxation in reducing coronary risk: four year follow up. British Medical Journal Volume 290. 1103-6. 15. Patel C et al. Controlled trial of biofeedback-aided behavioural methods in reducing mild hypertension.British Medical Journal 1981 Jun 20;282(6281):2005-8. Aivazyan TA et al. Efficacy of relaxation techniques in hypertensive patients. Health Psychol. 1988;7 Suppl:193-200. 16. Van Montfrans GA. Relaxation therapy and continuous ambulatory blood pressure in mild hypertension: a controlled study. BMJ 1990 May 26;300(6736):1368-72. 17. Malhotra V et al. Effect of Yoga asanas on nerve conduction in type 2 diabetes. Indian J Physiol Pharmacol 2002 Jul;46(3):298-306. 18. Sat Bir S. Khalsa. Applied Psychophysiology and Biofeedback, Vol. 29, No. 4, December 2004. 19. N. Janakiramaiah et al. Antidepressant efficacy of Sudarshan Kriya Yoga (SKY) in melancholia: a randomized comparison with electroconvulsive therapy (ECT) and imipramine. Journal of Affective Disorders 57 (2000) 255-259. 20. Nai-Ling Pan. The Role of Brain-Derived Neurotrophic Factor in the Antidepressant Effects of Sudarshan Kriya Yoga. Electronic Thesis and Dissertation System, P 72. http://etds.ncl.edu.tw/ theabs/english_site/detail_result_eng.jsp?id=095 NCKU5116008. 43
21. Yoga: The Strongest Stretch. Psychology Today Magazine, May/Jun 2007. 22. Carter J.J. et al. Two year study of four pilot studies using yoga as an adjunct to ordinary psychiatric treatment in war veterans suffering from PTSD. 2004. Vivekananda Yoga Research Institute and RMIT University, Melbourne, Australia. 23. A. Vedamurthachar et al. Antidepressant efficacy and hormonal effects of Sudarshana kriya Yoga (SKY) in alcohol dependent individuals. Journal of Affective Disorders 94 (2006) 249-253. 24. Kochupillai V et al. Effect of Rhythmic Breathing (Sudarshan Kriya and Pranayam) on Immune Functions and Tobacco Addiction. Annals of the New York Academy of Sciences. Volume 1056 Natural Products and Molecular Therapy Page 242252, November 2005. 25. Mani Baskaran et al. Intraocular Pressure Changes and Ocular Biometry during Sirsasana (Headstand Posture) in Yoga Practitioners. Ophthalmology, Volume 113, Issue 8, Pages 1327-1332. 26. Dimiter Robert Bertschinger et al. Yoga can be dangerous-glaucomatous visual field defect worsening due to postural yoga. British Journal of Ophthalmology 2007;91:1413-1414. 27. Stuart Brody et al. Intraocular pressure changes: the influence of psychological stress and the Valsalva maneuver. Biological Psychology Volume 51, Issue 1 October 1999, Pages 43-57. 28. Gert Kaluza et al. Stress reactivity of intraocular pressure after relaxation training in open-angle glaucoma patients. Journal of Behavoural Medicine. Volume 19, Number 6 / December, 1996. 29. Shirley Telles et al. Effect of yoga on self-rated visual discomfort in computer users. Head Face Med. 2006; 2: 46. Spiritual saints wherever they be Pray for every beings prosperity They love every one And have enmity with none.
Sant Gurmeet Ram Rahim Singh Insaan
HYDROCEPHALUS REQUIRING SHUNT SURGERY
CASE REPORT
Hydrocephalus Requiring Shunt Surgery as an Initial Presentation of Vogt-Koyanagi-Harada Syndrome
Subrata Mandal, Anusha V, Rajpal Insaan, Pradeep Venkatesh, Satpal Garg
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS
Abstract: We report a female patient who presented with fever, chills and rigor and headache. On neurological consultation meningitis with hydrocephalus was diagnosed. Ophthalmological examination showed only bilateral disc edema. She underwent ventriculo-peritoneal shunt surgery for hydrocephalus. In postoperative period she developed signs of uveitis and after ophthalmological evaluation Vogt-Koyanagi-Harada syndrome was diagnosed. Inflammation as well as vision improved after treatment with pulse and oral corticosteroids. Key words: Hydrocephalus; ventriculo-peritoneal shunt; Vogt-Koyanagi-Harada syndrome.
Vogt-Koyanagi-Harada syndrome (VKH) is an uveomeningoencephalitic syndrome involving the eye, ear, meninges and integumentary system for which no confirmatory diagnostic tests are available.1, 2 It usually affects persons in 2nd to 4th decades of life. Natural course of VKH comprises of four different stages. Firstly, there is a prodromal stage manifested as headache, flulike symptoms, auditory symptoms and aseptic meningitis. Then follows the ocular stage characterized by panuveitis with exudative retinal detachment and optic disc edema. In convalescent stage poliosis, vitiligo of skin and limbal area, depigmentation of retinal pigment epithelium (RPE), alopecia appears. Lastly chronic or recurrent stage manifests. We herein report a patient who underwent shunt surgery for hydrocephalus secondary to meningitis of unknown etiology and who subsequently developed typical features of VKH. Case Report A 27 year old female without any known systemic illness developed sudden onset fever with chills and rigor associated with headache, nausea and vomiting. She sought neurology consultation elsewhere. A series of investigations were done to rule out tuberculosis and connective tissue disorders. Ophthalmological
Subrata Mandal, Anusha V, Rajpal Insaan, Pradeep Venkatesh, Satpal Garg Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS New Delhi
examination revealed bilateral disc edema. Noncontrast computerized tomography scan of brain showed mild dilated lateral and third ventricles. Third ventricle transverse diameter was 8.2 mm and ventricular size index was 37%. Computerized tomography scan findings were suggestive of mild ventriculomegaly (Figure: 1A). She was diagnosed to have postmeningitic hydrocephalus and a ventriculo-peritoneal shunt surgery was performed on the 3rd week of illness for the same. She was put on antibiotics and anticonvulsant. Post shunting surgery cranial CT scan showed resolution of ventriculomegaly (Figure: 1B). In post operative period she developed redness of the both the eyes with pain and progressive dimness of vision. A diagnosis of uveitis was made and referred to our uvea clinic.
Figure 1A, B: pre and post shunt surgery CT scan of brain showing decrease in ventricular size.
During first ophthalmological examination best corrected visual acuity was 6/18 in both eyes. Poliosis was present in both the eyes (Figure: 2). 44
Figure 2: Poliosis
Fundus fluorescein angiography revealed multiple pinpoint areas of hyperfluorescence suggestive of serous detachment along with disc leakage (Figure: 5A, B). On systemic examination, alopecia but no skin lesion was found. She was diagnosed to have complete VKH syndrome and was treated with pulse dexamethasone therapy (1000mg OD intravenously for three days) to which she responded. After three days, systemic oral steroid (1 mg/kg body weight) was prescribed. One week after treatment initiation BCVA was OD-6/9 and OS-6/12. Ocular inflammation also reduced to the extent of occasional anterior chamber and retrolental cell.
Anterior segment examination revealed medium sized keratic precipitates and 3+ cells, flare and posterior synechiae (Figure: 3).
Figure 5A, B: fundus fluorescein angiography showing multiple pin point leakages.
Figure 3: Anterior segment examination photographs showing posterior synechiae and posterior subcapsular cataract.
Iris nodules or iris neovascularization were absent. Mild posterior subcapsular cataract was noted in both the eyes. Posterior segment examination shows bilateral disc edema and multiple small yellowish white lesions scattered diffusely all over the fundus (Figure: 4A, B).
Figure 4: fundus picture showing disc edema (A & B) followed by depigmented blonde looking fundus (C & D).
She was discharged on topical steroids and cycloplegics and systemic steroids and advised regular follow up. In the last visit (3 months) she is maintaining her vision on 20 mg oral steroid daily and fundus showed RPE depigmentation (Figure: 4C, D). Discussion Independently, Vogt, Koyanagi, and Harada described several patients during a 20-year period with bilateral uveitis, exudative retinal detachments, neurological abnormalities, and disorders of the integument. Despite differences in their patients, the manifestations appeared to represent a spectrum of disease and several authors suggested that the disorder should be termed Vogt-Koyanagi-Harada syndrome. The revised criteria defined 3 categories of disease: complete VKH, incomplete VKH, and probable VKH. Common to all forms of VKH disease are the requirements that: patients have no prior history of ocular trauma or surgery, patients have no evidence of another ocular disease based upon clinical or laboratory evidence, and patients have bilateral ocular involvement. Patients with complete VKH disease must also have evidence of neurological and auditory findings as well as integumentary signs. However, the neurological and auditory manifestations which include meningismus, cerebrospinal fluid pleocytosis, and tinnitus may have resolved before an ophthalmic examination. To be diagnosed with incomplete VKH disease, patients must have either the neurological and auditory manifestations or the integumentary signs. The most frequently encountered neurological associations of 45
uveitis are VKH disease, primary CNS lymphoma, multiple sclerosis, and herpes virus infections.3 Others are sarcoidosis, cytomegalovirus infection, collagen vascular diseases, disorders associated with disseminated intravascular coagulopathy, and malignant hypertension.4 The inflammatory aspects of VKH syndrome are attributed to the autoimmune destruction of melanocytes through immunological mechanisms. This mechanism would account for the high incidence of Harada's disease in dark-skinned patients.5 It may affect any organ containing melanocytes and if not treated early can cause advanced damage to the organ. Neurological signs in VKH syndrome are usually mild, the main finding being atypical headache,6 and this particularity delays diagnosis. Symptoms of meningitis usually do not need any active intervention. To our knowledge this is the first case report of VKH associated meningitis requiring ventriculo-peritoneal shunt surgery. In our case symptoms of meningitis were so prominent that disc edema was considered as a result of increased intra cranial pressure by neurologist. We think if the disease could be diagnosed early and treated it may not developed hydrocephalus. In conclusion, all cases of bilateral disc edema and meningitis should be carefully
examined for anterior chamber and vitreous reaction and if suspected fundus fluorescein angiography should be done to rule out multiple areas of pin point leakage suggestive of exudative detachment. Reference: 1. 2. 3. Sugiura S. Vogt-Koyanagi-Harada disease. Jpn J Ophthalmol 1978;22: 9-35 Snyder DA, Tessler HH. Vogt-Koyanagi-Harada syndrome. Am J Ophthalmol 1980; 90:69-75 J R Smith, J T Rosenbaum. Neurological concomitants of uveitis. Br J Ophthalmol 2004; 88:1498-1499 Wolfensberger TJ, Tufail A. Systemic disorders associated with detachment of the neurosensory retina and retinal pigment epithelium. Curr Opin Ophthalmol. 2000; 11(6):455-61 Ghipponi JP, Boitte JP, Rosier S et al. Harada's disease. Report of a case. Med Trop (Mars). 1995; 55(4 Pt 2):459-61 Beniz J, Forster DJ, Lean JS et al. Variations in clinical features of the Vogt-Koyanagi-Harada syndrome. Retina. 1991;11(3):275-80
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46
A CASE OF GIANT CHOROIDAL TUBERCULOMA MISDIAGNOSED
CASE REPORT
A case of giant choroidal tuberculoma misdiagnosed as amelanotic melanoma.
Anusha V, Rajpal Insaan, Pradeep Venkatesh, Satpal Garg, Subrata Mandal
Dr. Rajendra Prasad Centre for Ophthalmic Sciences, AIIMS. Madhav ratti, 30 yr old male presented with sudden painless loss of vision, especially the nasal field of the left eye within a duration of one month. The patient was seen at a private hospital and was diagnosed to a have total retinal detachment, a vitreo-retinal surgery was contemplated and the patient was referred to RPC for the same. The diagnosis was revised at another private hospital and the patient was referred to R.P.centre with a diagnosis of amelanotic melanoma for further management and enucleation if deemed necessary. The patient presented to our centre with the same complaints. He did not give a history of photopsia ,floaters or metamorphopsia. There was no history of ocular trauma. A detailed enquiry of his past revealed a history of tuberculous pleural effusion at the age of 8 years for which he had received anti-tuberculous treatment under supervision for 8 months. On examination, the patient had a vision of 20/20 in the right eye and PL+ PR inaccurate in two quadrants in the left. Slit lamp examination of the left eye showed the presence of pigment deposits on the corneal endothelium with 3+ cells and flare in the anterior chamber and 3+ retrolental cells suggesting an inflammatory etiology. Fundus examination of the left eye revealed a mass arising from the supero-temporal quadrant that was diffusely elevated with overlying blood vessels and haemorhages. There was an associated retinal detachment with shifting fluid pointing towards an exudative cause for the same.
(Figure - 1b)
Fundus examination of the right eye showed a yellowish lesion along the inferotemporal arcade with no associated vitritis.
(Figure - 2)
Ocular and systemic investigations were planned.
Address for correspondence:Dr. Anusha V. Dr. Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute of Medical Sciences (AIIMS), New Delhi - 110029 (Figure - 1a)
47
The ocular ultrasound of the left eye confirmed the presence of a mass in the posterior segment that showed moderate to high amplitude spikes with associated retinal detachment.
FFA of the other eye was however inconclusive.
(Figure - 3)
(Figure - 5)
Fluorescein angiography showed early hyperflourescence with increasing hyperflourescence and leakage in the late phases suggesting inflammation in the left eye.
Systemic investigations: Haemogram revealed a high ESR (57 mm/hour), the other parameters being normal. Peripheral blood smear was normal. The renal function testa and the liver function tests were unremarkable except for a mild elevation if the SGOT and SGPT liver enzymes. Mantoux was 15mm. HIV screening was done and was negative. Chest X-ray showed the presence of paratracheal widening suggestive of mediastinal lymphadenopathy.
(Figure - 4a)
(Figure - 6) (Figure - 4b)
48
MRI orbit showed the presence of a hyperintense lesion on T-1 and a hypointense non-homogenous lesion on T-2 weighted image with enhancement of the borders of the lesion with contrast suggesting an inflammatory abscess.
CECT chest and abdomen showed the presence of large necrotic rim enhancing mediastinal lymph nodes: possibly tuberculous in etiology.
(Figure - 8a) (Figure - 7a)
(Figure - 8b)
(Figure - 7b)
PET scan showed an increased FDG uptake in large orbital leson in the posteror part of the globe and multiple lymph nodes suggestive of disseminated tuberculosis. USG guided FNAC from the lt. supraclavicular lmyph node shows necrosis in which few Acid Fast Bacilli were detected. Features were consistent with TB. In the presence of a past history of tuberculosis, and with the above investigations suggesting a definite tubercular etiology a diagnosis of choroidal tuberculoma with exudative retinal detachment was made and the patient was started on anti tuberculosis treatment- category 2. (the case being one of relapse.) The age of the patient , the findings on the MRI and the presence of anterior chamber and retrolental activity with a systemic involvement refutes the diagnosis of amelanotic melanoma in this patient. The patient is now following up at a local DOTS centre. 49
(Figure - 7c)
Discussion: Choroidal tuberculoma results from hematogenous seeding from the primary complex or secondary lesions that may develop, where the bacilli may remain dormant for many years before reactivation. Progressive caseation necrosis, and rapid multiplication of the tubercular bacilli and tissue destruction lead to the formation of these tubercles It is seen in 1.4% to 60% in patients with different form of TB. The most characteristic clinical presentation of ocular TB is in the form of multifocal choroidal tubercles. It may occasionally present as solitary elevated mass like lesion(4-14mm). The tubercles appear as yellowish sub retinal mass with exudative detachment, rapid progression and sometimes even as ocular perforation.Patients with military TB and AIDS may present with sub retinal abscess. Investigations: The investigation considered as Gold standard in ocular TB is the isolation of mycobacteria by sub retinal fluid analysis that can help in the detection of TB foci . Others investigations to be undertaken are Mantoux, Chest X-ray and culture for tuberculosis if any specimen is obtainable. Ocular investigations: Ultrasound examination of the posterior segment may show a low reflectivity on A-scan but may show a solid elevated mass lesion in B-scan. Ocular fluid positivity for IS 6110 sequence in PCR is also suggestive of ocular TB. Angiographic studies of large size tuberculomas show an early hyperfluorescence within and around the lesion that increases in intensiy and size over the subsequent phases as the dye leaks into the surrounding RD with late leakage from the lesion . FFA can also be used to assess response to treatment which shows decreasing hyperfluoroscence of the lesion with treatment. The initial phases are said to have a ring of fire appearance. The late hyperfluorescence hasd been attributed to the presence of retinal pigment epithelitis. ICG angiography is also a useful method to determine the extent of the lesion. Diagnosis : There are definite guidelines for the diagnosis of ocular TB: A. Clinical signs: - Cellular reaction in AC/vitreous posterior synechiae - Vitreous snow ball opacities - Perivascular cuffing of inflammatory exudates - Solitary or multiple choroidal granulomas exudative RD 50
- Optic disc granuloma neuroretinitis - Sub retinal abscess B. Ocular investigations: - Demonstration of AFB from ocular fluids - Positive PCR C. Systemic investigations: Positive mantoux test Evidence of healed/active TB on chest X-ray Evidence of extra pulmonary TB (TB granuloma, AFB, culture)
D. Therapeutic test: positive response to ATT over 4-6 weeks. The presence of any one or more of the clinical signs with any one of the positive tests (B) is confirmatory for Ocular TB. In the presence of any one or more of the clinical signs with any one of the positive tests (C) or positive therapeutic trial(D): ocular TB is presumed. Management: There are no large studies available on the treatment of ocular TB. However, a multi drug therapy for atleast 6 months-15 months depending upon the patient's immune status and response to treatment has an efficacy of 95%. The recommendations by the american thoracic society and CDC and infectious disease society of america and by the WHO are as follows: Category 1: 2(HRZE) +4(HR) Category 2: 2(HRZES) +4(HRZE) Category 3: 2(HRZES) +1(HRZE) +5(HRE) The drug dosages are as follows: drug Daily dosage INH 5mg/kg rifampicin 10mg/kg pyrazinamide 15-30mg/kg ethambutol 15-25mg/kg streptomycin 15 mg/kg Thrice weekly 15mg/kg 10mg/kg 50-70mg/kg 25-30mg/kg 25-30mg/kg.
Ocular side effects: Ethambutol can cause optic neuritis,photophobia, extraocular muscle paresis. Visual field and colour vision testing every 4 weeks(>15mg/ kg); 3-6 months for lower doses is recommended. The complaints usually resolve by 3-12 months, otherwise parentral hydroxy cobalamin is indicated. The response to treatment is evident within 2-4 weeks. The use of low dose steroids, though controversial, for 46 weeks with ATT may limit damage to the ocular tissues from delayed hypersensitivity.
JOURNAL ABSTRACTS
DJO VOLUME 14 NUM 7 . JAN-MARCH 2008
JOURNAL ABSTRACTS
Dr. Shailesh G.M., MD, DNB, Dr. Munish Dhawan, MD Comparison of preoperative and postoperative anterior segment measurements with Pentacam in horizontal muscle surgery. Emre S, Cankaya C, Demirel S, Doganay S. Eur J Ophthalmol. 2008 Jan-Feb;18(1):7-12. Department of Ophthalmology, School of Medicine, Inonu University, Malatya, Turkey. mdsinanemre@ yahoo.com PURPOSE: To evaluate the effect of horizontal muscle surgery (recession or recession plus resection) on the anterior chamber parameters in patients after strabismus surgery. METHODS: The Scheimpflug of 18 eyes of 12 patients with horizontal deviations were recorded just before surgery and 1 month after surgery. The power of anterior surface of cornea in horizontal and vertical axis, thinnest corneal thickness, anterior chamber depth, anterior chamber volume, and cornea volume were analyzed. The clinical characteristics of patients, the size of the deviations, the surgical doses, and observed responses to surgery were reviewed. RESULTS: There were six male and six female patients with an average age of 11.4 years (range, 4 to 22 years). Mean preoperative deviation was 47.91 PD (range, 20 to 75 PD), eight patients had esotropia with 57.5 PD average deviation (range, 40 to 75 PD), and four patients had exotropia with 28.75 PD average deviation (range, 20 to 35 PD). Of these 18 eyes, 12 eyes had horizontal muscle recession and 6 eyes had recession plus resection surgery. At the end of 1 month, three patients were orthophoric and eight patients had residual deviations varying between 16 and 35 PD. Preoperative and postoperative comparison of the whole study group documented insignificant changes in anterior chamber parameters and in keratometer readings. However, after dividing patients into two groups-recession or recession plus resection group-only one parameter, anterior chamber volume, was significantly reduced in recession plus resection group. CONCLUSIONS: Patients with strabismus who undergo recession plus resection procedure are prone to change in anterior chamber volume. Study with larger groups and long follow-up is necessary for clearer documentation of alterations at anterior chamber parameters.
50
Laser-assisted subepithelial keratectomy for anisometropic amblyopia in children: outcomes at 1 year. Astle WF, Rahmat J, Ingram AD, Huang PT. J Cataract Refract Surg. 2007 Dec;33(12):2028-34. Vision Clinic, Alberta Children's Hospital, University of Calgary, Calgary, Alberta, Canada. william.astle@ calgaryhealthregion.ca PURPOSE: To assess the refractive, visual acuity, and binocular results of laser-assisted subepithelial keratectomy (LASEK) for anisomyopia, anisohyperopia, and anisoastigmatia in children with various levels of amblyopia secondary to the anisometropic causes. SETTING: Nonhospital surgical facility with follow-up in a hospital clinic setting. METHODS: This retrospective review was of 53 children with anisometropia who had LASEK to correct the refractive difference between eyes. All LASEK procedures were performed using general anesthesia. Patients were divided into 3 groups according to their anisometropia as follows: myopic difference greater than 3.00 diopters (D), astigmatic difference greater than 1.50 D, and hyperopic difference greater than 3.50 D. The children were followed for at least 1 year, and their refractive status, visual acuity, and binocular vision were assessed and recorded at 2 and 6 months as well as 1 year. RESULTS: The mean age at treatment was 8.4 years (range 10 months to 16 years). The mean preoperative anisometropic difference was 6.98 D in the entire group, 9.48 D in the anisomyopic group, 3.13 D in the anisoastigmatic group, and 5.50 D in the anisohyperopic group. One year after LASEK, the mean anisometropic difference decreased to 1.81 D, 2.43 D, 0.74 D, and 2.33 D, respectively, and 54% of all eyes were within +/-1.00 D of the fellow eye, 68% were within +/-2.00 D, and 80% were within +/-3.00 D. Preoperative visual acuity and binocular vision could be measured in 33 children. Postoperatively, 63.6% of children had an improvement in best corrected visual acuity (BCVA) and the remainder had no noted change. No patient had a reduction in BCVA or a loss in fusional ability after LASEK. Of the 33 children, 39.4% had positive stereopsis preoperatively and 87.9% had positive stereopsis 1 year after LASEK. CONCLUSION: Laser-assisted subepithelial keratectomy is an effective surgical alternative to improve visual acuity in anisometropic children unable to tolerate conventional methods of treatment or in whom these methods fail.
JOURNAL ABSTRACTS
JOURNAL ABSTRACTS
Effect of preoperative stability of alignment on outcome of strabismus surgery for infantile esotropia. Lueder GT, Galli ML. J AAPOS. 2008 Feb;12(1):66-8. Epub 2007 Dec 21. Departments of Ophthalmology and Visual Sciences and Pediatrics, St. Louis Children's Hospital at Washington University School of Medicine, St. Louis, Missouri, USA. INTRODUCTION: Some strabismus surgeons wait until the angle of deviation stabilizes prior to operating on patients with infantile esotropia. This study evaluated whether a preoperative increase in the angle of deviation affected surgical outcomes. METHODS: This was a retrospective comparative case series in which records of patients with infantile esotropia, who had surgery performed before age 2 years and who were followed for at least 2 years postoperatively, were reviewed to identify two groups for comparison: the first had </=5(Delta) change in the angle of deviation between the first office visit and time of surgery; the second had a >/=10(Delta) increase in the angle of deviation prior to surgery. In the latter group, surgery was performed for the angle present at the time of surgery. Outcomes were considered successful if the patients had microtropias. RESULTS: Fifteen patients were identified in each group. The interval between the first office visit and time of surgery was the same in both groups (mean, 2 months). Outcomes were successful in 11 of 15 (73%) in each group (no significant difference, p = 0.659). CONCLUSIONS: There was no difference in outcome between children whose angles of deviation were stable and those whose angles increased prior to surgery. This indicates that strabismus surgery does not need to be delayed while waiting for the angle of deviation to stabilize. Surgical correction may therefore be achieved at an earlier age, which may have a beneficial effect on outcome. Computer-assisted dosage calculation for strabismus therapy in myopic patients. Koch M, Priglinger S, Hoerantner R, Haslwanter T. Acta Ophthalmol (Oxf). 2008 Feb;86(1):53-7. Epub 2007 Aug 6. Department of Ophthalmology, University Hospital Graz, Graz, Austria. PURPOSE: The published dosage recommendations for the surgical correction of horizontal strabismus in nonmyopic patients show large, unexplained differences. For patients with high myopia, the situation becomes even more complex because the increase in the size of the bulb also affects the geometry of the oculomotor muscles. In this study, we wanted to investigate whether computer simulations of the oculomotor plant can be used to find accurate surgical parameters. METHODS: In a retrospective study, we investigated pre- and postoperative strabismus patterns in 13 patients affected by convergent (seven patients) or divergent (six patients) strabismus and high myopia. Postoperative checks were made 1 day, 1 week, 3 months and 1-6 years after the operation. For each patient, we simulated the presurgical strabismus pattern with SEE++ (see 'Further Information' for manufacturer details), a biomechanical simulation program of the oculomotor plant. The individual results of the simulations were then compared to the measured postoperative strabismus patterns. RESULTS: We found a trend of under-correction in the postoperative situation, resulting in four patients having a large remaining strabismus angle of more than 5 degrees. The computer simulations were able to reproduce this under-correction, and suggested an increase in dosage. CONCLUSION: We conclude that realistic biomechanical simulations of the oculomotor plant can predict the postoperative result for myopic patients accurately. The results of the computer simulation correlate well with the postoperative outcome of the patient.
51
INSTRUCTION TO CONTRIBUTORS
Aims of the Journal Delhi Journal of ophthalmology (DJO) is the quarterly journal published by Delhi Ophthalmological Society. The DJO aims to become an easily readable fully referenced journal which will provide the specialists with up to date information and the residents with articles that give expert's opinions that are backed with references. The journal aims to provide : 1. The views of experts on current advances in the field, in a clear and readable format. 2. Case Reports and clinical enigmas. 3. Original articles preferable of clinical relevance . 4. Articles on Diagnostic and surgical techniques. 5. Selections, annotated by experts, of the most interesting papers from the great wealth of original publications. 6. New ideas and innovations, new devices, instruments. 7. Book reviews and letters to editor. All correspondence shall be acknowledged within six weeks of receipt by the editorial board. Authors shall be intimated about the acceptance of their articles for publication within six weeks of the acknowledgement. The journal expects each contributor to have made a significant contribution in writing the article. The authors must take full responsibility to ensure that the manuscript contains no matter that is, to the best of contributors, knowledge, and libetous or unlawful, or infringes upon any Indian copyright laws. All accepted manuscripts are subject to editing. The contributors are responsible for the statements in his/her/their work including the changes made during editing. All contributors are requested to sign a letter of transmittal' at the time submitting their manuscript for submission of the manuscript. Submission of the manuscript Authors are requested to read these instructions carefully before submitting manuscripts All manuscripts/ contribution should be sent by post to Dr. Rajpal Insan: Editor DJO, Dr. R.P. Centre, AIIMS 4th Floor, Room No- 480. Ansari Nagar New Delhi-29 India. All manuscript and illustrations must be submitted in triplicate along with a CD. The authors should retain a copy for their future reference. To speed the process of review t he manuscript s may b e sub mit t ed electreonically be email to Dr. Rajpal Insan at drrajpal2001@yahoo.co.uk, drrajpal_editordjo @yahoo.co.in or on a disc. These should be in MS-Word format and the images should be in jpeg format (email) and Tiff format (Disc). Graphs and line drawing/diagrams must be sent in graphic format, i.e. EPS, LOTUS/EXCEL Spreadsheet files, PICT/CHART files, or Harvard graphic. Do not send graphs and diagrams in freehand. The disk should be labeled with the title of the article, author's name, the file name, software used including version. The disk should be sent in proper packaging to avoid damage and corruption of the information during transit. Unreadable disks will be returned to the author for substitution.
Armeta Essenz
(Refreshing eye wash)
52
FORTHCOMING EVENTS
FORTHCOMING EVENTS
April, 2008 4-9 CHICAGO (USA)
ACSRS (American Society of Cataract & Refractive Surgeons) CHICAGO, IL, USA
11-14 CANADA
Canadian Ophthalmological Society Fairmont Chateau Whistler Whistler, BC, Canada
19-22 WURZBURG, GERMANY

21st Annual Congress of the German Retina Society/8th Symposium of IntI Society of Ocular Trauma, Main Topic: Ocular Trauma Wurzburg, Germany http://www.retinologie.de
12-16 CHICAGO
ASCRSI ASOA Symposium and Congress CHICAGO, IL, USA Contact: ASCRS Tel: + 1 703 591 2220, Fax: + 1 703 591 0614 Web: www.ascrs.org
28 June - 2 July,
HONG KONG
19-20 GERMANY
Frankurt Retina Meeting Mainz, Germany
27 Apr.-1 May
USA
ARVO (Association for Research in Vision & Ophthalmology) Greater Fort Lauderdale/Broward Country Convention Center Fort Lauderdale, FL, USA
WOC (World Ophthalmology Congress) Secretariat Ms. Angela Cho Department of Ophthalmology & Visual Sciences The Chinese University of Hong Kong 3/F, Hong Kong Eye Hospital, 147K, Argyle Street, Kowloon, Hong Kong Tel: (852) 2762-3128, Fax: (852) 2194-0695 Email: ange1acho@woc2008hongkong.org
July, 2008 7-10 MONTREAL, CANADA

9th International Conference on Low Vision Rehabilitation - Vision 2008 Montreal, Province: QC (Canada) Contact: Beatrice Laham Phone: 514-906-1979, Fax: 514-395-1801 E-Mail: blaham@opus3.com September, 2008 5-7 NEW DELHI, INDIA Biennial Meeting SAARC Academy of Ophthalmology India Habitat Centre, New Delhi Contact: Dr. Namrata Sharma Phone: 011-26589810, E-Mail: namrata.sharma@gmail.com
May, 2008 21-24 JAPAN

18th International Visual Field & Imaging Symposium (IPS2008) Nara, Japan Contact: Chota Matsumoto Phone: 81-72-366-0221 ext 3335 Fax: 81-72-368-2559 E-Mail: ips2008@med.kindai.ac.jp
22-25 VIENNA, AUSTRIA

Euretina (European Society of Retina Specialist) Austria Centre, Vienna, Austria
28-31 BELGIUM
XI International Orthoptic Congress 2008 ANTWERP, BELGIUM Contact: Daisy Godts Tel: +32 3 8214845, Fax: +32 3 8251926 Email: daisy.godts@ioacongress2008.org Web: www.ioacongress2008.org
13-16 CZECH REPUBLIC

EVRS (European Vitreo-Retinal Soceity) Prague, Czech Republic
13-17 GERMANY
ESCRS Berlin, Germany December, 2008 National update on Ophthalmology at Shah Satnam Ji Super Speciality Hospital, Dr. Shaane-meet, Chairman Shah Satnam Ji Healthcare Society Contact : Dr. Aditya Insaan, Dr. Rajpal Insaan, Dr. Pradeep Sharma Insaan, Dr. Dinesh Talwar Insaan, Prof. V.K. Dada E-mail : drrajpal2001@yahoo.co.uk. 53
June, 2008 1-6 GERMANY

European Glaucoma Society Organizing Secretariat Viale G. Matteotti, 7 - 50121 Firenze, Italy Phone ++39/055/50351 Fax ++39/055/5001912-570227 E-mail: egs2008@oic.it Website: www.eugs.org
MOTIVATE FOR ORGAN DONATION

Contact organizations which are helping eye donation, blood donation and body donation campaign.
Prof. S. Ghose, Chief RP Centre, Prof. Radhika Tandon, Dr. Namarta Sharma National Eye Bank, Dr. R.P. Centre (AIIMS) Ansari Nagar, New Delhi-110029 Ph:26589461/26588500/26588700/ 26593444 Prof. B. Ghose Prof. Ritu Arora Guru Nanak Eye Centre Eye Bank Maharaja Ranjit Singh Marg, New Delhi-110002. Ph: 23234612/22, 23235145/23232400 Prof. KPS Malik Safdarjung Hospital Eye Bank, Safdarjung Hospital, Ansari Nagar, New Delhi-110029. Ph: 26198126/26707217 Prof. Madan Mohan Dr. Rishi Mohan Sewa Eye Bank, MM Eyetech 29 Link Road, Lajpat Nagar-III New Delhi-110024 Ph: 29841919/ 9212035119
Dr. Shaane-meet Jee President, Shah Satnaam Jee Health Care Wing Shah Satnam Ji Super Speciality Hospital, Dera Sacha Sauda, Sirsa Ph. 01666-245588,245688 E-mail: dss321@sancharnet.in No waiting list Dr. Umang Mathur Dr. Shroff's Charity Eye Bank Dr. Shroff's Charity Eye Hospital Dr. Umang Mathur 5027, Kedar Nath Road, Darya Ganj New Delhi-110002 Ph: 41564300-11 Extn 268, 9873208336/26 Email: sceh.org Dr. Ashok Grover Delhi Central Rotary Eye Bank Sir Ganga Ram Hospital, Rajendra Nagar, New Delhi-110060 Ph: 42251356/ 25861463 Extn 1356, 9811771213 Dr. S C Gupta Rotary Regency Gift of Sight Coordination & processing Centre Venu Eye Institute & Research Centre 1/31, Sheikh Sarai, Phase-II, New Delhi- 110017
Donation of blood, eye or other body organs is a noble deed which shall go a long way in helping the suffering humanity. It may be interesting to note that Dera Sacha Sauda, Sirsa (Haryana) under the spiritual guidance of Hazoor Maharaj Saint Gurmeet Ram Rahim Singh Ji Insaan has got the Guinness world record in blood donations and is now working for eye and other organ donations. Let us help motivate more people for this noble deed. For more information contact: 1. ORBO, Organ Retrieval Banking Organisation All India Institute of Medical Sciences Ansari Nagar, New Delhi-110029 Ph.: 1060 (24 hours helpline), 2659 3444, 2658 8360 Fax: 91-11-2658 8402 E-mail: orboindia@yahoo.com Website: www.orbo.org
2.
International Blood & Organ Donation Bank Shah Satnam Ji Super Speciality Hospital, Dera Sacha Sauda, Sirsa (Haryana) Ph. 01666-245588,245688 E-mail: dss321@sancharnet.in Website : www.derasachasauda.org
54
TRAINING PROGRAMME
Training programmes
Institute 1. 2. Aditya Jyot Eye Hospital, Mumbai Aravind Eye Hospital, Madurai Aso-Palov Eye Hospital, Ahmedabad Bangalore West Lions Eye Hospital, Bangalore Bombay City Eye Institute, Mumbai Disha Eye Hospital, Barrackpore Giridhar Eye Institute, Kochi 1 8. 9. Grewal Eye Institute Lions NAB Eye Hospital, Mid Miraj 1 6 3 3+ 1 2 1 2 2 2 1 1+1 3+ 3 1 1 2 6+, 12 . 6++, 12+ 24+ , 24, 4*+, 6 24* 21. Dr. R.P. Centre, New Delhi 22. Choudhary Eye Care, New Delhi A total of 18 observerships of varing duration are available in all subspecialities A total of 18 observerships of varing duration are available in all subspecialities 1 1 2 4 3+3 4 2 1 4 3 8 4(DOMS) 1 1 6 4 6 20 24+ 12+ 1 12++,12+o 1 6+, 6oo,24+ 64 100 2 2$ 1 24* 1 6 3, 12= 4.1 2 4 Ant. Segment Glaucoma, Cornea/cataract Uveitis Orbit & Plastics Pediatric Ophthal. Retina Vitreous 1(DNB) 2 7 General Ophthal. 1(DNB) 10 72t, 49++24|| 24 , 20*, 12 12 48* 10 4(DNB) 6 16+, 16t 6 52 104 Shot Term Fellowship Observer ship
Several shot term paramedical courses 3. 4. 5. 6. 7. 6
10. L.V. Prasad Eye Institute, Hyderabad 11. Mahatme Eye Bank & Eye Hospital, Nagpur 12. Prakash Netra Kendr 13. Rajan Eye Care Hospital, Chennai 14. Shankar Nethralaya, Chennai 15. Sri Sankaradeva Nethralaya, Guwahati 16. Dr. S.B. Sohan Singh Eye Hospital, Amritsar 17. Shri Ganapathi Netralaya, Jalna 18. Shroffs Charity Eye Hospital, New Delhi 19. Suraj Eye Institute, Nagpur 20. Venu Eye Institute, New Delhi
2+
Optometry fellowship (2yrs + 1yr internship) 5+5/ observership in cornea, glaucoma, med retina, ped. Ophthal. 4 years BSc in Optometric Practices, 30seats 3 years Bsc in Optometric Practices, 10seats
* Indirect ophthalmoscopy; tIOL microsurgery; +phacoemulsification; Cornea; Glaucoma; 4 every 2 weeks, ++Lasers in diabetic retinopathy +Contact lens, Instruments maintenance; *Community outreach;00 low vision; **Manual SICS; **1 every 2 Weeks in phacoemulsification & refactive surgery, +Eye banking, 0Counselling, 00Paediatric ocular anaesthesia.
1.
2. 3.
4.
5. 6.
Aditya Jyot Eye Hospital Plot No. 153, Road No. 9 Opp. SIWS College Near Five Gardens, Wadala Mumbai - 400 031 Aravind Eye Hospital Anna Nagar Madurai - 625 020 Aso-Palov Eye Hospital Near Under Bridge Rajbhavan Road, shahibag Ahmedabad - 380 004 Bangalore West Lions Eye Hospital and Cornea Grafting Centre 56/2, H Siddaiah Road Bangalore - 570 002 Bombay City Eye Institute 5, Babulnath Road Mumbai - 400 007 Disha Eye Hospital & Research Centre Barrackpore, North 24 Parganas West Bengal - 743 120
7. 8. 9. 10. 11. 12. 13. 14.
Giridhar Eye Institute 28/2576, A. Kadavanthra Kochi - 682 020, Kerala Grewal Eye Institute Sector 9C, Madhya Marg Chandigarh 160009 Lion NAB Eye Hospital Plot No. P-31, Mide Miraj- 416 410 Sangli Dist L.V. Prasad Eye Institute L.V. Prasad Marg, Banjara Hills Hyderabad - 500 034 Mahatma Eye Bank & Hospital 16, Central Excise Colony Ring Road, Nagpur - 440 015 Prakash Netra Kendr N H 2, Vipul- Khand IV Gomti Nagar 226010 Rajan Eye Care Hospital No. 5, Vidyodaya East ll Street T Nagar, Chennai - 600 017 Dr. R.P. Centre for Ophthalmic sciences AIIMS, Ansari Nagar New Delhi - 110 029
15. Sankara Nethralaya Medical Research Foundation 18 College Road Chennai - 600 006 16. Sri Sankaradeva Nethralaya Beltola - 28, Guwahathi 17. Dr. S.B. Sohan singh Eye Hospital, Katra Sher Singh Amritsar - 143 006 18. Shri Ganapati Netralaya Head Post Office Road Jalna - 431 203 19. Dr. Shroff's Charity Eye Hospital 5027, Kedar Nath Road, Daryaganj, New Delhi- 110002 20. Suraj Eye Institute 559, new colony Nagpur - 440 001 21. Venu Eye Institute 1/31 Institutional Aera Sheikh Sarai Phase- ll New Delhi- 110 017 22.
Choudhary Eye Care New Delhi
55

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DJO VOLUME 14 NUM 7. JAN.

Editor Dr. Rajpal Insaan

Delhi Journal of Ophthalmology

Chief Editor : Rajpal Insaan

Delhi Journal of Ophthalmology

National advisory board:

From Darkness to Light

Delhi Ophthalmological Society

DERA SACHA SAUDA

Delhi Journal of Ophthalmology

The Science of Spirituality

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Never forget that the image on the retina is inverted.

Temporal half of right retina

Lateral geniculate body

Primary visual area (= striate cortex)

Figure 1: Visual Pathway

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Figure 2: central scotoma in case of optic neuritis

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Figure 4: Junctional scotoma

Figure 3: Bitemporal hemianopia in a case of pituitary adenoma

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Figure 5: Right homonymous hemianopia in a case of left parietal lobe granuloma

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Doctor Today's Request For

MISTY EYE DROPS

0.5%w/v 0.005%w/v q.s.

Moxifloxacin Hydrochlorida equivalent to Moxifloxacin Sterile aqueous vehicle

GO-3 EYE DROPS

ZENTOB-F EYE DROPS

ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Regression of neovascularization Elsewhere(NVE)

ROLE OF AVASTIN IN MANAGEMENT OF DIABETIC RETINOPATHY

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Preoperatively in Diabetic vitrectomy

CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

PHACOEMULSIFICATION/TYPE OF IOL/PCO IN PATIENTS WITH DIABETES

CATARACT SURGERY IN PATIENTS WITH DIABETES MELLITUS

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

DIRECT EVIDENCE 1. Examination of Smear and Staining for Acid-Fast Organisms

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Exclusion of Other Uveitis Entities

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

Ocular Side Effects of Anti-Tubercular Drugs

OBESITY AND EYE DISEASES

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

OBESITY AND EYE DISEASES

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008

CURRENT TRENDS IN MANAGEMENT OF AMBLYOPIA

DJO VOLUME 14 NUM 7 . JAN.-MARCH 2008