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Pars Planitis
- 1. PARS PLANITIS Shah-Noor HassanFCPS,FRCS(Glasgow) Vitreo-Retina Consultant Bangladesh Eye Hospital & Institute
- 2. History • Cyclitis- Fuchsin 1908, Duke-Elder 1941 • Peripheral uveitis- Schepens-1950 • Peripheral cyclitis- Brockhurst et.al. - 1960 • Pars planitis- Welch et.al. - 1960 • Chronic cyclitis- Hogan & Kimura in 1961 • Vitritis- Gass et.al. - 1968 • Intermediate uveitis- IUSG- 1987 • SUN working group-2004
- 3. Nomenclature • Standardization ofUveitis Nomenclature working group classification • Idiopathic form of intermediate uveitis • Includes snowballs and snowbanking • If associated with diseases like Sarcoidosis and Lyme disease then included in intermediate uveitis
- 4. Epidemiology • 10-25 %of all the uveitis cases • Children and young adults • Can occur at any age • Both sexes are equally affected • 80% are bilateral • Less in Chinese and Japanese population
- 5. Etiology • Idiopathic • Noknown hereditary or environmental factors • Some isolated cases of familial pars planitis • Associated with various systemic diseases • Most common- multiple sclerosis, sarcoidosis
- 6. Pathogenesis • Immune mediatedresponse • But the antigenic stimulus remains speculative • Davis and colleagues – Stage 1- immunologically mediated – Stage 2- Non specific breakdown of intraocular regulatory mechanisms (Not necessarily an autoimmune mechanism but even exogenous viral or bacterial antigens may be responsible)
- 7. Pathogenesis • Escape fromregulatory control of Helper T cells directed against these antigens • Defective intraocular T cell regulation of B cells • Decreased helper to suppressor T cell ratios in aqueous and peripheral blood • Other mechanisms – Anterior chamber associated immune deviation – Auto retinal antibodies – Related to Demyelination – HLA-DR15 and HLA-A28 positivity – Nucleoporin like protien-nup36
- 8. Pathology • Peripheral retinaand ciliary body demonstrate condensed vitreous , fibroblasts, spindle cells, lymphocytes and blood vessels • Prominent lymphocyte cuffing of retinal veins • Pars plana exudates – Loose fibrovascular layer containing scattered mononuclear inflammatory cells and a few fibrocyte like cells – Fibroglial tissue consists of vitreous collagen, mullers cells and probable fibrous astrocytes
- 9. Clinical features • Floatersand hazy vision • No pain, photophobia, redness • First episode is associated with a more severe and symptomatic iridocyclitis • Subsequent episodes have a chronic course……. • One eye symptomatic other eye may be asymptomatic and even show signs of active disease
- 10. Presentation • VISION LOSS •CME, ERM • PSC • Vitreous Opacification • Membranes • Retinal Detachment • Vitreous Hemorrhage
- 11. Presentation • Cells, flare,KPs in AC, synechiae (Spill over anterior segment inflammation) • Snow balls (organized vitreous inflammatory cells ) • Snow banking (exudates at pars plana) • May be localised to inferior half
- 12. Presentation • Peripheral vasculitis •CME, Peripapillary retinal edema • Vitritis, Cyclitis • Vitreous hemorrhage • Band shaped keratopathy
- 13. Effect on macula •Macular edema (CME) and maculopathy (12- 82 %) • Most common cause of visual loss • Incidence increases with duration and severity of disease
- 14. Vitreous involvement • Vitritis •Snowball formation • Vitreous membranes and floaters • Vitreous hemorrhage
- 15. Retinal involvement • Retinalvascular changes – Tortuosity of arterioles and venules – Peripheral vascular sheathing (Periphlebitis-16-36 %) – Neovascularizations (6.5%) – Retinal detachment (2.2-51 %) • Causes of RD – Vitreous traction due to long standing inflammation and subsequent hole formation – Exudative detachment secondary to uvietis inflammation
- 16. Optic nerve involvement •Disc edema- 3-38% • Optic neuritis with or without multiple sclerosis was seen in 7.4 %
- 17. Complications • Glaucoma – Acuteuveitis- 7.6 % – Chronic – 6.5% at one year, 11.1 at 5 years • Causes of glaucoma – Active inflammation – Steroid usage – Increasing age – Number of years since diagnosis
- 18. Cataract • 15-50% ofeyes • Posterior or anterior subcapsular • At times posterior cortical even posterior polar have been reported • Incidence increases with duration and severity of disease • If treated earlier with immunosuppressive rather than corticosteroids cataract formation is less severe
- 19. Types Of RetinalDetachment • Exudative RD in 5-17% • Vitreoretinal traction - in 3-22% TRRD • Brockhurst and Schepens – 4 types of RRD Type I: - Low lying, chronic, associated with demarcation lines - Small breaks near ora with exudates - Benign course
- 20. Types Of RetinalDetachment Type II: - Large dialysis at the posterior edge of the pars plana exudate - Slowly progressive - May resolve spontaneously if VR exudation occludes the break - Seen in pts with a mild chronic inflammatory course Type III: - Rapidly progressive - Large breaks associated with NVVB and circumferential pars plana exudates. - Associated with severe chronic uveitis.
- 21. Pars planitis inchildren • More so as an intermediate uveitis • JIA most common cause (30%) • 1.8-29% of all uveitis • Of which 25 % are pars planitis • Mean age 8.5-10.9 years • Male preponderence • Bilateral 84-94 % • Resolves over several years • Severe visual loss is uncommon
- 22.
- 23. Natural course Self limited 10% Smoldering 59% Recurrent 31 %
- 24. Diagnosis CLINICAL FEATURES OPHTHALMIC INVESTIGATIIONS TO RULEOUT SECONDARY CAUSES
- 25. Diagnosis: Clinical • History •Clinical findings • Duration of symptoms, recurrences • Fever , fatigue or night sweats are typical signs - Sarcoidosis & TB • Loss of sensitivity or paresthesias of hands, arms or legs - Multiple sclerosis • Dermatitis, Arthritis– Lyme • Contact with cats – possibility of Bartonella infection
- 26. Ophthalmic investigations • V/A •SL biomicroscopy • IOP and • Fundus examination with scleral depression • Amsler grid
- 27. • OCT -Macular oedema • Fluorescein Angiogram- Vasculitis ,CNP areas , New vessels & CME • B scan (Hazy media) • UBM • Diagnostic vitrectomy Ophthalmic investigations
- 28. To rule outsecondary causes… • Complete hemogram • ELISA for tuberculosis and toxoplasma • CXR • Galium Scan and Chest CT Lab Inv: - ACE levels- elevated in 60-90% of active sarcoid patients - Lysozyme level - Elevated in granulomatous disorders viz sarcoid, TB, and leprosy - Elevated antibody titre against Borrelia burgdorferi • Sarcoidosis • Tuberculosis.
- 29. Differential diagnosis • Noninfectious – Multiple sclerosis (3-27 %) – Sarcoidosis (23-26%, IU developing sarcoidosis- 2- 10%) – Intraocular lymphoma (PCNSL- 10-20% have vitreous inflam) • Infectious conditions – Tuberculosis – Syphilis (10.3%) – Lyme disease – Toxoplasma – Toxocariasis – HTLV-1, EBV, Cat scratch disease – Endogenous endophthalmitis – ARN, Eales, VKH, Fuch’s
- 30.
- 31. Four Step Approach(Kaplan et al)
- 32. Modified 5 stepprogram: S.Foster et al Topical +/ Periocular corticosteroids Oral +/ Topical NSAID After 3rd injection Systemic C steroids Inflammation persists or recurs Peripheral retinal cryopexy /BIOL Recur following 6th regional steroid injection PPV/ Immunosupression Recalcitrant inflammation
- 33. Addition of systemicsteroid or immunosuppressive agents Periocular steroid Cryo or peripheral LASER Vitrectomy
- 34. Corticosteroids • Drop inVA due to vitritis, CME, progression of neovascularization at the vitreous base • Periocular steroids- – Long acting Methyl prednisone (40 mg ) – Triamcinolone acetonide (20 mg) • Complications- – Glaucoma – Cataract – Aponeurotic ptosis – Enophthalmos – Orbital scarring
- 35. Corticosteroids • IVTA canbe given in cases of severe macular edema • Complications Cataract Glaucoma Endophthalmitis
- 36. Oral steroids • Indicatedif the disease activity is not controlled with periocular steroids • Prednisolone 1 mg/kg/day tapered once response occurs
- 37. Immunosuppressive agents • Antimetabolites: Methotrexate , Azathioprine • Alkylating Agents : Cyclophosphamide , Chlorambucil • Immunomodulators : Cyclosporine , Tacrolimus • Complications – GI upset – Hepatotoxicity – Bone marrow suppression
- 38. Methotrexate • Folate analoguewhich inhibits dihydrofolate reductase • 7.5-25 mg per week oral/subcutaneous • Can also lead to pneumonitis • Effective and safe for chronic anterior and IU in children
- 39. Azathioprine • Purine nucleosideanalogue • Alters purine metabolism • 50-150 mg per day • GI upset and hepatotoxicity Mycophenolate mofetil • Inhibits purine synthesis • Prevents replication of T and B lymphocytes • 1-3 mg per day • Mycophenolate is faster amongst the 3 in controlling inflammation
- 40. Inhibitors of T-cellsignaling • Cyclosporine and Tacrolimus – Inhibit NF-AT (Nuclear Factor of Activated T-cells ) – Nephrotoxicity and hypertension are important complications • Biological response modifiers – Daclizumab – Infliximab – Eternacept – Interferon alpha
- 41. Biological response modifiers •Daclizumab – Humanized monoclonal ant-IL-2 receptor alpha antibody – Suppresses auto reactive T-cells – 1 mg/kg IV every 2 weeks for 5 doses – Increase risk of infection
- 42. Biological response modifiers •Infliximab – Binds to TNF and prevents its action on target tissues • Eternacept – Dimeric, fully human, soluble TNF receptor – Binds tightly and specifically to circulating and cell-bound TNF • Adalimumab – Can be self administered as a subcutaneous injection – Fully humanized so less chances of antibody formation • Disseminated tuberculosis is one of the fatal complications
- 43. Newer steroid implants •Retisert – Fluocinolone acetonide implant – Duration of 30 months • Ozurdex – Dexamethasone implant
- 44. Ablative procedures • Faileddrug therapy • At times cryotherapy is preferred before immunosuppressive Rx • Aim – To treat neovascularization associated with the exudates – To destroy the peripheral vessels which bring in the inflammatory mediators
- 45. • Double row,single freeze • Apply to pars plana and posterior to it • CONFLUENT BURNS • Extend 1 clock hr on either side of all areas affected by inflammation • EFFECTS – Decreases vitritis and improves VA – Decrease in fluorescein in the treated area – Induce regression of this NVVB and consequently stabilize inflammation Cryo ablation
- 46. LASER ablation • LASERphotocoagulation works as effective as cryo • 3-4 rows of burns are placed at the pars plana and peripheral retina • Works on the same mechanism as cryo
- 47. Vitrectomy • Vitrectomy foruveitis began in late 1970s • Aims – Get rid of inflammatory mediators and immunologically competent cells – Clear the media • Indications – Refractory uveitis – Vision loss due to densely opacified vitreous – Scar tissue pulling on ciliary body causing hypotony – CME, ERM – Dense PCO – TRD
- 48. MANAGEMENT OF CATARACT: •Eye - quiet for 3 months – Preoperative – Start steroids 3 days prior – Postoperative - slow taper. • Technique – – As preferred by surgeon – Minimal trauma – Preferably heparin coated IOL
- 49. What’s new…. • AntiVEGF agents are being evaluated in cases of uveitis with macular edema • Lucentis and Avastin have been proved to be effective in cases of uveitic CME
- 50. Nevanac in parsplanitis • Case 1: - Short term benefit in cases of recurrent intermediate uveitis
- 51. Case 2 • Rapidresolution of vitritis in uncomplicated case of intermediate uveitis
- 52. Case 3 • Freshcase of pars planitis with CME • Nevanac improved the CME
- 53. Summary • Examination ofpars plana • Diagnose macular edema • Rule out secondary causes • Plan appropriate treatment modility • Bold use of steroids and immunosuppressive agents to prevent vision loss due to macular involvement • Look out for complications • Surgical management in resistant cases and to clear the media
- 54.