presentation made during uveitis session.

1. Bipin Bista
Resident
Ophthalmology
NMCTH

2.  Diagnosis of intermediate uveitis is made by
inflammation primarily involves vitreous &
peripheral retina.
 In 1960 Brockhurst & colleagues described it as
inflammation characterized by white
accumulation on pars plana.
 International Uveitis Study Group : intraocular
inflammation predominantly involving
vitreous & peripheral retina.

3.  National Institute of Health – 2.077 per 100000
persons.
 No gender or race predilection.
 Usually affects after the age of 40.
 HLA Association.

4.  Blurred vision
 Floaters
 Decreased visual acquity
 If inflammation persists , severe visual loss.
 Sudden loss of vision.
 Anterior segment involvement – minimal.
 AS involvement common in children.

5.  Presence of vitreous
cells (+1)
 Vitreous snowball :
white & yellow
colored aggregates .
 Coalesce to form
material : snowbank
 Periarteritis
 Perivasculitis
 Vascular cyclitic
membrane

7.  Snowbank may be discontinuous, usually
located inferiorly but can extend upto 3600
 cystoid macular oedema – FA
 Rhegmatogenous RD.
 Chronic intermediate uveitis : long standing
macular oedema – development of retinal
pigment epithelial stippling in macula.
Disc oedema, optic atrophy & optic disc
neovascularization.

8.  BENIGN
 MILD
 CHRONIC
 SEVERELY CHRONIC

9.  Sarcoidosis
 Multiple sclerosis
 IBD
 Lyme disease
 Toxocariasis
 Intraocular
Lymphoma
 Retinoblastoma
 Whipple’s Disease
 Iridocyclitis
 Multifocal choroiditis
 Irvine-Gass syndrome
 Amyloidosis
 Interstitial nephritis &
uveitis syndrome
 Cat scratch disease
 Hepatitis C
 Crohn’s Disease

11.  Optic neuritis (>50%)
 Intermediate uveitis,
anterior uveitis &
periphlebitis.
 Multiple sclerosis had
serum antibodies to
arrestin (retinal S-
antigen).

12.  Exudation
 Periphlebitis : leads to breakdown of blood-
ocular barrier.
 Snow-banking

13.  Collapsed vitreous, blood
vessels, fibroglial cells
including fibrous
astrocytes & scattered
inflammatory cells,
predominately
lymphocytes.
 Peripheral vein :
lymphocytic cuffing &
infiltration.
 Composed of epitheloid
cells & multinucleated
giant cells.
 Absent in uvea & primary
site may be vitreous.

14.  Glial tissue in the snowbank & extensive
peripheral vascular disease with perivascular
infiltration of lymphocytes & MHC II antigen.
 No substantial choroidal inflammation.

15.  Increased level of immune markers :
• Interleukin-2
• Intercellular adhesion molecule-1

16.  Exclude the possibility of underlying infectious
disease or malignancy.
 Therapy

17.  Mainstay of therapy.
 Topical not much effective.
 Systemic or periocular.
 40mg triamcinolone – 2-3 times in 8 weeks.
 Systemic – bilateral IU.
 0.5-1 mg/kg/day – Prednisolone

18.  Steroid resistant cases.
 Cyclosporin – watch for toxicity.
 Azathioprine, methotrexate, cyclophospamide,
mycophenolate mofetil.

19.  Anti – TNF monoclonal antibodies :
Daclizumab.

20.  Cryotherapy
 Vitrectomy

21.  Destroys the vascular component of peripheral
retinitis or vitreitis & eliminates the entrance
site for inflammatory mediators into the eye.
 Combined with periocular steroid injections.
 Evident within several weeks & lasts for 3-6
months.
 Complication : transient increased vitreal
inflammation, reduced accomodation, cataract
& hyphaema.

22.  Chronic inflammation
 2/3rd improvement.

23. Reference:
- Nussenblatt and whitecup 4th edition
- Myron yanoff 4th edition