It provide clear and in short knowledge about uveitis.

1. UVEITIS
PREPARED BY:
RAHUL BIKRAM SAH
BAMS 23RD BATCH

2. Introduction
Uveitis is a complex intraocular inflammatory
process that involves the uveal and retinal tissues.
Anatomy of Uvea
The uvea is a pigmented vascular structures consisting
of iris ,ciliary body and choroids .

3. Choroid, ciliary body and iris - the uveal tract
• Posteriorly, the choroid acts as a conduit for branches of the ophthalmic artery
and veins. The choriocapillaris, a network of wide- bore, fenestrated capillaries,
abuts the retinal pigment epithelium. The ciliary body forms the junction
between the choroid and the iris, and lies just inferior to the limbus. Anteriorly,
its ciliary processes produce aqueous (fluid) that circulates through the pupil
into the anterior chamber. Posteriorly, it constitutes the pars plana and forms
the attachments for the suspensory ligaments. of the lens. The ciliary muscle
encircles the eye within the ciliary body. Contraction of this muscle relaxes the
suspensory ligaments of the lens, bringing near objects into focus.
• The iris bows gently forwards as it lies against the lens. It is divided into a
pupillary zone, containing the circumferential sphincter pupillae muscle, and a
ciliary zone, containing the dilator pupillae.

4. Function of Uveal Tract
Highly vascular system that cools the retina. It supply outer 5 layers of retina by
choriocapillaries.
The iris with its central opening, pupil, controls the amount of light entering the
eyes.
The ciliary body secretes aqueous humor and contains smooth muscles
responsible for changing the shape of the lens during accommodation.
The inner surface of ciliary body is divided into two regions:
1. Pars plicata: Anterior part; about 70 plications are visible. Microscopically,
they have ciliary processes responsible for the production of aqueous.
2. Pars plana: Posterior smooth part. They are covered by two layers of
epithelium, continuous with the iris anteriorly, and retina posteriorly. Ciliary
body extends backward as far as the ora serrata. At this point the retina proper
begins abruptly.
The choroid, a vascular layer, provides the blood supply to the retinal pigment
epithelium and the outer half of the sensory retina. Also Some of the light
absorbed by sclera,then remaining light absorbed by choroid so there is no
blurring of vision.

6. A.Anatomical classification of Standardization of Uveitis
Nomenclature(SUN)
Type Primary site of
inflammation
Includes
Anterior Anterior • Iritis chamber
• Anterior cyclitis
• Iridocyclitis
intermediate Vitreous Pars planitis
Posterior Choroid or retina •Focal,
multifocal or diffuse
choroiditis
• Chorioretinitis
•Retinochoroiditis •
Retinitis
• Neuroretinitis
Panuveitis Anterior Chamber,Vitreous
and Choroid or retina

7. B. CLINICAL CLASSIFICATION
• ACUTE UVEITIS: It has got a sudden symptomatic onset and the disease
lasts for about 6 weeks to 3months.
• CHRONIC UVEITIS:It frequently has an insidious (gradual) and
asymptomatic onset. It persists longer than 3 months to even years and is
usually diagnosed when it causes defective vision.
• RECURRENT UVEITIS:This is characterised by repeated episodes separated
by inactive periods of >3 months without treatment.

8. C. PATHOLOGICAL CLASSIFICATION
1.SUPPURATIVE UVEITIS: Composed or containing of pus. Occurs as a result of
exogenous infection by pyogenic organisms which include- Staphylococcus,
Streptococcus, Pseudomonas, Pneumococcus and Gonococcus.
2.NON- SUPPURATIVE UVEITIS:It has been further subdivided into two groups (
Woods classification)
• Non granulomatous uveitis and
• Granulomatous uveitis - characterized by the formation of granulomas.

9. granulomatous uveitis Non granulomatous uveit
Insidious onset and chronic course Acute onset and short course
Tuberculosis, sarcoidosis, leprosy, etc. are usually
responsible
Mainly idiopathic and allergic in nature
Nodules (Keoppe’s and Bussaca’s) on the iris No such nodules on the iris
Medium to large KPs (often mutton-fat type) Fine keratic precipitates (KPs)
Mild flare *Intense flare,often with heavy fibrinous exudates.

10. D.ETIOLOGICAL CLASSIFICATION
Idiopathic
• Anterior uveitis often associated with the HLA-B27 haplotype,
• even in the absence of other manifestations
Rheumatological
• HLA-B27-associated (seronegative) spondyloarthropathies: ankylosing
spondylitis, psoriatic arthritis, reactive arthritis • Juvenile idiopathic arthritis
Systemic vasculitides
• Behçet's disease
• Polyarteritis nodosa
• Granulomatosis with
• polyangiitis (Wegener's)

12. Inflammatory bowel disease
(Crohn's disease, ulcerative colitis)
Systemic conditions of unknown cause
Multiple sclerosis
Sarcoidosis
Systemic infections (only the more
common causes are listed)
• Brucellosis
• Herpes virus infections (cytomegalovirus,
herpes simplex virus, varicella zoster
virus)
• Leptospirosis
• Gastrointestinal conditions
• Lyme borreliosis
• Syphilis
• Toxoplasmosis
• Tuberculosis
• Whipple's disease

13. Basic pathomechanisms in uveitis
• Vasodilatation
• Increased capillary permeability
• Migration of inflammatory cells into the ocular cavities

14. ANTERIOR UVEITIS (IRIDOCYCLITIS)
• Inflammation of iris and ciliary body (pars plicata) is called ANTERIOR
UVEITIS commonly known as iridocyclitis.
• Incudes Iritis , Anterior cyclitis and Iridocyclitis.
• Pain: Acute, severe with radiation along the branches of the 5th nerve. It
is typically worse at night . Also pain is felt on forehead,scalp,
cheeks,malar bone and sometime to nose and teeth.
• Redness: It is due to vasodilatation
• Photophobia
• Lacrimation
• Dimness of vision: It is due to:
Plasmoid (turbid) aqueous ,Vitreous exudates ,Exudates in the pupillary
area, Cystoid macular edema ,Secondary glaucoma ,Ciliary muscle spasm,
Complicated cataract.

15. Ocular Signs
• Circumcorneal ciliary congestion (CCC):It is one of the hallmarks of acute anterior uveitis.
• Circumcorneal congestion is marked in acute iridocyditis and minimal in chronic iridocyditis.
• Keratic Precipitates: They are cellular deposits on the corneal endothelium.
Anterior chamber signs
1.Aqueous cells: It is due to exudation of inflammatory cells into the aqueous presence of cells in aqueous
always indicates active inflammation.
2. Aqueous flare:
• flare is protein, it appears finer, like smoke.
• earliest sign of acute anterior uveitis
• occurs due to leakage of protein particles into the aqueous humour
from damaged blood vessels.

16. 3. Hypopyon
• When exudates are heavy and thick, they settle down in lower part of
the anterior chamber as hypopyon (sterile pus in the anterior
chamber)

17. Iris
• Muddy iris or loss of iris pattern: This is due to accumulation of fluid
and exudates over the surface of the iris.
• Iris nodules: It is seen in granulomatous uveitis.
1.Koeppe’s nodule: At the pupillary border, and smaller in size. „
2.Busacca’s nodule : On the surface of the iris, away from the pupil.

18. Synechiae ;
• Posterior synechia: It is the adhesion between the anterior lens
surface and the iris.
− Ring (annular) synechiae: Posterior synechiae extending for 3600
around the pupil (seclusio pupillae), prevent the passage of aqueous
from the posterior to the anterior chamber. This gives rise to forward
bowing of the peripheral iris causing an iris bombe . This may lead to
elevation of intraocular pressure due to secondary angle closure by the
peripheral iris

19. − Total posterior synechiae: Adhesion of entire iris with the anterior
lens capsule.
-Anterior synechiae: Adhesion of iris with the corneal endothelium. It is
usually peripheral and secondary to iris bombe.

20. Pupillary signs
l. Narrow pupil
occurs in acute attact.Due to irritation of sphincter pupillae by toxin, Iris oedema and
engorged radial vessels of iris.
2. Irregular pupil shape(festooned pupil)
• It results from segmental posterior synechiae formation.
3. Ectropion pupillae ( evertion of pupillary margin)
• It may develop due to contraction of fibrinous exudate on the anterior surface of the iris.
4. Pupillary reaction becomes sluggish or may even be
• absent due to oedema and hyperaemia of iris which
• hamper its movements.

22. Changes in the lens
I. Pigment dispersal on the anterior capsule of lens
II. Exudates may be deposited on the lens
III.Complicated cataract may develop as a complication of persistent
iridocyclitis

23. Sequelae and Complications of Anterior Uveitis
• Secondary glaucoma: It is due to:
-Ring synechiae → seclusio pupillae → iris bombe → peripheral anterior
synechiae → secondary angle closure glaucoma
-Albuminous aqueous blocking the angle. Associated trabeculitis and
trabecular edema.
Phthisis (atrophic) bulbi: It prolonged cyclitis → ciliary body atrophy →
less secretion of aqueous → atrophic bulbi

24. Investigations
• Routine hemogram
• Serological tests: Antinuclear antibody (ANA); rheumatoid factor (RF); HLA-
typing; Venereal disease research laboratory (VDRL) and fluorscent
treponemal antibody absorption (FTA-ABS) (for syphilis); ELISA, etc.
• Skin tests: (a) mantoux test (tuberculosis) (b) kveim test (sarcoidosis)
• X-ray (a) chest—for tuberculosis and sarcoidosis (b) joints—arthritis group
• Gallium scan: For sarcoidosis z Urine culture: Urethritis z Anterior
chamber paracentesis for polymerase chain reaction (PCR) to diagnose
organisms and cellular analysis

25. • Gallium scan: For sarcoidosis
• Urine culture: Urethritis
• Anterior chamber paracentesis for polymerase chain reaction (PCR)
to diagnose organisms and cellular analysis

26. • Distinguishing features between acute conjunctivitis, acute
iridocyclitis and acute congestive glaucoma

27. Treatment
A. Local therapy
1. Cyclogenic drugs
Most effective during acute phase of iridocyclitis.
Commonly used drugs is 1% atropine sulfate eye ointment or drop
instilled 2-3 times a day.
2. Corticosteroid
Reduced inflammation.
Used in allergic type of uveitis.
Eye drop – 4-6 times a day
Eye ointment - bed times
Anterior sub – tenon injection in severe case

28. B. Systemic therapy
1. Corticosteroid
- When applied systemically plays definite role in non-granulomatous
iridocyclitis
- DOSE - high dose of prednisolone (60- 100 mg) or equivalent quantities
and other steroid is given.
- In absence of acute disease, alternate day therapy regime should be chosen.
- Dose of steroids should be decreased by a week’s interval because it has
many side effect like steroid induced glaucoma and cataract.
2. Non-steroidal anti-inflammatory drugs (NSAIDS)
- Aspirin are used when steroid are contraindicated.
- Phenylbutazone and oxyphenbutazone can be used in uveitis associated with
rheumatoid disease

29. 3. Immunesuppressive drug
- Only used in extremely serious cases of uveitis.
- Are dangerous and should be used with great caution.
C. Physical therapy
a. Hot fomentation – can be done by dry heat or wet heat , increase
circulation diminishes pain and reduces venous stasis.
b. Dark goggles – feeling of comfort, reduces photophobia, lacrimation.

30. SPECIFIC TREATMENT
• Treat the disease associated to it.
• Treat the complication like glaucoma, cataract, retinal detachment,
phthisis bubli etc .

31. INTERMEDIATE UVEITIS
• Intermediate uveitis refers to inflammation involving pars plana of
ciliaris, peripheral retina, choroid and vitreous base.
• The exact cause is still not clear. It is thought to be due to some
immunological reactions at the pars plana and outer layers of the
peripheral retina.
• Known causes (15% cases) include tuberculosis, syphilis, sarcoidosis,
Lyme disease and multiple sclerosis.

32. Clinical Features
1.Age: Second to fourth decade.
2. Sex: It can affect either sex.
3. Laterality: It usually bilateral (80%).
Incidence: In 5–15% of all uveitic patients.
Symptoms:
Floaters and blurring of vision
Pain, photophobia and redness are absent

33. Signs
Anterior segment signs
• Eye looks white and quiet.
• Anterior segment may or may not show signs of minimal activity in
the form of:
• Low-grade flare and cells,
• Few KPs
• Lens may show complicated cataract in late stages

34. Posterior segment signs
• Vitreous cells and vitreous flares.
• Snowball or cotton ball opacities (Ant's eggs) refers to typical
exudates present near the ora serrate in the inferior quadrant.
• Snow banking, i.e. grey white fibrovascular plaque over the pars
plana.

35. Complications (Causes of Visual Loss)
• Complicated cataract
• Cystoid macular edema (CME)
• Vitreous hemorrhage
• Retinal detachment (tractional).

36. Treatment
• Mild cases are self-limiting, and do not require any treatment except
periodic observation.
• But, in moderate to severe cases (vision less than 6/12) or in the
evidence of CME, the treatment is: Sub-Tenon injection of depot
steroid every 2–3 weeks. systemic corticosteroids—oral prednisolone
(60 mg/day) for two weeks— then tapered off slowly. „
Cryotherapy—if
above treatment fails. Parsplana vitrectomy—if cryotherapy is
ineffective. Immunosuppressive agents, very rarely

37. POSTERIOR UVEITIS
• Posterior uveitis refers to inflammation of the choroid (choroiditis) and
sometimes inflammation is spreads to retina (chorioretinitis).
Etiology
• Infectious: Toxoplasmosis, tuberculosis, syphilis, etc.
• Autoimmune
• Idiopathic.
Symptoms
• Floaters: More with peripheral lesions.
• Impaired vision: Mainly with lesions involving the fovea and
papillomacular bundle.
• Photopsia i.e. sensation of flashes of light.
• Black spot floating in front of eye.

38. SIGNS
• No external sign is present except the KPs, which are seen on slit lamp
examination.
• Others signs may includes
1. Vitreous opacities
2. Patched of choroiditis
3. Vitritis
4. Cystoid macular oedema (fluid accumulation in the area of central
vision)

39. TREATMENT
Systemic steroids are the main line of treatment along with specific
treatment for causative disease.

40. Panuveitis:
It is the severe form of uveitis which involves the whole uveal tract.
Choroid+ retina Chorioretinitis
Localised Diffuse
Anterior Uveitis
Panuveitis

41. Common causes are as follows:
• Sympathetic ophthalmitis
• Vogt-Koyanagi-Harada syndrome
• Sarcoidosis
• Behcet’s disease.