Uploaded byDr Mohd Najmussadiq Khan
Uveitis
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.
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Uveitis
- 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 themiddle 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 extendsfrom 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 portionof 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 symptomsof 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 developmentanomalies-- 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 ocularpathology-- 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 (nongranulomatous)--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 (granulomatousuveitis)-- 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 symptomsof 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 aqueouscells 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 appearas 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--Adhesionbetween 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/chroniccyclitis — 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 (usuallychronic 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 posterioruveitis— 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-- AnteriorUveitis— 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 casesare 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-- Formationof 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 tovitreous 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 ofuveitis-- 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 isthe 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 intraocularcontents, 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 Retinaldetachment 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 ofall 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 autoimmunedisease 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 (sympatheticuveitis) 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 iscaused 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 macularoedema 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 (Fuchss 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 Anklyosingspondylitis (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—Itis 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 granulomatusdisease 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--Idiopathicmulti-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 isa 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—ocularcomplications 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 causedby 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 causea 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 forsmall 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