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Pars Planitis (Intermediate Uveitis)

A chronic bilateral inflammation of the vitreous and pars plana producing snowballs (vitreous opacities) and snowbanking (peripheral retinal exudate); classically idiopathic in young adults but may be associated with multiple sclerosis, sarcoidosis, Lyme disease, or tuberculosis.

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

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What is Pars Planitis (Intermediate Uveitis)?

Intermediate uveitis is inflammation centered on the vitreous, pars plana, and peripheral retina, classified by SUN Working Group as one of four anatomic subtypes of uveitis (anterior, intermediate, posterior, panuveitis). Pars planitis specifically refers to the idiopathic subtype with snowballs and snowbanking and accounts for 50–60 percent of intermediate uveitis cases.

Etiology of intermediate uveitis: idiopathic (pars planitis, 50–60 percent), multiple sclerosis (15–20 percent — bilateral intermediate uveitis with vasculitis is highly suggestive of MS, especially in young women with optic neuritis history), sarcoidosis (10–15 percent — granulomatous, snowballs, periphlebitis with candle-wax drippings), Lyme disease, syphilis, tuberculosis, HTLV-1, Epstein-Barr virus, cat-scratch disease (Bartonella), Behçet disease, juvenile idiopathic arthritis. Workup includes MRI brain (MS), chest X-ray and serum ACE / lysozyme (sarcoid), Lyme serology, RPR / FTA-ABS (syphilis), QuantiFERON-TB (TB), serum calcium / 1,25-OH vitamin D.

Diagnosis: comprehensive examination with dilated indirect ophthalmoscopy with scleral indentation (essential to detect snowbanking on inferior pars plana), slit-lamp examination of anterior chamber (mild anterior segment inflammation), B-scan ultrasound (vitreous opacities), OCT (CME — leading cause of vision loss), fluorescein angiography (peripheral vasculitis, CME, neovascularization). Complications include CME (most common cause of permanent vision loss), epiretinal membrane, vitreous hemorrhage from neovascularization, peripheral retinoschisis, retinal detachment, cataract, secondary glaucoma.

Symptoms

Painless floaters (most common — from vitreous opacities and snowballs)
Blurred vision (from cystoid macular edema)
Bilateral involvement (often asymmetric)
Mild redness, photophobia (less prominent than anterior uveitis)
No pain in most cases
Reduced visual acuity progressively
Floaters described as cobwebs, threads, or snow-like specks
Onset typically in children, adolescents, or young adults (5–40 years)

Risk Factors

Young age (5–40 years, peak in second-third decades)
Female sex (slight predominance)
HLA-DR15 (associated with idiopathic pars planitis and MS)
Personal or family history of multiple sclerosis
Sarcoidosis (systemic granulomatous disease)
Tick exposure in Lyme-endemic regions
Tuberculosis exposure or risk factors
Autoimmune predisposition

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • New onset floaters, especially bilateral
  • Blurred or decreased vision in young adult
  • Floaters with mild eye discomfort
  • Family history of multiple sclerosis with new visual symptoms
  • Known sarcoidosis with visual changes
  • Known intermediate uveitis with vision worsening (CME progression)
  • Sudden vision loss in known uveitis (vitreous hemorrhage, retinal detachment)

Treatment Methods

01
Comprehensive workup: dilated fundus exam with scleral indentation, OCT macula (CME), fluorescein angiography, B-scan, MRI brain (MS workup), chest X-ray, serum ACE / lysozyme / calcium (sarcoid), Lyme serology, RPR / FTA-ABS, QuantiFERON-TB
02
Step 1 — periocular corticosteroid (sub-Tenon triamcinolone 40 mg, repeat every 6–12 weeks as needed) for unilateral or asymmetric disease with CME
03
Intravitreal triamcinolone acetonide (4 mg) or dexamethasone implant (Ozurdex 0.7 mg, lasts 4–6 months) for refractory CME
04
Step 2 — systemic corticosteroid (oral prednisone 1 mg/kg/day, taper over 6–12 weeks) for bilateral or vision-threatening disease; gastroprotection, calcium / vitamin D, bone density monitoring
05
Step 3 — corticosteroid-sparing immunomodulator: methotrexate 15–25 mg weekly, mycophenolate mofetil 1–1.5 g BID, azathioprine, cyclosporine; choice based on side-effect profile and comorbidities
06
Step 4 — biologic anti-TNF (infliximab 5 mg/kg every 4–8 weeks, adalimumab 40 mg every 2 weeks — FDA-approved for non-infectious uveitis) for refractory CME or vision-threatening disease
07
Pars plana vitrectomy for vitreous opacities causing chronic floaters, vitreous hemorrhage, epiretinal membrane, or persistent CME despite medical therapy; may also have therapeutic effect on inflammation
08
Treat underlying systemic disease: MS (disease-modifying therapy with neurology), sarcoidosis (steroids, methotrexate), Lyme (doxycycline / ceftriaxone), TB (4-drug regimen), syphilis (penicillin)
09
Long-term follow-up every 1–3 months with OCT macula (CME monitoring), visual acuity, IOP (steroid response); manage cataract and glaucoma as they develop

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Health Disclaimer: The information on this page is prepared for general informational purposes only. It does not replace medical diagnosis and treatment. Please consult your physician for your complaints. Saygı Hospital does not accept responsibility for actions taken based on the information on this page.