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Pars Planitis

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Pars Planitis is a disease of the eye that is characterized by inflammation of the narrowed area (pars plana) between the colored part of the eye (iris) and the choroid. This may lead to blurred vision; dark, floating spots in the vision; and progressive vision loss.

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Pars Planitis

  1. 1. PARS PLANITIS Shah-Noor Hassan FCPS,FRCS(Glasgow) Vitreo-Retina Consultant Bangladesh Eye Hospital & Institute
  2. 2. History • Cyclitis- Fuchs in 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. 3. Nomenclature • Standardization of Uveitis 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. 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. 5. Etiology • Idiopathic • No known hereditary or environmental factors • Some isolated cases of familial pars planitis • Associated with various systemic diseases • Most common- multiple sclerosis, sarcoidosis
  6. 6. Pathogenesis • Immune mediated response • 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. 7. Pathogenesis • Escape from regulatory 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. 8. Pathology • Peripheral retina and 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. 9. Clinical features • Floaters and 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. 10. Presentation • VISION LOSS • CME, ERM • PSC • Vitreous Opacification • Membranes • Retinal Detachment • Vitreous Hemorrhage
  11. 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. 12. Presentation • Peripheral vasculitis • CME, Peripapillary retinal edema • Vitritis, Cyclitis • Vitreous hemorrhage • Band shaped keratopathy
  13. 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. 14. Vitreous involvement • Vitritis • Snowball formation • Vitreous membranes and floaters • Vitreous hemorrhage
  15. 15. Retinal involvement • Retinal vascular 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. 16. Optic nerve involvement • Disc edema- 3-38% • Optic neuritis with or without multiple sclerosis was seen in 7.4 %
  17. 17. Complications • Glaucoma – Acute uveitis- 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. 18. Cataract • 15-50% of eyes • 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. 19. Types Of Retinal Detachment • 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. 20. Types Of Retinal Detachment 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. 21. Pars planitis in children • 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. 22. STANDARDIZATION OF UVEITIS NOMENCLATURE
  23. 23. Natural course Self limited 10 % Smoldering 59% Recurrent 31 %
  24. 24. Diagnosis CLINICAL FEATURES OPHTHALMIC INVESTIGATIIONS TO RULE OUT SECONDARY CAUSES
  25. 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. 26. Ophthalmic investigations • V/A • SL biomicroscopy • IOP and • Fundus examination with scleral depression • Amsler grid
  27. 27. • OCT - Macular oedema • Fluorescein Angiogram- Vasculitis ,CNP areas , New vessels & CME • B scan (Hazy media) • UBM • Diagnostic vitrectomy Ophthalmic investigations
  28. 28. To rule out secondary 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. 29. Differential diagnosis • Non infectious – 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. 30. MANAGEMENT
  31. 31. Four Step Approach (Kaplan et al)
  32. 32. Modified 5 step program: 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. 33. Addition of systemic steroid or immunosuppressive agents Periocular steroid Cryo or peripheral LASER Vitrectomy
  34. 34. Corticosteroids • Drop in VA 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. 35. Corticosteroids • IVTA can be given in cases of severe macular edema • Complications Cataract Glaucoma Endophthalmitis
  36. 36. Oral steroids • Indicated if the disease activity is not controlled with periocular steroids • Prednisolone 1 mg/kg/day tapered once response occurs
  37. 37. Immunosuppressive agents • Antimetabolites : Methotrexate , Azathioprine • Alkylating Agents : Cyclophosphamide , Chlorambucil • Immunomodulators : Cyclosporine , Tacrolimus • Complications – GI upset – Hepatotoxicity – Bone marrow suppression
  38. 38. Methotrexate • Folate analogue which 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. 39. Azathioprine • Purine nucleoside analogue • 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. 40. Inhibitors of T-cell signaling • 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. 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. 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. 43. Newer steroid implants • Retisert – Fluocinolone acetonide implant – Duration of 30 months • Ozurdex – Dexamethasone implant
  44. 44. Ablative procedures • Failed drug 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. 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. 46. LASER ablation • LASER photocoagulation 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. 47. Vitrectomy • Vitrectomy for uveitis 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. 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. 49. What’s new…. • Anti VEGF 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. 50. Nevanac in pars planitis • Case 1: - Short term benefit in cases of recurrent intermediate uveitis
  51. 51. Case 2 • Rapid resolution of vitritis in uncomplicated case of intermediate uveitis
  52. 52. Case 3 • Fresh case of pars planitis with CME • Nevanac improved the CME
  53. 53. Summary • Examination of pars 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. 54. Thank you…

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