The document provides information on the uveal tract, which consists of the iris, ciliary body, and choroid. It describes the anatomy, histology, and functions of each part of the uvea. Signs and symptoms of uveal inflammation/uveitis are discussed, including anterior uveitis characterized by pain, photophobia, cells and flare in the anterior chamber, and keratic precipitates. Chronic/granulomatous uveitis can cause nodules on the iris and chronic inflammation. Posterior uveitis may involve the choroid and retina without anterior chamber signs.

1. D R . M O H D N A J M U S S A D I Q K H A N
M S ( O P H T H ) D I S S O ( E S A S O )
Uveal Tract

2. UVEA
 Is the middle coat of the eye consists of iris, ciliary
body and choroid.
Iris--It is the anterior extension of the ciliary body. Its
anterior surface is divided by an irregular circular line
called collarette into a large ciliary and small pupillary
zones, it contains a round aperture (pupil) in the
middle. Histologically it consist of--
 Endothelium (continuous with corneal endothelium
and anterior limiting layer)
 Stroma (contains sphincter and dilator pupillae
muscles, vessels, nerve, pigment cells)
 Posterior pigment epithelium (continues with pigment
epithelium)
 Function-- controls amount of light entering the eye

3. Ciliary body--It extends from anterior end of choroid to the
root of iris about 6mm length. Grossly it consists of 2
zones, pars plicata (cornea ciliaris) which contains ciliary
processes (2 mm anterior) & pars plana smoother and
flatter ( 4 mm posteriorly). Histologically--
 Ciliary muscles (longitudinal, circular, radial fibres)
 Stroma (vessels, nerve, pigment cells)
 Basal lamina
 Epithelium--external pigment and internal non pigment,
both of which continues as pigment layer over posterior
surface of iris
 Functions--
 Aqueous secretion into posterior chamber
 Contraction and relaxation of zonule for near and far vision
(by ciliary muscles contraction (accommodation)

4. Choroid--The posterior portion of uvea and it lies
between sclera and retina. It extends from the
edge of optic nerve posteriorly to ciliary body
anteriorly at ora serrata. Highly vascular and
consists mainly of blood vessels. The largest
vessels are nearer to sclera while smallest vessels
(choriocapillaries) are towards retina being
separated from retinal pigment epithelium by
Bruch s membrane.
 Suprachoroid is on either sides of stroma--
avascular layer of collagen and elastic fibres.
 Function--nutrition of outer part of retina

5. Signs and symptoms of uveal diseases--Depends on site
of uvea affected
 Pain, redness, visual loss, floaters
 Iritis---pain, photophobia
 Iridocyclitis---ciliary injection, pain
 Most diseases of ciliary body---disturb accommodation
 Inflammation of choroid---no ciliary injection, no pain if
affect retina--- interfere with vision
 Pupil distortion in anterior uveitis
 Release of cells and protein in the anterior chamber (iritis)
and vitreous cavity (choroiditis)
 Keratic precipitates (Kps) in iridocyclitis
 Ophthalmoscopically chorioretinal involvement in
choroiditis

6. Congenital and development anomalies--
 Coloboma iridis--failure of complete iris development
(in 6 clocks and bilateral)
 Aniridia--failure of anterior growth and differentiation
of optic disc ---- rudimentary iris, iris not visible, black
cornea, 60% is autosomal dominant inheritance.
 Albinism--patient with photophobia and myopia
 Heterochromia iridis--the 2 irises different in colour
 Iridocorneal endothelial syndrome---glaucoma, iris
atrophy, abnormal corneal endothelium. P.A.S, multiple
iris nodules, transparent membrane covering anterior
surface of iris.
 Rubeosis iridis--neovascularization of the iris occur as
irregularly, distributed networks of new vessels on
surface and stroma of iris and they may cover
trabecular meshwork, peripheral anterior synechae
formation, angle closer glaucoma, more common in
diabetics, intraocular tumours.

7. Inflammation of Uvea (Uveitis)
Iris Ciliary body Choroid
Iritis Cyclitis Choroiditis
Iridocyclitis
(Anterior uvitis ) (Posterior uveitis)
Classification
Anatomical classification—
 Anterior uveitis— iritis and iridocyclitis
 Intermediate uveitis—pars planitis
 Posterior uveitis—choroiditis and chorioretinitis
 Panuveitis
Clinical classification—
 Acute (for 3 month or less)
 Chronic (more than 3 months)
 Recurrent
 Healed uveitis (no sign of inflammation)
Others classify uveitis—
 Granulomatus (chronic)
 Non granulomatus (acute)

8. Aetiological classification---
 Idiopathic–25-30% of cases
 Infections---either exo or endogenous
 Exogenous--introduction of microorganisms after
perforated wound or ulcer
 Endogenous--spread of infection from other site in the
body
 Bacterial (T.B, Syphilis)
 Viral (mumps, herpes, influenza)
 Parasites (Toxoplasma, malaria)
 Fungal (candidiasis)
 Allergy--delayed bacterial allergy to T.B
 Autoimmune (sympathetic ophthalmia)
 Trauma--after contusion or surgery

9. Secondary to ocular pathology--
 Suppurative keratitis, scleritis, retinitis
 Hyper-mature cataract
 Orbital cellulitis
 After extra-capsular cataract extraction
 Dislocated lens
 Intraocular tumours
 Intraocular haemorrhage
Secondary to systemic diseases—sarcoidosis, T.B, Crohn s
diseases, behcet s disease, ulcerative colitis, Vogt–
Koyanagi syndrome, Still disease, rheumatoid arthritis,
Reiter syndrome
Malignant tumours (masquerade syndrome)
Sinusitis, otitis media, tonsillitis
Specific HLA type (B-27 in acute anterior uveitis, B-5 in
behcets disease, DW-22j in VKH syndrome)

10. Acute uveitis (non granulomatous)--mostly anterior
uveitis, non suppurative, recurrent inflammation of
uveal tract characterized by oedema, capillary
dilatation, exudation of inflammatory cells (PMN,
Lymphocytes, plasma cells)
 Onset is acute, marked pain, photophobia, blurred
vision (symptoms are severe)
 Ciliary injection, fine Keratic precipitates, exudation in
to A.C, posterior synechiae
 No nodules on iris
 In most cases it affects anterior uvea but posterior
uvea (choroid) is rarely affected
 In acute uveitis---retinal oedema without exudation,
fine opacities in vitreous
 Generally idiopathic in nature

11. Chronic uveitis (granulomatous uveitis)--
 Progressive inflammation of uveal tract associated
with cellular infiltration by chronic inflammatory cells
(macrophages, mononuclear, epithelioid cells) with
fibrosis
 Onset is insidious and anterior or posterior uvea or
both may be affected
 In anterior uvea involvement---minimal signs of
inflammation and minimal pain, photophobia, blurred
vision, slight ciliary injection or none, mutton fat
Keratic precipitates.
 The eye is relatively white
 In post uvea involvement---slight retinal oedema with
exudation, heavy vitreous opacities, heavy choroidal
exudation
 T.B, sarcoidosis and leprosy

12. Signs and symptoms of uveitis
Anterior uveitis--
Symptoms—
 pain, photophobia
 Lacrimation (marked in acute phase, minimal or absent in chronic
phase)
 Blurred vision (more severe in chronic phase)
Signs--
 Ciliary injection--due to dilatation and congestion of anterior
ciliary arteries supplying iris and ciliary body (must be able to
distinguish it from conjunctival injection). In acute phase it may
be associated with episcleral and conjunctival injection and it is
absent or slight in chronic uveitis.
 Exudation in anterior chamber--the inflammatory process
release prostaglandins---break down blood aqueous barrier
(BAB)---increase protein fibres and inflammatory cells in aqueous
 Increase protein cause--aqueous flare and in the absence of
cells it is not indicative of active inflammation. It can be graded
as faint +1, moderate +2, marked (iris details hazy) +3 and
intense with fibrinous exudates +4.

14.  The aqueous cells are sign of active inflammation
and graded by 3mm long and 1 mm wide slit beam
as <5 cells +/-, 5-10cells +1, 11-20 ceels +2, 21-
50 cells +3 and >50cells +4.
 Inflammatory cells adhere to posterior surface of
cornea causing Keratic precipitations (K.Ps) and due
to toxic inflammatory reaction the endothelial cells
of cornea shed off---precipitate inflammatory cells
increase on posterior lower surface of cornea
 The 2 types of K.Ps occur--Small fine white
punctate accumulations of lymphocytes and plasma
cells in acute phase. Large heavy greasy
composed of macrophages, phagocytes pigment
called mutton fat K.Ps in chronic phase.
Occasionally in acute anterior uveitis so many
inflammatory cells present that a (hypopyon) forms
A.C.

19.  Macrophages appear as nodules at pupillary
margin k/a koeppe nodule and on the surface of
iris k/a Basacca nodule (less common) and on
lens surface
 In anterior chamber angle---- OAG as in
phagolyitc glaucoma of lens
 In acute phase--oedema of iris---constriction or
mid-dilation of pupil blurred or muddy iris
 In chronic phase--nodules due to proliferation of
iris pigment epithelium or infiltration of iris with
macrophages---granulomatus nodules---iris
atrophy (floccules of Busacca)

22.  Posterior synechiae--Adhesion between iris and lens---cause pupil to
be small irregular constricted non reactive to light (complete or partial)
 Ring or annular synechiae—causing seclusion pupillae and iris
bombe
 Total posterior synechiae
 Peripheral anterior synechiae
 Constricted pupil (miosis)--due to toxin and irritation of iris
sphincter muscles contraction leads to constriction of pupil and
sluggish or non reacting pupil or irregular festooned pupil after
dilatation
 If posterior synechiae involves whole pupillary margin then aqueous
humour cannot flow from posterior to anterior chambers leading to
pupillary block (occlusion papillae)---iris bombe---2ry glaucoma
 Lens changes—
 Anterior surface pigmentation
 Complicated cataract with polychromatic lusture and bread crum
appearance
 Cyclitic m embrane behind the lens

25. Intermediate uveitis/pars Planitis/chronic cyclitis — it is
due to some immunological reaction at the pars plana and
outer layers of the peripheral retina. It is an idiopathic,
insidious, generally bilateral (80%) inflammatory disease of
pars plana, peripheral retina and underlying choroid. 10-15%
patients develop multiple sclerosis due to common HLA-DR
15. The symptoms are floaters and impairment of visual
acuity in young adults of either sex in 2-4th decade of life and
the signs are
 Some signs of anterior uveitis
 Vitritis showing snowballs, cotton balls or sheet like
opacities with a few cells in the anterior chamber
 Peripheral retinal periphlebitis
 Greyish white plaque like snowbanking involving inferior
pars plana
 Absence of focal lesions in the posterior fundus
 Complications are cystoids macular oedema, cyclitic
membrane formation, secondary cataract and tractional
retinal detachment

28. Posterior Uveitis (usually chronic form)—the symptoms
are floaters and impaired vision. The important signs are
 Vitreous flare, cells, opacities---occur because of
exudation of inflammatory cells and protein rich fluid with
RBC and this appears as black dots ( more intense in
chronic phase)
 Posterior hyaloids phase may be covered by
inflammatory precipitates
 Choroiditis—active lesions appear as greyish white or
greyish yellow area with ill defined borders surrounded by
normal fundus (with ophthalmoscope) while inactive lesions
appear as white well defined atrophic areas with pigmented
borders.
 Retina is nearly always involved (retinitis)---retina
oedematous, opaque, obscuration of retinal vessels
 Vasculitis—involving retinal veins (periphlebitis) more in
comparisons to retinal arteries (periarteritis)
 Spill over anterior uveitis is common

31. Classification of posterior uveitis—
 Focal—toxoplasmosis
 Multifocal—birdshot retinochoroidopathy
 Geographical—cytomegalovirus retinitis
Diagnosis of uveitis--
 History--symptoms, any systemic disease
 Clinical exam--ophthalmic exam for red eye, KPs,
vitreous clouding aqueous flare
 General exam for systemic disease
 Lab exam--important in non responsive uveitis to
treatment chronic uveitis trying to find the etiology
 Skin tests for T.B, histoplasmosis
 Test for syphilis, toxoplasmosis, rheumatoid arthritis
 X-rays

32. Treatment of uveitis--
Anterior Uveitis—
 Treat the cause of known (T.B, Sarcoidosis)
 Mydriatics and cycloplegics like long acting atropine 1% (up to 2
weeks) drops or ointment or short acting like cyclopentolate 24
hours, tropicamide 6 hours and phenylephrine (no cycloplegia) 3
hours which will produce dilation of pupil to prevent posterior
synechiae and relaxation of ciliary muscle will relief pain caused by
its spasm.
 Systemic steroids like oral prednisolone or I/M injections of ACTH
 Topical corticosteroids like betamethesone, dexamethasone,
prednisolone e. d. and eye ointment
 Subconjunctival /anterior or posterior subtenon injections of
dexamethasone/prednisolone/triamcinolone
 Nonsteroiddal anti-inflammatory drugs if steroids are
contraindicated
 Local hot compresses 4 times/day and dark goggles.
 Analgesics if needed
 Immunosuppressive agents antimetabolites like azathioprine 1-3
mg/kg/day in Behcets disease, methotrexate 7.5-25 mg single
dose once/week, mycophenolate mofetil 1 gm b d and T-cell
inhibitors like cyclosporine 2-5 mg/kg/day, tacrolimus (FK-506)
0.05-0.15 mg/kg/day

33. Intermediate uveitis—Mild cases are self limiting, in
severe cases--
 Topical corticosteroid
 Sub tenon injection of depot steroids every 2-3 weeks
 Systemic steroids for 2 weeks then tapering
 Rarely immune suppressive agents
 Cryotherapy if above treatment fails
 Pars plana vitrectomy
Posterior uveitis--
 Treat the cause
 Atropine 1%
 Posterior sub tenon injection of long acting steroids
 Intravitreal injection of triamcinolone is under
evaluation
 Systemic corticosteroids

35. Treatment of complications--
 Iris bombe--LASER iridotomy
 2ry glaucoma--decrease corticosteroids
 Systemic carbonic anhydrase inhibitor
 Local timolol, epinephrine
 Surgery for synechiae ,trabecular meshwork damage
 Cataract--surgery if vision is poor
 Phthisis bulbi--enucleation of eye if painful
and still infected

36. Complications of uveitis--
Formation of synechiae--
 Anterior (decrease aqueous out flow at angle of A.C---
Glaucoma)
 Posterior (occlusion of pupil by organized exudates causing
adhesion of pupillary borders to lens (occlusion pupillae)---
increase pressure behind iris---iris bombe---2ry angle
closure angle
Change in IOP (2ry Glaucoma)--In the early stage uveitis
cause hypo-secretion of aqueous humour and decrease IOP.
But later on IOP becomes high due to--
 Inflammation or occlusion of trabecular meshwork by
inflammatory cells and protein (OAG)
 Topical corticosteroids in genetically susceptible person
causes resistance of aqueous out flow from AC (OAG)
 Posterior synechiae causes pupillary block---prevent passage
of aqueous from posterior to A.C---Iris bombe---2ry angle
closure glaucoma (ACG )
 Peripheral anterior synechiae (between iris and cornea)---
2ry angle closure glaucoma (ACG )

37.  Pseudoglioma--due to vitreous exudation
 Band shaped keratopathy—more in children with juvenile
rheumatoid arthritis and chronic iridocyclitis
 Keratitis and keratopathy--Cornea can be affected in uveitis due
to histological contraction. Keratitis-–damage to corneal
endothelium, vascularization of cornea, deposition of KPs, band
keratopathy (calcium deposition in Bowman s zone)
 Phthisis bulbi—in severe uveitis---atrophy of ciliary body---no
aqueous humour secretion--–shrinking of eyeball
 Cataract—it is due to interference with lens metabolism---
posterior sub-capsular cataract. In severe cases anterior and
posterior sub-capsular cataract
 Retinal detachment (traction detachment)—it is due to fibro-
vascular proliferation after exudation in vitreous causes traction of
sensory retina. Severe effusion from uveal tract causes elevation of
retina
 Cystoid macular oedema--Capillaries of central retina become
abnormally permeable---oedema of posterior pole
 Macular ischaemia, epiretinal membrane formation
 Choroidal neovascularisation
 Consecutive optic neuropathy

38. Differential diagnosis of uveitis--
 Acute conjunctivitis--normal vision, gradual
onset, normal pupillary responses, normal
iris, slight pain, conjunctival (not ciliary)
injection
 Acute angle closure glaucoma--sudden
onset, increase IOP, marked decrease vision,
pupil mid dilated, no posterior synechiae,
steamy cornea
 Acute iritis
 Ulcerative keratit

39. Suppurative uveitis
It is the inflammation of uvea with pus formation. The
causes are staphylococci, proteus, pseudomonas,
bacillus subtitis, and fungi. Organisms introduced
into eye after--
 Accidental injury or surgery penetration wound
 Rupture of corneal ulcer
 Through filtration bleb in glaucoma surgery
 Endogenous cause--Septic emboli in bacterial
endocarditis, meningococcemia, bacteraemia,
Viraemia, fungaemia
 After urologic surgery
 Spread from adjacent structure--Orbital abscess,
Pharyngeal phycomycosis

40. Types--
A)Endophthalmitis--Suppurative inflammation of
intraocular contents, starts in uveal tract then some other
tissues are 2ry affected.
Clinically--
 Severe pain, photophobia, diminution of vision,
 Lacrimation, red tender oedematous lids, chemotic
conjunctiva with mixed (conjunctiva and ciliary) injection
 Hazy cornea with KPs, muddy iris (pus in vitreous, yellow
reflex)
 Cloudy vitreous, fundus not seen clearly
 Cloudy aqueous
 Decreased IOP
 No Proptosis
 No restriction of ocular movement
 Ultimately no perception of light (PL –ve)

41. Complications--
 Panophthalmitis
 Retinal detachment
 Shrinking eyeball
Treatment of endophthalmitis--
 Aqueous and vitreous tap with gram stain, KOH
preparation, culture for bacteria and fundus
 Intra-vitreal injections of gentamicin / vancomycin /
ceftazidime / amikacin / amphotericin-B, dexamethasone
 Antibiotics (local, subconjunctival injection, systemic)
 Systemic antifungal drugs like ketoconazole/fluconazole
 Systemic corticosteriods
 Pars plana vitrectomy in some case if medical treatment
fails to control within 48-72 hours
 If eye still infected, blind, painful then enucleation

42. B)Panophthalmitis--Suppurative inflammation of all parts
of the eye.
Clinically--
 Same symptoms as endophthalmitis but more severe
 Same signs as endophthalmitis with--
 Restriction of ocular movements
 Corneal necrosis (hypopyon, corneal abscess)
 Proptosis
 Finally shrinking of eyeball (phthisis bulbi)
Treatment—
 Systemic and local antibiotic
 Systemic corticosteroids
 If no cure then evisceration--removal of contents of eye
ball leaving the sclera around optic nerve to avoid opening
of meninges which can cause fatal meningitis
 So Enucleation is contraindication in panophthalmitis, fear
of spread of infection along sheaths of optic nerve to brain
and causing meningitis

43. C)Lens–induced uveitis--An autoimmune disease
2ry to lens antigens liberated in hyper-mature
cataract or traumatic rupture of lens capsule.
Lens material passes into A.C causing an
inflammatory reaction.
D)Endophthalmitis phacoanaphylactica--More
severe form of lens induced uveitis and occurs
after extra-capsular lens extraction where the eye
become sensitive to its own lens material left
behind in the operation, causing Ag–Ab reaction.
Phacolytic glaucoma is a common complication of
lens induced uveitis
 Treatment--Removal of all lens material and
local corticosteriods

44. Sympathetic ophthalmia (sympathetic uveitis)
Very rare diffuse granulomatus bilateral panuveitis which
may occur 10 days to years after perforating eye injury
or intraocular surgery (very rare).
 Cause is unknown may be autoimmune response to
uveal pigment. The injured (exciting) eye becomes
inflamed first then the fellow (sympathizing) eye
becomes inflamed within 3 months of injury in most
cases.
 65% cases between 2 weeks and 3 months after initial
injury and 90% cases within 1 year after trauma.
Pathology--
 It is an auto immune reaction to antigens in the uveal
tissue, uveal pigments and retinal antigens.
 Nodular aggregation of lymphocytes and plasma cells
in the uveal tract
 Pigment cell of uveal tissue proliferates with epitheloid
cells and macrophages to form Dalen-Fuchs nonules

45. Symptoms and signs--
 In sympathising eye pain, photophpbia (1st symptom),
difficult accommodation
 In exciting eye pain, irritation, redness
 Signs in exciting eye ciliary congestion and traumatic
injury
 Signs in sympathising eye retrolental flare(1st sign),
signs of granulomatous uveitis, posterior fundus shows
yellow white Dalen Fuchs nodules, perivasculitis, retina
oedema, multifocal choroiditis and optic disc swelling.
Treatment--
 In case of severe injury blind eye---immediate eye
excision to prevent sympathetic uveitis within 2 weeks.
 If inflammation appear in fellow eye---local steroid,
atropine, systemic corticosteroids (80-100 mg/day) or
cyclosporine

46. Toxoplasmic uveitis--Toxoplasmosis is caused by Toxoplasma
gondi a protozoon parasite (cat is definitive host). There are
two clinical types--
 Congenital--due to intrauterine infection (more severe)
 Acquired--infection in later life (ingestion of oocyst)
Clinically there is chorioretinitis which appear in early stage as
white elevated masses covered by hazy vitreous. In congenital
toxoplasmosis chorioretinitis, convulsions and
calcification (3 Cs)
Symptoms and signs—
 Visual loss due to media opacities, cystoids macular oedema,
maculopapillary bundle or fovea or optic disc involvement
 In most patient bilateral healed choriretinal scars detected in
later life
 Occasionally anterior uveitis
 Severe vitritis and focal necrotising retinitis
 papillitis
 In late stage--punched out pigmented chorioretinal lesion

50. Complications--
 Cystoids macular oedema
 Sub retinal neovascularisation
 Tractional retinal detachment
 Retinal and choroidal atrophy and loss of vision
Diagnosis--
 Dye test (Sabin–Feldman)
 ELISA for toxoplasmic antibody
 Indirect fluorescein test
Treatment--
 Sulphonamides (2 gm loading dose then 1 gm q i d)
 Clindamycine orally 300 mg q i d for 3 weeks
 Pyrimethamine 100 mg loading dose then 25 mg qid
(Daraprim). It is given with 10 mg/day folinic acid

51. Heterochromatic uveitis (Fuchs s iridocyclitis)--
Inflammation of anterior uvea with pigmentary changes in
iris. There is non granulomatus anterior uveitis with insidious
onset and generally unilateral in middle aged adults.
 Unknown cause
 Iris and ciliary body show atrophy but posterior synechiae
typically absent
 Eyes are of different colour
 Enlarged pupil (mydrasis) due to atrophy of sphincter
pupillae
 Insidious onset
 No synechiae--so no mydriatic is needed
 Fine Kps scattered throughout the entire corneal
endothelium
 flare and cells in A.C
 fine neovascularisation of iris (rubeosis iridis) and angle
(Amsler sign)
 Vitreous opacities
 No symptoms until complicated cataract develops--blurred
vision
 Glaucoma may also occur
Treatment—topcal corticosteroids and cataract surgery

57. Uveitis associated with
spondylarthropathies
Anklyosing spondylitis (AS)— it is a chronic
inflammatory arthritis of unknown aetiology, affecting
mainly sacroiliac joint and axial skeleton. Males only
affected (20-40 yr) where in females it has benign
course. More than 90% of patients carry the histo-
compatibility antigen HLA – B27
Ocular manifestations--
 Acute unilateral non granulomatus iridocyclitis
 Dusting on corneal endothelium then small white KPs
 Usually acute course < 6 weeks
Diagnosis :_
 X-rays (Sacroiliac joint)
 Tissue typing for HLA – B27

58. Reiter s syndrome—It is defined as an episode of
peripheral arthritis of more than one month duration. There
is triad of
Urethritis/cervicitis
Conjunctivitis bilateral mucoprulent
Arthritis (seronegative )
 70% of patients show HLA-B27 and males more affected
 60% of patients have associated sacroiliitis
 The aetiology is unknown but some patients are presented
with previous bacillary dysentery or previous venereal
diseases gonococci and joint problem.
 Other less common features are keratoderma of palm and
sole, nail dystrophy.
Ocular manifestation--
 Conjunctivitis (mucopurulent)
 Keratitis (punctate, sub-epithelial)
 Iridocyclitis (unilateral acute non granulomatous anterior
uveitis in 20% of patient at 1st or recurrent attacks)

60. Psoriatic arthritis—affects 7% patients with
psoriasis and associated with HLA-B27 & B17
 Anterior uveitis—acute/chronic
 Conjunctivitis
 Keratitis
 Secondary Sjogren syndrome

61. Uveitis in Juvenile (rheumatoid
arthritis) still disease
 It is a inflammatory arthritis of at least 6 weeks duration in
children before 16 years of age. Patients are seronegative for
IgM rheumatoid factor. 20% of patients develop a chronic
bilateral (in 70%) non granulomatus iridocyclitis. The female
are more affected.
 In most cases the onset is insidious; the disease discovered
only when child noted to have difference of colour of two
eyes, difference in size, shape of pupil or strabismus.
Clinically—
 Eye is typically white (white iritis)
 Band keratopathy, white medium sized KPs
 Posterior synechiae very common
 Hypopyon does not develop even in acute phase
Complications--
 Complicated cataract
 2ry glaucoma
 Band shaped keratopathy is very common

64. Sarcoidosis-- Chronic granulomatus disease of unknown cause
characterized by multiple cutaneous and subcutaneous nodules with
similar invasion in viscera
 Onset > 30 yr
 Tissue reaction < T. B
 No caseation
 If parotid gland affected---uveo-parotid fever (Heerfordt s disease)
 If Lacrimal gland affected---Mikulicz s syndrome
Clinically—in 30% of cases chronic bilateral anterior uveitis (less
commonly posterior uveitis)
 Anterior uveitis nodules may lead to cataract and 2ry glaucoma,
papilloedema, optic atrophy
 In posterior uveitis--multiple yellow retinal exudates--snow ball
floaters, occasionally severe periphlebitis (candlewax drippings),
BRVO, choroiditis with granuloma, optic disc granulomas, peripheral
retinal neovascularisation & palsy of extraocular muscles
Diagnosis--
 Chest x rays showing bilateral hilar lymphadenopathy
 Skin biopsy of nodules
 Kveim test
Treatment--corticosteroids
In case of sarcoidosis in acute stage unilateral eye and in chronic
stage bilateral eye involvement

70. Behcet s disease--Idiopathic multi-systemic disease, common
in young (3-4th decade) men of Middle East, mediterranean
region and Japan. + ve for HLA–B5. Present theory is
obliterative vasculitis caused by abnormal circulating immune
complex
Clinically--
 Recurrent oral ulcer
 Genital ulcers 90%
 Skin lesions (erythema nodosum, pustules, ulcers)
 70% bilateral non granulomatus iridocyclitis or sometime
posterior uveitis
 Conjunctivitis, keratitis, episcleritis, transient hypopyon,
posterior uveitis, retinitis, retnal vasculitis, massive retinal
exudation, vitritis
 Less common--- thrombophlebitis, cerebral ivolvement
(meningioencephalitis)
 Poor visual prognosis due to phthisis bulbi
Treatment--
 Topical and systemic steroids
 Oral chlorambucil

75. Vogt-koyanagi-harada (VKH) syndrome—it
is a idiopathic, bilateral, granulomatous severe
panuveitis associated with cutaneous (alopecia,
vitiligo, poliosis), neurological (headache,
convulsion, cranial nerve palsy) and auditory
(tinnitus, vertigo, deafness) involvement.
 More in japaneese with HLA-B 22j
 Bilateral serofibrinous granulomatous
iridocyclitis
 Multifocal exudative choroiditis
 Exudative retinal detachment
 Optic neuritis in some cases

79. AIDS and uveitis—ocular complications occur in
75% patients of AIDS patients.
 The lesions are retinal micro-vasculoangiopathy
with cotton wool spots and superficial and deep
haemorrhages
 Kaposi sarcoma of eye lids and conjunctiva. It
appears as bright red mass
 Opportunistic infectios--like CMV retinitis
(commonest), herpes zoster ophthalmicus,
candida endophthalmitis, toxoplasma
retinochoroiditis, herpes simplex infection,
molluscum contagiosum of lid

84. Toxocariasis—it is caused by toxocara canis and cati
which are common intestinal worms of dog and cat.
Human infected by accidental ingestion of
contaminated soil or food (usually children between 2-
9 years)
Clinically--
 Choroidal granuloma
 Macular oedema
 Mild anterior uveitis
 Chronic endophthalmitis with vitreous clouding
 Retinal detachment
 Cataract severe cyclitic membrane
 Granuloma in fundus
 Diagnosed by ELISA
Treatment--Majority of cases come late so no effective
treatment (thiabendozole, pars plana vitrectomy)

89. Tuberculous uveitis--T.B cause a granulomatus
uveitis (rare 1%). It is in the form of
chorioretinitis
Clinically--
 Hazy vitreous
 Yellow exudates on retina
 If anterior segment involved--iris nodules, mutton
fat KPs
Treatment--
 Systemic anti–Tuberculous drugs & Atropine 1%

91. Tumours--
a) Melanoma benign (naevus)—flat or slightly elevated
lesions less than 3 disc diameter and generally asymptomatic
b) Malignant melanoma-- most common primary intra ocular
tumour in adults affecting choroid (vision may 6/6). Average
age being 50 years, more in males and its always unilateral
Clinically divided into 4 stages—
Quiscent stage
Glaucomatous stage
Stage of extra ocular extension
Stage of metastasis
 Decrease vision defects in visual field
 C A Glaucoma
 Ophthalmoscopically appears as solitary unilateral brown
pigmented mass with choroidal folds, sub retinal and vitreous
haemorrhages
 Cataract and posterior uveitis
 Spread to orbit
 Metastasis to liver

92. Investigations—
 General examination, liver function test, X-ray chest
 Indirect ophthalmoscopy
 Fundus photography
 Fluorescein angioscopy
 A & B-scan(ultrasound)
 CT & MRI
Differential diagnosis—
 Rhegmatogenous retinal detachment
 Metastatic tumour of choroid
 Choroidal haemangioma
 Large chorpidal naevus
 Choroidal detachment

93. Management—
 Observation for small and slow growing tumours, age
more than 65 years, with liver metastasis
 Enucleation for very large melanoma when vision loss
is irreversible
 Radioactive sclera plaques of cobalt 60 for medium
sized melanoma
 Heavy charged particle irradiation (proton or helium)
 Photocoagulation with xenon arc or argon laser for
small tumours away from fovea
 Choroidectomy (local resection) but very difficult
 Palliative therapy with chemotherapy or
immunotherapy for cases with distant metastasis