Clinical Dry Eye After LASIK Dr. Sivakami, MS Resident, Aravind Eye Hospital, Madurai LASIK has now become the standard of care in cornea - based refractive surgery. An increasing number of patients are undergoing this procedure. This has led to an increasing interest in our attempts to understand the post LASIK changes in the ocular surface health. There has been much interest in dry eye symptoms affecting patients who have undergone LASIK. Dry eye is considered as the most common complication of LASIK. Ocular surface and tear film before LASIK Complications during LASIK and even after LASIK can be influenced by the state of the ocular surface and tear film before surgery. Implications of pre-existing dry eye symptoms and ocular surface and tear film disorders on LASIK outcomes Dry eye and associated contact lens intolerance motivate individuals to consider refractive surgery. Pre-existing ocular surface and tear film disorders can have a negative impact on the outcome of keratorefractive surgery in a number of ways. Dry eye symptoms and signs before LASIK are a significant risk factor for experiencing dry eye after LASIK. Poor tear secretion before surgery (Schirmer test value less than 10mm) is a significant risk factor for experiencing dry eye symptoms after surgery. In addition, patients diagnosed with dry eye before surgery have, prolonged recovery of corneal sensation, and more severe and sustained dry eye symptoms after surgery compared to those without dry eye before LASIK. Ocular surface and tear film disorders before surgery may adversely affect LASIK refractive outcome. Disorders of the ocular surface and tear film before LASIK have been implicated in increasing the risk of complications during and after LASIK, including epithelial defects and epithelial in growth, flap folds, wrinkles and displacement, diffuse lamellar keratitis, and infectious keratitis. Factors adversely affecting the ocular surface and tear film before LASIK Contact lens wear Contact lens wear before LASIK can reduce the predictability of refractive surgical outcome by inducing corneal warpage, and altering tear proteins, ocular surface morphology, corneal physiology, barrier function, pachymetry and sensation. These factors may increase the potential for complications during and after refractive surgery. In LASIK studies, tear secretion and corneal sensitivity before and 6 months after LASIK were significantly more depressed in long-term contact lens wearers, compared to non-contact lens wearers. A history of contact lens intolerance can serve as a red flag for the potential exacerbation of dry eye problems after LASIK. Eyelid disease Anterior blepharitis and Meibomian gland dysfunction must be managed before LASIK to minimize the risk of complications after surgery. Staphylococcus aureus has been isolated in appreciable frequency from patients with anterior blepharitis and was reported to be the most prevalent causative microorganism for microbial keratitis after LASIK. Ocular allergy Ocular allergy has the potential to impact on surgical outcomes due to increased incidence of toxicity reactions to medications and their preservatives. Increased mucous in the tear film may lodge in the microkeratome gears and cause incomplete flaps.
2 AECS Illumination Also, there is potential for inflammation after surgery due to increased levels of cytokines and chemical mediators released from the inflamed conjunctival and subconjunctival tissues. Herpetic keratitis Patients with a history of actual or suspected herpetic keratitis are advised not to have elective refractive surgery. Epithelial basement membrane dystrophy Patients with epithelial basement membrane disorders before surgery have an increased risk of incurring epithelial defects during and after LASIK. LASIK should not be performed in eyes with this condition due to the increased risk of epithelial in growth and loss of best spectacle - corrected visual acuity. Lid-related anomalies Several disorders of lid aperture, lid/globe congruity, and blinking can pose a problem for the LASIK surgeon and must be recognized and managed before LASIK can be considered. Conjunctivochalasis, large fleshy pterygia, exophthalmos, lagophthalmos, and incomplete blinking should be managed prior to LASIK. Age, gender and medical conditions Old age is one of the risk factors for epithelial defects during surgery. This has been attributed to both decreased epithelial adhesion and increased friction from drier eyes in the older patients. In terms of gender, there is some evidence to suggest that females may have inferior outcomes after LASIK compared to males. Although further research is required, clinical experience suggests that the hormonal changes (particularly the reduction in androgen levels) experienced by older females contribute to the dry eye symptoms, abnormal healing, and less than optimal LASIK results observed in this demographic group. In terms of medical conditions, patients with Diabetes require particular attention. Diabetes has been associated with reductions in tear quality, tear volume, ocular surface epithelial health, goblet cell density, and corneal sensation. Ocular surface and tear film during LASIK Use of topical anaesthetics Excessive and / or repeated dosing of anaesthetic can be toxic to the corneal epithelium and stromal keratocytes. Overuse of topical anaesthetic can result in epithelial toxicity, epithelial defects, diffuse lamellar keratitis, and epithelial in growth. Topical anaesthetic should be used just before surgery to minimize epithelial damage during surgery. Flap reference marking Gentian violet dye used for flap reference marking is toxic to the corneal epithelium and stroma and it has been implicated in causing diffuse lamellar keratitis. Signs of LASIK-induced dry eye Myopic LASIK can cause punctate epitheliopathy, elevated tear osmolarity, decrease in tear secretion, tear volume, tear clearance, tear film stability, goblet cell density, and blink rate. Mechanisms of LASIK-induced dry eye Surgical trauma to the ocular surface All ocular surgical procedures disrupt the ocular surface and tear film. Trauma to the ocular surface that occurs during LASIK has been proposed as a cause of tear film instability, punctate epitheliopathy, and recurrent corneal erosions after LASIK. Trauma from the suction ring could be a contributing factor to the loss of perilimbal conjunctival goblet cells after LASIK. The shearing forces of the traversing microkeratome and excessive drying and wiping of the ocular surface during surgery could damage the microvilli of the superficial epithelium. Ocular surface sensory denervation LASIK disrupts the normal organization of corneal innervation and induces a corneal anaesthesia or hypoaesthesia, lasting up to 6 months. However, in patients with dry eye before LASIK, patients who have worn contact lenses long-term before surgery, or patients who have superior hinged flaps or deeper
Vol. XII, No.2, April - June 2012 3 ablations, the return of corneal sensation to levels observed before surgery appears to take longer than 6 months and is associated with more persistent dry eye signs and symptoms. Another study reports that corneal sensation after LASIK recovers within 6 months and that nasally hinged flaps were associated with a significantly greater decrease in corneal sensation than superior hinged flaps. Investigative studies have suggested that this loss of sensory denervation is one of the leading causes of tear film anomalies and punctate epitheliopathy after LASIK. Reduced corneal and conjunctival sensitivity results in reduced tear secretion, tear clearance, goblet cell density, and blink frequency, as well as increased tear osmolarity and ocular surface staining. All of these anomalies are features of the eye after LASIK and support neurotrophic mechanisms as a main cause for dry eye after LASIK. As sensory denervation can mask symptoms of ocular surface irritation, patients who have LASIKinduced tear film and ocular surface problems may only become aware of symptoms as the damaged nerves regenerate. This temporal feature of sensory denervation makes it difficult to correlate symptoms and signs after LASIK. Inflammation The inflammatory changes observed after LASIK may contribute to chronic dry eye symptoms and signs after LASIK. Reduction in tear secretion and tear clearance in eyes after LASIK have been proposed to cause an increase in the concentration of pro-inflammatory cytokines and matrix degrading enzymes in the tear film. This could stimulate up regulation of other inflammatory mediators, leading to further inflammation and damage to the ocular surface. Increased cytokine levels in the tear film may exacerbate the LASIK induced corneal nerve damage, thus further decreasing corneal sensation and further impairing lacrimal gland function. These theories are yet to be verified in experimental studies. Alterations to surface topography and corneal curvature A number of studies have linked changes in corneal profile after LASIK to symptoms and signs of dry eye. Irregularities within the interface, together with the gutter of the flap and the irregular shape of the cornea after LASIK, have the potential to alter the normal relationship between the lids and the corneal surface and hence, change the spreading of the tear film across the ocular surface. A reduction in the spread of tears during blinking could create areas of non wetting or stagnation of tears. This could result in increased tear evaporation and areas of ocular surface desiccation. Type of correction, characteristics of the flap and ablation profile Evidence suggests that tear film and ocular surface problems and dry eye symptoms after LASIK may be affected by the type of correction performed, the characteristics of the flap, and the ablation profile. LASIK for hyperopia appears to induce more severe and more sustained dry eye symptoms and greater adverse effects on the ocular surface and tear film, compared to LASIK for myopia. This may reflect greater corneal sensory denervation effects with hyperopic LASIK due to the larger flap and midperipheral ablation. Also, an increased number of older patients, who are more likely to experience dry eye, have hyperopic LASIK. Management of the ocular surface and tear film after LASIK Artificial tears are a critical component of the ocular surface and tear film management strategy after LASIK. Carboxymethyl cellulose-based, hydroxypropyl methylcellulose-based, and sodium hyaluronate-based artificial tears have been recommended to protect and regenerate the ocular surface and tear film.
Vol. XII, No.2, April - June 2012 4 Reference 1. Golas L, Manche EE. Dry eye after laser in situ keratomileusis with femtosecond laser and mechanical keratome. J Cataract Refract Surg. 2011 Aug;37(8):1476 80. 2. Shoja MR, Besharati MR. Dry eye after LASIK for myopia: Incidence and risk factors. Eur J Ophthalmol. 2007 Feb;17(1):1 6. 3. Salomão MQ, Ambrósio R Jr, Wilson SE. Dry eye associated with laser in situ keratomileusis: Mechanical microkeratome versus femtosecond laser. J Cataract Refract Surg. 2009 Oct;35(10):1756 60. 4. Mian SI, Li AY, Dutta S, Musch DC, Shtein RM. Dry eyes and corneal sensation after laser in situ keratomileusis with femtosecond laser flap creation Effect of hinge position, hinge angle, and flap thickness. J Cataract Refract Surg. 2009 Dec;35(12):2092 8. 5. Toda I. LASIK and dry eye. Compr Ophthalmol Update. 2007 Apr;8(2):79 85; discussion 87 89. 6. Ambrósio R Jr, Tervo T, Wilson SE. LASIK-associated dry eye and neurotrophic epitheliopathy: pathophysiology and strategies for prevention and treatment. J Refract Surg. 2008 Apr;24(4): 396-407. 7. Shtein RM. Post-LASIK dry eye. Expert review of ophthalmology. 2011 Oct;6(5):575 82. 8. Nettune GR, Pflugfelder SC. Post-LASIK tear dysfunction and dysesthesia. Ocul Surf. 2010 Jul;8(3):135-45. 9. Toda I, Yoshida A, Sakai C, Hori-Komai Y, Tsubota K. Visual performance after reduced blinking in eyes with soft contact lenses or after LASIK. J Refract Surg. 2009 Jan;25(1):69-73.
Clinical Pneumatic Retinopexy Dr.R.Ramakrishnan,Chief Medical Officer, Aravind Eye Hospital, Tirunelveli Definition Pneumatic retinopexy consists of an intravitreal gas injection with retinochroidal adhesive procedure (e.g. transconjunctival cryopexy) and appropriate head positioning. Indications 1. Isolated break of less than one clock hour in the superior 8 clock hours of retina 2. Multiple breaks within one clock hour of retina in the superior 9 clock hours 3. Mascular breaks and other posterior retinal breaks 4. Redetachment after scleral buckling due to superior open break 5. Fish mouthing after RD surgery. Contraindications 1. Multiple breaks extending over more than one clock hour of retina 2. Single break larger than one clock hour 3. Breaks in the inferior 4 clock hour of retina 4. Presence of PVR of grade C or more 5. Mental retardation 6. Physical disability precluding maintenance of the required positioning 7. Uncontrolled glaucoma 8. Difficulty in assessment of retina due to media haze. Important notes 1. The selected gas is drawn through a Milipore filter (0.22µm). 2. A few ml.of gas drawn into the syringe is discarded and the syringe is refilled. 3. A disposable 30 gauge, ½ inch needle should be used for gas injection. 4. Gas should be injected moderately briskly, not too briskly nor too slowly. 5. Air travel is contraindicated for longer period of time with C3F8 due to risk of increased IOP during the ascent of the airplane. 6. Proper positioning after gas injection is a must 7. IOP should be checked of the selected gas and thereafter 8. Paracentasis may be done if required to lower the IOP 9. I/O should be done after gas injection to evaluate central retinal artery Possible complications 1. New or missed breaks 2. PVR 3. Redetachment 4. Persistent SRF 5. Macular pucker formation 6. ERM formation 7. Incarceration of Vitreous 8. Vitreous haze 9. Reopening of original break 10. Subconjunctival / subretinal gas 11. Increase IOP / Glaucoma 12. Lens Opacities 13. Dislocation of IOL 14. Bulbous Keratopathy 15. Subretinal pigment migration 16. Uveitis Geometry of intraocular gas bubble Arc of bubble contact (Degrees) Vitreous Diameter 21 mm 24 mm 90 0.28 ml 0.42 ml 120 0.75 ml 1.13 ml 150 1.49 ml 2.24 ml 180 2.40 ml 3.62 ml
6 AECS Illumination Different types of gases used for PR Gas Dose (%) Max.rate of expansion Max expansion Average time Average time of expansion Longevity Total Duration Air 0.8ml. No expansion No expansion No expansion 5-7 days SF6 0.5ml. 6 hours 24-48 hours 1.9-2 times 10-14 days C3F8 0.3ml. 6-8 hours 72-96 hours 4 times 55-65 days C2F6 0.3ml 6-8 hours 72-96 hours 3.3 times 30-35 days Reference 1. Hutter J, Luu H, Schroeder L. A biological model of tamponade gases following pneumatic retinopexy. Curr. Eye Res. 2002 Oct;25(4):197 206. 2. Friberg TR. Inverted pneumatic retinopexy. Ophthalmology. 2003 Nov;110(11):2261; author reply 2261 2262. 3. Schechter RJ. Inverted pneumatic retinopexy. Ophthalmology. 2003 Nov;110(11):2260 2261; author reply 2261. 4. Chang TS, Pelzek CD, Nguyen RL, Purohit SS, Scott GR, Hay D. Inverted pneumatic retinopexy: a method of treating retinal detachments associated with inferior retinal breaks. Ophthalmology. 2003 Mar;110(3):589 94. 5. Greenberg PB, Baumal CR. Laser therapy for rhegmatogenous retinal detachment. Curr Opin Ophthalmol. 2001 Jun;12(3):171 4. 6. Georgalas I, Papaconstantinou D, Karagiannis D, Ladas I. Pneumatic displacement of acute submacular hemorrhage with and without the use of tpa. Eur J Ophthalmol. 2011 Apr;21(2):220; author reply 221. 7. Coe RP, Eller AW, Friberg TR. Pneumatic retinopexy. Arch. Ophthalmol. 2011 Aug;129(8):1110 1111; author reply 1111. 8. McGimpsey SJ, Cooke CA, Best RM. Pneumatic retinopexy. Ophthalmology. 2007 Feb;114(2):401 2. 9. Mansour AM. Pneumatic retinopexy for inferior retinal breaks. Ophthalmology. 2005 Oct;112(10):1771 6. 10. Yeung L, Kokame GT, Brod RD, Lightman DA, Lai JC. Pneumatic retinopexy for retinal detachment associated with severe choroidal detachment. Retina (Philadelphia, Pa.). 2011 Jan;31(1):87 92. 11. Chan CK, Lin SG, Nuthi ASD, Salib DM. Pneumatic retinopexy for the repair of retinal detachments: a comprehensive review (1986-2007). Surv Ophthalmol. 2008 Oct;53(5):443 78. 12. Ross WH, Lavina A. Pneumatic retinopexy, scleral buckling, and vitrectomy surgery in the management of pseudophakic retinal detachments. Can. J. Ophthalmol. 2008 Feb;43(1):65 72. 13. Kleinmann G, Rechtman E, Pollack A, Schechtman E, Bukelman A. Pneumatic retinopexy: results in eyes with classic vs relative indications. Arch. Ophthalmol. 2002 Nov;120(11):1455 9. 14. Zaidi AA, Alvarado R, Irvine A. Pneumatic retinopexy: success rate and complications. Br J Ophthalmol. 2006 Apr;90(4):427 8. 15. Schaal S, Sherman MP, Barr CC, Kaplan HJ. Primary retinal detachment repair: comparison of 1-year outcomes of four surgical techniques. Retina (Philadelphia, Pa.). 2011 Sep;31(8):1500 4. 16. Sharma T, Gopal L. Recent developments in vitreoretinal surgery. J Indian Med Assoc. 2000 Dec;98(12):754 8, 760 2.
Clinical Retinal Vasculitis Approach to Diagnosis and Management Retinal vasculitis is a sight threatening inflammatory eye disease which involves the retinal blood vessels, predominantly retinal veins. Clinically, it presents as fluffy white perivascular infiltrates in the retina with aqueous and vitreous inflammatory cells. Fluorescein angiogram shows staining and diffuse leakage from the retinal blood vessels with or without cystoid macular odema. The etiology of the disease is varied. It may occur as an isolated ocular condition, as a manifestation of infectious, or neoplastic disorders or in association with systemic inflammatory diseases. Hence, it is essential that a complete history, ocular and systemic examination and a detailed laboratory work up is done in all patients with retinal vasculitis. Classification The causes of Retinal vasculities can be classified as follows 1. Systemic diseases 2. Infectious diseases 3. Ocular diseases 4. Malignancies 5. Drug Induced Systemic diseases Sarcoidosis, Behcet s disease, Multiple sclerosis, Systemic lupus erythematosus, Wegeners granulomatosis, Polyarteritis nodosa, Relapsing polychondroitis, Seronegative arthropathies, Polymyositis, Dermatomyositis, Antiphospholipid antibody syndrome, Takayasu arteritis Crohn s disease. Infectious disease Tuberculosis, Toxoplasmosis, Syphilis, Herpes, Cytomegalovirus, Leptospirosis, Cat scratch disease, Candidiasis, Rickettsia, Amoebiasis, Brucellosis. Ocular disease Idiopathic, Intermediate uveitis, Eales disease, Birdshot retinochoroidopathy, Frosted branch angitis, Serpiginous choroiditis, Idiopathic retinal Vasculitis, aneurysms and neuroretinitis. Masquerades Leukemia, Lymphoma, Retinoblastoma Drug induced Immunoglobulins, Ripabutin methamphetamines Systemic disease associated with retinal vasculitis Behcet s disease It is a multisystem inflammatory disease which is diagnosed by the clinical triad of recurrent orogenital ulcers, skin lesions and uveitis. Erythema nodosum arthralgia and meningoencephalitis are also commonly seen. Ocular involvement is seen in 70% of patients. It usually presents as recurrent vasoocclusive retinopathy which affects both arterioles and veins in the posterior pole. Fundus examination shows retinal hemorrhages, Yellow, White retinal infiltrates, retinal odema and optic disc odema with hyperemic in the acute stage. Chronic stage of the disease shows macular ischemia neovascularization of retina and disc sheathed vessels and optic atrophy. Sarcoidosis This disease typically affects young adults and presents with bilateral hilar lymphadenopathy and ocular and skin lesions. Retinal vasculitis is a characteristic feature and mainly involves retinal veins. These venules are usually mid peripheral or peripheral in location and show short segments
8 AECS Illumination of perivascular cuffing associated with retinal infiltrates, Sarcoid nodules and snow ball vitreous opacities. Yellow perivenous exudates, classically described candle wax drippings (taches de bougie) may also be seen. Wegeners granulomatosis It is a granulomatous necrotizing vasculitic condition that primarily affects upper and lower respiratory tracts and kidneys. In addition to retinal vasculitis, other clinical findings include necrotizing scleritis, peripheral ulcerative keratitis, dacryocystitis and proptosis. Systemic lupus erythematosus Patients present with malaise, fatigue, anorexia and low grade fever. They may also have arthritis, Facial rash, alopecia and pleurisy. Fundus examination shows multiple cotton wool spots; dilated, tortuous arterioles and intraretinal haemorrhages. Retinal vasculitis is usually uncommon but very devastating. It causes severe vaso-occlusive diseases leading to retinal ischemia and proliferative retinopathy. Infectious diseases associated with retinal vasculitis Tuberculosis Though choroiditis is the most common ocular feature of tuberculosis, periphlebitis is also commonly present. It occurs either by direct infection or by hypersensitivity reaction to Mycobacterial antigens. It is associated with vitritis and retinal hemorrhages and may lead to branch or central retinal vein occlusion leading to neovascularization and vitreous hemorrhage. Toxoplasmosis Toxoplasmic retinochoroiditis is commonly associated with retinal periphlebitis. Retinal veins show continuous sheathing with narrowing near acute lesions. Perivasculitis is believed to be caused by an Arthus-type reaction. Locally produced antigens diffuse into the vessel walls and react with circulating antibodies, activate complement and recruit inflammatory cells that form a perivascular cuff. Focal periarterial exudates or plaques, called kyrieleis arterialitis are also seen near the active focus and these lesions do not cause vascular obstruction or leakage. Syphilis Syphilis can have protean ocular manifestations. Retinal vasculitis is rare and has been described in secondary and tertiary syphilis causing venous or arterial occlusion. Other clinical findings can be vitritis, chorioretinitis, neuro retinitis, optic neuritis, subretinal neovascularization and exudative retinal detachment. Herpes virus Retinal infections with herpes group of viruses cause necrotizing retinits, vasculitis, and retinal hemorrhages. Acute retinal necrosis caused by herpes simplex and varicella zoster viruses is a fulminant peripheral necrotizing retinitis with severe vitritis and occlusive vasculitis affecting arterioles in the retina and choroids. Cytomegalovirus in immunocompromised patients causes fluffy white necrotic lesions along the vascular arcades of the posterior pole with retinal hemorrhages and vasculitis. The vasculitis is caused by perivascular neutrophilic infiltration of both arteries and veins. Ocular diseases associated with retinal vasculitis Intermediate Uveitis is characterized by vitritis, snowball exudates, peripheral retinal periphlebitis and pars plana exudates. Eales disease is an idiopathic obliterative periphlebitis which commonly occurs in healthy young males between 15-40 years of age. It starts anterior to the equator and progresses posteriorly and ultimately involves multiple quadrants of the retina. This inflammation induced vascular occlusion leads to proliferative vascular retinopathy with sequelae as recurrent vitreous hemorrhage and tractional retinal detachment. The etiology of this disease is still unknown however it is believed to be due to hypersensitivity to tuberculoprotein.
Vol. XII, No.2, April - June 2012 9 Birdshot Retinochoroidopathy is a bilateral panuveitis where fundus examination shows cream colored, deep, round lesions, retinal vasculitis and cystoid macular odema. Frosted branch angiitis is a rare vasculitis where thick inflammatory infiltrates surround the retinal arterioles and venules creating an appearance of frosted tree branches. The sheathing of the blood vessels is so extensive that the underlying vessels are obscured. Mostly it is idiopathic, but cases have been reported in herpes, rubella, cytomegalovirus infections and malignancies. Pathogenesis Retinal vasculitis is presumed to be an immunologically medicated condition. It is an autoimmune phenomenon and various studies have shown the presence of CD4+ve T cells within and surrounding the retinal vessels in patients with retinal vasculitis. Thus, cell medicated immunity plays a major role in the pathogenesis, however humoral immunity and immune complex formation can also be involved. Symptoms Patients usually complain of gradual painless loss of vision except where vasculitis involved the macular and there is sudden loss of vision. Presence of floaters is due to inflammatory exudates in the vitreous cavity. Scotomas, photopsias, Color vision alterations metamorphopsia may also be profound. Slit lamp examination may show-aqueous or vitreous vells, aqueous flare, keratic precipitates, posterior synechiae and posterior subcapsular cataract. Fundus examination reveals fluffy white exudates around retinal vessels in the form of either continuous skip lesions. Vascular sheathing, retinal hemorrhage retinal odema and anterior - venous anastomoses are seen in cases where venules are the site of inflammation. Cotton - wool spots which represent nerve fibre layer infarcts are mainly seen in systemic vasculitic diseases. Intra-retinal infiltrates are characteristic of infectious causes of retinal vasculitis except for Behcet s disease. Vitreous snow ball exudates and cystoid macular odema are seen in intermediate uveitis, sarcoidosis and tuberculosis. Chronic stage of the disease shows vascular occlusion, neovascularization of the disc or retina, vitreous hemorrhage, branch retinal vein occlusion, sclerosed vessels and optic atrophy. Involvement of retinal venules is more common in conditions like Behcet s disease, tuberculosis, sarcoidosis, Eales disease, multiple sclerosis, inflammatory bowel disease and sero negative arthropathies. Retinal arterioles are involved in systemic vasculitis and viral retinitis. Retinal capillary involvement occurs commonly in syphilis and whipples disease. Management Investigation As retinal vasculitis is associated with various systemic, ocular and infectious disease, a detailed laboratory work up is always essential. A thorough medical history and physical examination should be the basis for a focused diagnostic evaluation. The initial evaluation should include complete blood count, erythrocyte sedimentation rate, C-reactive protein, VDRL, FTA-ABS, mantoux test, angiotensin converting enzyme, rheumatoid factor (RA), antinuclear antibody (ANA) and chest x-ray. If an infectious etiology is suspected, especially in retinal vasculitis associated with dense vitritis investigations should include ocular fluid cultures, serological tests and polymerase chain reaction. Serological tests are done for toxoplasma, syphilis, lyme disease and cat-scratch disease. Polymerase chain reaction in ocular fluid specimens has been extremely useful in identifying herpes simplex, varicella zoster, cytomegalovirus, Mycobacterium tuberculosis and toxoplama gondii. In patients with non-infectious systemic diseases, diagnostic tests should be focused on systemic vasculitic syndromes. Laboratory work up includes rheumatoid factor, antinuclear antibody, anti-double stranded DNA antibodies, anti-neutrophil cytoplasmic antibodies, anticardiolipin antibodies, complement levels, and imaging studies.
10 AECS Illumination Human leukocyte antigen (HLA) testing is another useful technique in certain diseases. These HLA associations include Behcet s disease and HLA-B51, birdshot retinochoroidopathy and HLA-A29 and systemic lupus erythematosus and HLA-DR3, Finally, MRI and CT scan can be considered in patients with multiple sclerosis and primary central nervous system lymphoma. Fluorescein angiography can be done in active or healed vasculitis. It shows staining and leakage of retinal veins, areas of capillary non-perfusion, retinal neovascularization, sclerosis of vessels, optic disc leakage, cystoid macular odema, vascular occlusion and macular ischemia. Optical coherence tomography may also be done in cases of refractory macular odema to follow them and see the response of treatment when it is not clinically apparent. Treatment The main goal of treatment in retinal vasculitis is suppression of intraocular inflammation in order to prevent visual loss and long-term complications. The mainstay of therapy is corticosteroids and immuno suppressives. In case of an infective lesion, specific therapy against the infective agent with or without corticosteroids may be required. Corticosteroids may be given either systemically or by posterior subtenon s injection. Periocular steroids are useful in patients with unilateral and mild inflammation. Though this route avoids the systemic side effects, it carries a risk of raised intraocular pressure and globe perforation. Oral corticosteroids are given in patients with moderate to severe bilateral inflammation and a marked decrease in visual acuity. Severe cases of sight threatening retinal vasculitis involving the posterior pole may require intravenous methyl prednisolone followed by oral corticosteroids and immunosuppressives. Intravitreal steroid injections can also be given in cases of refractory macular odema. In cases, where retinal vasculitis does not respond or shows inadequate control to oral corticosteroids, steroid sparing immunosuppressive agents are useful. These drugs are also used in patients who develop intolerable side effects to oral steroids. Various immunosuppressive agents used for treatment of retinal vasculitis include azathioprine, cyclosporine, cyclophosphamide, methotrexate, mycophenolate mofetil and infliximab. The choice of immunosuppressive agent should be individualized for each patient with a specific systemic disease. Azathioprine, cyclosporine and inflicimab are used in-behcets disease. Alkylating agents like cyclophosphamide are often used with systemic corticosteroids in vasculitis associated with systemic autoimmune diseases like Wegeners granulomatosis and systemic lupus erythematosus. Topical steroids with cycloplegics are given in cases with co-existing iridocyclitis. Other modalities of treatment in retinal vasculitis are laser photocoagulation and vitrectomy. Laser photocoagulation is indicated in patients with retinal neovascularization with recurrent or non clearing vitreous hemorrhage and neovascular glaucoma. As photocoagulation may induce cystoid macular odema, intraocular inflammation must be adequately controlled prior to laser treatment. Vitrectomy is useful in patients with non-clearing vitreous hemorrhage, tractional retinal detachment and epiretinal membrane removal. Conclusion In summary, retinal vasculitis is not only a potentially blinding intraocular inflammatory condition, it can also be the first sign of a lethal systemic disease. A detailed history, ocular and physical examination with a focuses laboratory work up can help in prompt diagnosis and appropriate management of the disease.
Vol. XII, No.2, April - June 2012 11 Reference 1. Biswas J, Sharma T, Gopal L, Madhavan HN, Sulochana KN, Ramakrishnan S. Eales disease--an update. Surv Ophthalmol. 2002 Jun;47(3):197 214. 2. Natarajan S. From the editor s desk - vasculitis my brief synopsis. Indian J Ophthalmol. 2011 Aug;59(4):271 2. 3. Nourinia R, Montahai T, Amoohashemi N, Hassanpour H, Soheilian M. Idiopathic retinal vasculitis, aneurysms and neuroretinitis syndrome associated with positive perinuclear antineutrophil cytoplasmic antibody. J Ophthalmic Vis Res. 2011 Oct;6(4):330 3. 4. Pantanelli SM, Khalifa YM. Retinal manifestations of autoimmune and inflammatory disease. Int Ophthalmol Clin. 2012;52(1):25 46. 5. Levy-Clarke GA, Nussenblatt R. Retinal vasculitis. Int Ophthalmol Clin. 2005;45(2):99 113. 6. Sanders MD, Graham EM. Retinal vasculitis. Postgrad Med J. 1988 Jul;64(753):488 96. 7. Shrestha JK, Khadka D, Lamichhane G, Khanal S. Retinal vasculitis. Nepal J Ophthalmol. 2009 Jun;1(1):66 71. 8. Rahi AH, Tabbara KF. Retinal vasculitis: pathogenesis and laboratory investigations. Int Ophthalmol Clin. 1995;35(3):93 105. 9. Brydak-Godowska J, Dróbecka-Brydak E. [Retinal vasculitis--causes, diagnosis, treatment]. Klin Oczna. 2007;109(1-3):71 3. 10. Stanford MR, Graham EM. Systemic associations of retinal vasculitis. Int Ophthalmol Clin. 1991;31(3):23 33.