Experts Corner. two conditions, I would perform PPD skin test and chest x-ray/ HRCT. If PPD skin test is

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1 Experts Corner S.P. Garg Uveitis is a common and confusing entity in the practice of ophthalmology. Improper diagnosis or management lead to sight threatening complications. Medications used in treating cases of uveitis may have serious systemic side effects. So it is imperative to properly analyse cases before initiating by Senior Resident Uvea and Vitreo-retina services from R.P. Centre for Ophthalmic Sciences, All India Institute for Medical Sciences, Ansari Nagar, New Delhi. MD, MNAMS, Consultant, Vitreo Retina Service, Vision Eye Center, Siri Fort Road, New Delhi MS, FMRF, FNAMS, FIC Path., FAICO, Director of Uveitis and Ocular Pathology Department, Sankara Nethralaya, 18, College Road, Nungambakkam, Chennai. Additional Professor, Advanced Eye Centre, Post Graduate Institute of Medical Education and Research, Chandigarh Consultant, Uvea Service, L.V. Prasad Eye Institute, Kallam Anji Reddy Campus, Banjara Hills, Hyderabad, Telangana. MS, FRCSEd, FRCOphth, FMRF, Uveitis and Retina Services, Shroff Eye Centre, East of Kailash, New Delhi. does not merit investigation. A case of recurrent / chronic uveitis, or granulomatous uveitis or history/examination suggestive of systemic disease should be investigated. As a routine for most cases we do a chest X-ray and mantoux test. A CT chest and serum ACE levels are done usually in cases of granulomatous uveitis or chronic anterior uveitis. If history is suggestive suggest an associated collagen vascular disease or in children where JRA is suspected. Rare cases of leprosy would require a skin consultation. Syphilis is now seen rarely but if suspected a VDRL and a TPHA test is done. order any investigations as the outcome is usually quite good. However, in cases of recurrent anterior uveitis, based on the morphologic pattern, I order investigations. In non-granulomatous anterior uveitis, I order HLA B27, ESR, and ANA. In granulomatous uveitis, I order Mantoux, QuantiFERON TB gold test, sarcoid work up (serum angiotensin converting enzyme, serum lysozyme assay, serum calcium and inorganic phosphorus), and HRCT chest. If the patient has presented with granulomatous anterior uveitis and his IOP is two conditions, I would perform PPD skin test and chest x-ray/ HRCT. If PPD skin test is Jyotirmay Biswas Vishali Gupta Somasheila Murthy Shishir Narain www. dosonline.org l 15

2 Experts Corner: Uvea positive (induration of 10mm or more after 72 hours) and lymphadenopathy, I would consider TB as diagnosis. On the other hand, if PPD skin test is negative, and chest shows hilar gland enlargement, I would think of sarcoidosis and do ACE levels as well as consult pulmonologist for trans bronchial lung biopsy or bronchoalveloar lavage for proceed with quantiferon TB Gold or PCR to establish the diagnosis of TB. In another situation of a patient presenting with granulomatous anterior uveitis with raised IOP, I would like to rule out viral etiology and would look for features PCR from the aqueous tap. On the other hand, if patient has come with an acute attack of non-granulomatous anterior uveitis, I would like to rule out sacroilitis and HLA-B27 related spondyloarthritides. The simplest test in these patients would be x-ray sacroiliac spine to look for any evidence of sacroilitis. HLA B27 if available adds to the diagnosis but is not must. In a child presenting with chronic anterior uveitis with band shaped keratopathy, I would like to do ANA to rule out juvenile idiopathic arthritis. In other less common diseases like TINU syndrome etc, the investigations shall be customized depending upon the differential diagnosis. I investigate most cases of non-granulomatous uveitis when in young male or female (uniliateral or bilateral), when recurrent and when severe. The investigations I prefer are: HLA B27 in males and RA, ANA and CRP in young female patients. In bilateral granulomatous anterior uveitis, I usually ask for CBC, ESR, X Ray chest, PPD, S. ACE and sometimes VDRL. In case of unilateral anterior uveitis, with elevated IOP, I would consider it as Viral and not investigate. I would also rule out FHC and not investigate in those cases. Approach to Anterior uveitis: Is it painful symptomatic uveitis? HLA B27 related is usually very painful with obvious photophobia. One important aspect is the absence of posterior segment involvement except CME. Will like to know the HLA status, whether negative or positive as it affects systemic screening and dosage of treatment and possibility of ankylosis in early life. Is it painless, asymptomatic uveitis? In a child this is very crucial. If it is a girl child then investigate with ANA and keep JIA in differential diagnosis. If there is mild anterior uveitis, look for intermediate uveitis as it needs more aggressive management in children compared to adults. In adults with unilateral anterior uveitis rule out fuch s uveitis (FHU). If the diagnosis is FHU do not investigate or treat the disease except when more symptomatic. If suspecting CMV anterior uveitis can do AC tap antimicrobial treatment. Aim of FFA in posterior uveitis is to identify any typical pattern of leakage which may suggest / help So where we do suspect VKH, MEWDS, APMPPE we do perform FFA. CME or a secondary choroidal neovascular membrane can now be picked up easily by OCT. So an FFA for these would only be done in case there is some doubt on OCT. I perform an FFA in all cases of posterior uveitis, except in Toxoplasmic retinochoroiditis, where I do not. Quite frequently in patients with posterior uveitis especially in patients with retinal vasculitis to look non-perfusion and any neovascularisation. I would also do it at presentation in entities like VKH, sympathetic picture is diagnostic and helps in making the diagnosis. Less frequently for some of the conditions like cystoid macular edema where I have switched over to OCTs. Also for conditions like Serpiginous choroidits, we Very rare as I mainly see more of anterior FFA is rapidly being substituted by choroidopathy For Diagnosis especially to differentiate CSR and VKH as the treatment are reverse. For Treatment to look for areas of CNP especially prophylactic laser in such situations. As mentioned above we do not do a battery of tests and depending on any systemic history or examination and the ocular examination / chronicity of the disease we and should rather be condemned. HIV / Toxoplasma / Toxocara serology where there is a clinical suspicion. Viral serology for Herpes / CMV again does not give any meaningful results. 16 l DOS Times - Vol. 20, No. 3 September, 2014

3 Uvea I do serum ELISA for Toxoplasmosis in clinically suspected Toxoplasma retinochoroiditis. I value both IgM and IgG titres. Even in undiluted serum, positivity is quite relevant in suspected cases. I also do an ELISA for HIV in suspected viral retinitis, especially CMV retinitis and acute retinal necrosis (ARN). In most of the infectious conditions serological tests are unhelpful and should not be done especially for disease like TB or viral infections. We rely on the serological tests for very few infectious diseases like syphilis and toxoplasmosis. However, analysis of local intraocular antibody production by analyzing paired serum and aqueous samples for presence of antibodies against CMV, toxoplasmosis, HSV and VZV can be useful. Serological tests may be useful in certain autoimmune conditions like Systemic lupus erythematosus, polymyositis/dermatomyositis, connective tissue disease, and polyarteritis nodosa etc. Obvious infective etiologies like toxoplasma to be ruled out. The clinical diagnosis is of paramount importance and the serological tests are performed to support or refute the diagnosis. Please interpret the tests in the light of immune status, present systemic treatment, false negative and positive indices. For example, if the IgG Toxoplasma is negative then the likelihood of the retinal lesion being due to Toxoplasma is unlikely. Vice versa does not necessarily hold true, as it is often a positive test. We do routinely investigate for tuberculosis, sarcoidosis and syphilis. For this we generally do a chest X-ray, Mantoux, serum ACE level and VDRL as baseline. If suspicion is high due to any granulomatous nature of or a child with severe vasculitis a CT chest would also be done. Other tests depend on associated ocular and systemic Yes, I recommend investigations to rule out sarcoidosis, Behçet s disease, collagen vascular diseases, and tuberculosis. Nowadays, I do HRCT chest in all cases of Eales disease. Certainly yes. I personally use the term retinal vasculitis and in my practice all the cases of the underlying aetiology. However we would do only tailored investigations. The investigations would depend characteristics, associated systemic diseases etc. e.g., in a patient with occlusive vasculitis, I would think of TB and Behcets. If the patient has active periphlebitis with areas of capillary non-perfusion, with or without neovascularization or associated choroiditis lesions, I would consider the diagnosis of TB very likely and would investigate him for that. On the other hand, if he has patches of retinitis from the capillaries and also gives history of oral/genital ulcers, I would think about Behcets disease. The further investigation will be tailored towards the shortlisted differential diagnosis. If you mean retinal vascultis, then I would try to investigate to rule out TB/Sarcoid/Syphilis/Lyme s disease if there is such a history or assume a viral etiology and may periphlebitis like Eale s disease, still prefer to do a TB work up. Yes. Retinal phlebitis may have serious consequences if it involves the posterior pole. Rule out Sarcoidosis and TB hypersensitivity status and look for systemic auto-immune vasculitis with screening using ANA titres. We do UBM in cases of chronic hypotony to distinguish between ciliary body atrophy or formation of membranes over the ciliary body. In case of the latter a vitrectomy with removal of membranes may be planned. A few cases of mild recurrent chronic uveitis due to IOL haptic contact with ciliary body have been detected on UBM. Yes. UBM can be done in cases with small pupil, where peripheral retina is not seen to rule out pars planitis, particularly in the presence of vitreous cells or in with hypotony to rule out ciliary body pathology and in caterpillar hair induced uveitis. UBM helps in looking at the pathologies in the ciliary body region that may otherwise be obscured due to the development of synichae or media opacities. It can be used to diagnose granuloma of ciliary body in conditions like TB, a foreign body, haptic of an IOL in sulcus rubbing against the ciliary body, caterpillar hair or a mass in the ciliary body region in case of Masquerade syndromes. In patients with hypotony, UBM helps in diagnosing the cause for hypotony e.g., ciliary body atrophy or presence of a cyclitic membrane over the ciliary body. This would also help us in planning the strategy as in patients with complicated cataract, hypotony and ciliary membrane in a child with JIA, we would prefer pars plana lensectomy and vitrectomy with peeling of the ciliary membrane and silicon oil tamponade if required. We will not consider doing phacoaspiration with IOL implant in such a situation. www. dosonline.org l 17

4 Experts Corner: Uvea Yes, I routinely ask for UBM in cases with cataract and chronic hypotony, in cases of post-cataract surgery uveitis to rule out UGH like syndrome and chronic pars planitis. Helps in assessing response to treatment in cases of VKH also. Yes. In a selected group of patients with persistent hypotony to look for cyclitic membranes and atrophy of ciliary processes. This is crucial in advanced cases where mercenary vitreo-retinal procedures with long term silicone oil tamponade may be considered in desperate situations. We are generally doing a vitreous biopsy where a masquerade syndrome is suspected. Most commonly here we are looking for lymphoma. So a cytology after cytospin is generally ordered. Rarely in some cases we would do a vitreous biopsy for viral markers like HSV, HZV, CMV. Routinely we donot do these tests and would rather treat empirically on basis of clinical presentation. intraocular lymphoma. I also do a vitreous tap in suspected viral retinitis, suspected tubercular uveitis, and endogenous endophthalmitis. I do a smear, culture and PCR for detection of bacteria, especially Mycobacterium, fungus and virus. My indications for the vitreous biopsy are as follows: 1. Suspicion of intraocular malignancy. 2. Atypical presentation of uveitis where other noninvasive investigations are non contributory 3. In certain cases of suspected infectious uveitis, where we would like to collect vitreous sample for treatment. Whenever we plan a vitreous biopsy, handling of the specimen is of utmost importance as otherwise the cells will degenerate by the time the specimen reaches laboratory and no positive information can be obtained. One needs a very expert cytologist who can tell the precise cell morphology as the cells are very few. In addition, we also do molecular diagnostic tests depending upon the suspected pathology and cytokines e.g., IL 6 and IL 10 in cases of suspected primary vitreoretinal lymphomas. Unilateral pan or posterior uveitis with dense lesions suggestive of abscess. Masquerade like lymphoma. Perform microbiology and histopah to rule out fungus, PCR for HSV, CMV, VZV in cases looking like viral retinitis, ARN, and histopath for lymphoma. Usually to rule out intraocular lymphoma best detected with vitreous biopsy. Needs an expert cytologist to settle the diagnostic dilemma. Keep high index of suspicion even in cases with normal MR imaging of brain in some cases. steroid/ intravitreal steroid/ intravitreal Ozurdex Our preferred treatment of intermediate uveitis and many cases of serpigenous choroiditis, idiopathic vasculitis and multifocal choroiditis with panuveitis is posterior subtenon steroid. Most cases do respond well. If properly given, as far posteriorly as possible the incidence of glaucoma is also not very high. We rarely give intravitreal tricort / Ozurdex for uveitis. I give posterior subtenon steroid injection as a as it can cause ptosis and steroid-induced glaucoma, I give it less frequently. I give intravitreal steroid in recalcitrant cystoid macular edema (CME) in intermediate uveitis. If in these cases, the CME is huge, I prefer an intravitreal implant of Ozurdex. Local corticosteroid treatment is the mainstay of therapy in patients with unilateral non-infectious variety of uveitis e.g., pars planitis with cystoid macular edema. I personally prefer intravitreal ozurdex implants in uveitic eyes as it gives a sustained release of drug over a period of time. In other autoimmune conditions associated with systemic manifestations, the patients would need systemic immunosuppressive drugs but adding intravitreal ozurdex implant rather than administering high dose of systemic corticosteroids can manage the local unilateral exacerbations in these eyes. In cases of unilateral intermediate/posterior uveitis where infection has been ruled out, and patients have CME. Or post-op patients after cataract surgery, sometime combine with cataract surgery. Intermediate uveitis with CME in cases who are not steroid responders. Intravitreal ozurdex can also be used for recalcitrant treatment of peri-operative CME. For unilateral CME our preferred treatment is posterior subtenon tricort. Risk of glaucoma is explained to the patient. Even for bilateral cases we would initially start 18 l DOS Times - Vol. 20, No. 3 September, 2014

5 Uvea the patient on oral steroids and give a subtenon tricort in one eye if there are no additional risk factors of glaucoma. can be given in both eyes in case of a relapse. In case risk of glaucoma is perceived to be high or the patient is not willing to take the risk of glaucoma, oral steroids and in recurrent cases steroids with immunosuppressants are used. In case of unilateral CME, I give posterior intravitreal Ozurdex injection. In bilateral CME, I give immunosuppressive agents like Mycophenolate mofetil with low dose oral steroids. I add Nepafenac eyedrops three times daily in both eyes. Firstly I would investigate the patients with would have an underlying disease like TB, syphilis etc. etiology, this becomes pars planitis. The main cause of vision decrease in these patients is cystoid macular edema. element as the presence of vitreomacular traction would be an indication for pars plana vitrectomy. For unilateral edema, I prefer intravitreal ozurdex implant whereas for bilateral condition it can be systemic therapy with corticosteroids/ immmunosppressives with addition of local therapy to the worse eye if needed. The presence of concomitant pathologies like vitritis, choroiditis etc would Uniliateral; generally regional steroids, Ozurdex if affording, bilateral: oral steroids and other immunumodulators. For u/l cases sub-tenon steroids are the preferred choice of treatment. In bilateral IU with b/l CME, I prefer to investigate thoroughly for a systemic cause and prefer systemic oral steroids, and may need a steroid sparing immunosuppressive if the disease requires long term systemic treatment. Our preferred management is with sulfamethoxazole and trimethoprim followed by oral steroids. In cases which relapse frequently, therapy with a combination of Clindamycin and Azithromycin can also be tried. We do not have much experience with Intravitreal Clindamycin. I always give anti-toxoplasma treatment whatever the location of the lesion (ie) posterior pole or periphery. My preferred drug of choice is Clindamycin 300 mg 1 tablet 4 times daily for 6 weeks. I add tablet Prednisolone 1 mg/kg body weight after 48 hours of starting Clindamycin. I combine tablet Azithromycin 250mg 2 tablets stat and 1 tablet daily for 6 weeks. The diagnosis of Toxoplasmosis is based on the typical appearance of focal necrotizing retinitis and I generally do not wait for the serology results or obtain initiating treatment. I use a convenient combination of a dihydrofolate reductase inhibitor and sulfonamide that is trimethoprim/sulfamethoxazole (Bactrim, Septran) in the dose of double strength tablet (Trimethoprim 160mg; sulphamethaxazole 800 mg) per oral twice daily. Another convenient alternative drug is Clindamycin in the dose of 300 mg four times a day. The corticosteroids in the dose of mg per day are started 24 hours after initiating the antibiotic therapy. With regard to duration of therapy, I would continue corticosteroids until lesion borders begin to become more sharply demarcated and distinct that generally occurs by 4 to 6 weeks, at which time I will rapidly taper and discontinue corticosteroids and then stop antimicrobials completely after corticosteroids have been stopped. Antibiotics should not be tapered. Recently we have started treating our patients with local intravitreal injections of clindamycin (1.5 mg/0.1 ml) and dexamethasone (400 microg/0.1 ml) weekly for 4 weeks and are getting very encouraging results. This strategy can be used even in patients where systemic therapy may be contraindicated as in pregnancy or not tolerated. Usually with Bactrim DS or Clindamycin. Any lesion at or threatening the macula needs immediate anti-toxo agent, usually clindamycin and start with oral steroids within hrs after initiating co-trimoxazole and some cases may require prolonged treatment to prevent recurrences. Pyrimethamine along with sulphamethoxazole (Daraprim) can cause decreased platelet count and is now less commonly available at drug counters. Concomitant Folic acid treatment prevents bone marrow suppression. Recent reports show an increasing trend for using intravitreal clindamycin (with dexamethasone), is seen more commonly in recent practice with good results. Average case needs two to three injections per eye to bring about control of Retinochoroiditis. We would give ATT if there is evidence of systemic tuberculosis like a positive chest X-ray / CT chest or proven active extrapulmonary tuberculosis of any other organ. Only on the basis of a positive mantoux or Quantiferon gold test we will not start ATT. www. dosonline.org l 19

6 Experts Corner: Uvea I give ATT in multifocal serpiginoid choroiditis when Mantoux or QuantiFERON TB gold tests are positive and/or HRCT chest shows lesions suggestive of TB. In our clinic, all the patients of Serpiginouslike choroiditis are investigated for TB. The initial tests include Mantoux skin test and x-ray/cect of the chest and if Mantoux shows an induration of more than 10mm after hilar lymph nodes / Ghons focus, the patient receives ATT. In situations where these tests are equivocal, and the clinical indicators point towards the diagnosis of possible tubercular etiology, I would do quantiferon TB gold and if that too is negative, PCR from the vitreous humor for detection of Mycobacterial DNA. It is important to remember that the disease represents hypersentivity reaction to Mycobacterium tuberculosis and would need concomitant systemic steroids in the dose of 1-1.5mg/kg/day till the lesions are healed (4-6 weeks) following which steroids can be tapered and ATT continued. Failure to give systemic steroids may result in continued progression and paradoxical worsening of the lesions. If Mantoux positive, almost always. Generally start with high dose oral steroids (and IVMP if macula is involved). If investigation results suggest TB hypersensitivity add ATT after a week or so). Sometimes there may be a paradoxical reaction, which is largely initiation of ATT. We generally admit the patient and start IV Acylovir for about a week and then switch to oral acyclovir for 6-8 wks. After 48 hours of IV acyclovir oral steroids are also added. Despite aggressive therapy some patient s would develop retinal detachment and would require vitreo-retinal surgery with silicon oil injection. Role of prophylactic laser posterior to areas of necrotic retina to prevent retinal detachment is controversial We donot do prophylactic laser at margins of necrotic retina unless a distinct break is visible. I always give I.V Acyclovir 500 mg every 8th hourly for 7 days, followed by oral Acyclovir 800 mg 5 times daily or Valacyclovir 1 g 3 times daily for 12 weeks. I add tablet Prednisolone 1 mg/kg body weight after 48 hours. Yes, there is a role for prophylactic laser. I do it posterior to the lesion to create a new ora serrata once the lesion has healed completely to prevent retinal detachment, although its role is doubtful. We still treat our patients of ARN in a conservative manner where the patient is hospitalized and receives induction dose of intravenous acyclovis typically in the doses of 10-15mg per kg every 8 hours for one week for three to four months. Recently, we have also started treating some of patients on oral valacyclovir at 2 g TID that can achieve systemic levels similar to intravenous acyclovir but is more expensive than former. In addition, patients with severe disease may receive intravitreal injections of foscarnet (2.4 mg /0.1 ml) or ganciclovir in the dose of 2 mg/0.1 ml per injection given two or three times weekly. Prednisolone in the dose of 1-1.5mg/kg/day is started hours after the initiation of anti-viral therapy and aspirin added to minimize vascular thrombosis. The use of laser photocoagulation in patients with ARN is controversial, and the level of evidence supporting its use is generally weak. Currently, I am not doing any prophylactic laser in these patients. Usually with oral valacyclovir at therapeutic dose for 4 to 6 weeks, at the early breaks. Again the same scenario to other infectious empirical antimicrobial treatment with a strong clinical systemic tests. We start with IV aciclovir 500mg/m2 TDS and add systemic steroids after 24-48hrs later to prevent necrosis of retina. In patients not willing for IV treatment, alernatively Valaciclovir 1000mg tds is a good option. We with clear media, we do barrage laser to ward off the necrotic retina and prevent posterior RD from developing following large breaks, Usually RD occurs typically following acute These require extensive vitreoretinal surgery with long term silicone oil tamponade to prevent recurrence of RD. Primary immunosuppressive therapy is mostly considered in cases of VKH, Sympathetic Ophthalmia, Behcet s disease with panuveitis and necrotising scleritis. Secondary immunotherapy for steroid dependent or frequently relapsing chronic intermediate uveitis and similar steroid dependent or frequently relapsing chronic serpigeneous choroiditis or multifocal choroiditis with panuveitis. I give immunosuppressive therapy for Behçet s disease, sympathetic ophthalmia, Vogt- Koyanagi-Harada disease (once the acute phase is over), 20 l DOS Times - Vol. 20, No. 3 September, 2014

7 Uvea recalcitrant intermediate uveitis and JIA associated uveitis (methotrexate). I give immunosuppressive therapy in steroidresistant non-infectious uveitis like intermediate uveitis (mycophenolate mofetil). Most of my patients with chronic, recurrent noninfectious variety who need a maintaince dose of more than control would need immunosuppressive therapy. in patients with Behcets disease provided his PPD skin test is not positive and patient can afford it. Steroids in most cases of non-infectious bilateral panuveitis, intermediate uveitis, retinal vasculitisetc,and other immunosuppressive agents in most of these cases, which I would start either right away (for example in VKH or in Pars planitis) or after one month. Also prefer some immunosuppressant treatment if VKH or sympathetic ophthalmia is the clinical diagnosis. Another area of primary immunosuppressive agents is ANCA positive necrotizing scleritis. In children JIA associated uveitis requires primary immunosuppressive therapy. Secondary immunosuppressive treatment is used as steroid-sparing low dose maintenance in chronic diseases. We generally use Methotrexate or Azathioprine. I choose the agent according to the disease. I use Cyclosporine in Behçet s disease, mycophenolate mofetil in intermediate uveitis, azathioprine in non-tubercular serpiginous choroiditis, methotrexate in JIA associated uveitis, cyclophosphamide in Wegener s granulomatosis. We prefer oral azathioprine a lot as it seems to work very well in our population and is well tolerated. Also it is easy to monitor during the follow up. If patient is not responding to azathioprine, we do add/switch to methotraete that is also preferred drug in children and can be given by subcutaneous weekly injections. One needs to remember that most of these drugs extinguisher. Also it is important to remember that unlike corticosteroids, immunosuppressive drugs are started in lower dose and then the dose is gradually increased. It is very important to administer these drugs under the supervision of an internist who can monitor the toxic effects of these drugs. Azathioprine, methotrexate, Mycophemolate, cyclosporine and Cyclophosphmide, based on indication and affordability. Any agent which you are most familiar with and take shared responsibility to monitor and manage. Usually antimetabolites either Azathiprin or methotrexate or mycophenolate mofetil are easier to monitor. Cyclophosphamide is helpful in scleritis and needs rheumatology / internist supervision, Likewise Cyclosporin needs blood pressure and creatinine level monitoring and physician assistance. Before initiating immunosuppressive treatment we take an informed consent from every patient requiring these agents. Cases of secondary uveitis like those due to nucleus drop or intravitreal cysticercosis. Cases of intermediate uveitis where too high a dose of steroids and or immunosuppressives are required. Some cases of pars membranes. Cases of hypotony due to cyclitic membrane I advise vitrectomy in uveitis in recalcitrant intermediate uveitis and panuveitis. I would consider therapeutic vitrectomy in patients with suspected endogenous endophthalmitis, primary vitreoretinal lymphomas, vitreomacular traction, vitreous haemorrhage and tractional retinal detachment. Non-responsive dense vitirits as therapy, also where biopsy is needed, in JIA, comnine with PPL. Diagnostic vitrectomy as a procedure for obtaining vitreous specimen in infectious situations or suspected masquerade syndromes. Therapeutic vitrectomy in possible infective pathology including post-operative situations like P Acnes related chronic uveitis also requiring IOL explanation. In severe vitritis, vitrectomy alongside clearing the media also helps in removing the sequestered antigen and sometimes bring about remission in uveitis. In severe hyportony related uveitis vitrectomy with long term silicone oil tamponade is helpful. Most cases of CMV retinitis that we see today are already on HAART therapy. If not they are started on HAART therapy. In all cases intravenous ganciclovir therapy is given for 1 wk as induction therapy followed by oral valgancylovir. Duration of therapy depends on level of immune recovery and the clinical picture. For zone 1 unilateral cases intravitreal ganciclovir twice a week for 2-4 www. dosonline.org l 21

8 Experts Corner: Uvea wks followed by once a week intravitreal injections and simultaneous oral valgancyclovir therapy is given. These patients also can develop retinal detachment due to breaks at the edges of necrotic retina. This would require a vitreoretinal surgery with silicon oil injection. I give I.V Ganciclovir 5 mg/kg body weight every 12th hourly for days. If the patient is unable to afford, I give intravitreal ganciclovir. If the patient can afford, I give tablet valganciclovir 900 mg BD orally. HAART is the most important weapon in treating CMV retinitis. Sustained immune reconstitution (maintaining CD4 cells above 100/ mm³) generally allows discontinuation of anti-cmv treatment that otherwise must immune status, location and severity of the retinitis, concomitant medications and compliance with therapy. Therapy is induced at high doses for two to three weeks or until the retinitis stabilizes. The induction therapy includes intravenous ganciclovir 5mg/kg twice daily for 2 weeks with a maintaince dose of 5mg/kg/day. Alternately, Oral ganciclovir 1gm three times a day can be used for maintaince. Other alternatives include using intravenous foscarnet in the dose of 60mg/kg every night for 14 days with a maintaince dose of 90mg/kg/day. This is combined with local intravitreal injections of ganciclovir 2mg twice weekly for 3 weeks with maintaince of 2mg every week or intravitreal foscarnet 2.4 mg twice weekly for 3 weeks and maintaince of 2.4mg/weekly. Drug resistance may develop in 25-35% of cases and would need detection in case of replapses seen after long term therapy. Intravitreal gancyclovir at repeated intervals (two per week). My retinal colleagues manage. Frank CMV retinitis requires intravitreal ganciclovir injections with good response. If the disease is secondary to systemic immunosuppression (HIV related or drug related) then systemic intravenous ganciclovir and recently available oral val-ganciclovir can be added to the regimen. Peripheral suspected small CMV retinitis patches may be observed and all forms of systemic or periocular steroids avoided. If you want to sell your used Ophthalmic Equipments at Good Price OR If you are Interested to Purchase Second hand Ophthalmic Equipments at Reasonable Prices in Good Condition Please Contact: Manoj Pandey B-503, Plot No. 23, Sector-6, Dwarka, NEW DELHI-75 Ph.: , pandeymanoj67@yahoo.co.in 22 l DOS Times - Vol. 20, No. 3 September, 2014