UVEA

 UVEA

ANATOMY-

/LAYERS OF THE IRIS-

1.Anterior endothelium.

2 .Iris stroma

3. Smooth ms- Sphincter pupillae

                     -Dilator pupillae

4.Posterior  2 layers of epithelium

NERVE SUPPLY OF IRIS-

• Sensory- Nasociliary N
• Sphincter pupillae- III N
• Dilator pupillae- Sympathetic chain

Q. Which is the safe zone of the eye ?

A  Pars plana- as it is avascular

Avascular struc in eye-cornea,lens,pars plana,vitreous.

MAJOR ARTERIAL CIRCLE-

Formed by- 2 Long posterior ciliary As + 7 Anterior ciliary As

CHOROID- 3 layers of BVs-

1. Outer- large vessel layer of Haller
2. Middle-medium vessel layer of Sattler
3. Choriocapillaries

   CHOROID- layers-

1. Suprachoroidal lamina
2. Stroma-Haller’s layer & Sattler’s layer
3. Choriocapillaries
4. Bruch’s membrane

BRUCH’ MEMBRANE-layers

1. BM of RPE
2. Inner collagen layer
3. Middle elastic layer
4. Outer collagen layer
5. BM of choriocapillaries

MUTTON FAT KPs-

• Tb
• Leprosy
• Fungal
• Syphillis
• Sarcoidosis
• Sym oph
• VKH syn
• Toxoplasm

TRANSILLUMINATION DEFECTS-

• Peri-pupillary- PXF
• Mid-peripheral-PDS
• Diffuse- Albinism, Senile iris atrophy
• Sectorial- Herpes zoster iritis, Iris prolapse in phaco

CLASSN OF UVEITIS-

a) ANATOMICAL

1.Anterior- Iritis

                -Ant. Cyclitis

                -iridocyclitis

2.Intermediate-Post cyclitis

                      -Pars planitis

                      -Hyalitis

                      -Basal retinochoroiditis

3.Posterior-Choroiditis-Focal

                                   -Multifocal

                                   -Diffuse

                - Chorioretinitis

                -Retinochoroiditis

                -Neurouveitis

4.Panuveitis

b) CLINICAL-

Acute- < 3 wks

Chronic > 3 wks

c) PATHOLOGICAL-

GRANULOMATOUS UVEITIS [type-IV hypersens]	NON-GRANULOMATOUS UVEITIS / EXUDATIVE
Insidious onset & chronic course	Acute onset & short course
Nodules [Koeppe,s & Bussaca,s ]	No nodules
Mutton fat KPs [lymphocytes derived from the aqueous]	Fine KPs [lymphoid cells & polymorphs]
Mild flare	Intense flare
Ant uvea & retina- choroid equally inv	Mainly limited to ant  uvea
Tb,leprosy,sarcoidosis	Idiopathic & allergic
Minimum inflammation	Exudative

c) AETIOLOGICAL CLASS-

1. Infective-

-Exogenous- D/t introd of org into eye thru a perforating wound/ulcer [ usually acute iridocyclitis & suppurative type]

-Endogenous-Other organ of body→bld cir→eye

-Secondary inf-Spread from other ocular tiss-cor,sclera,retina

\-…

BACTERIAL-             VIRAL-                PROTOZOA-

• Tb                           * Mumps                * Toxoplasma
• Syphillis                  * Smallpox
• Gonorrhoea              * Influenza
• Brucellosis

2. Immune-mediated

Prim source of inf→spread thru bld stream→eye gets sensitized→renewal of activity→org/proteins meet the sensitized tiss→excite an immune response→deposition of immune complexes

3. Hypersensitivity to autologous tiss-

• Still’s dis
• SLE
• Weg gr
• Sarcoidosis
• Ankylosing spond
• Reiter,s dis
• Behc\et,s syn
• RA

4.NEOPLASTIC

• RB
• Iris melanoma
• Reticulum sarcoma
• Leukemia                      →
• Lymphoma                    → + uveitis→ Masquerade syn    
• Histiocytic cell sarcoma→

5.TRAUMA-

Blunt

Perforating

Surgery- Cataract

• Trab
• VR surg

     INVESTIGATIONS  IN  UVEITIS

1] HAEMATOLOGICAL-

1 ) Hb ,TLC, DLC, ESR-

Important wen antimetabolites are to be started

2) CD4 / CD8  lymphocyte ratio- 2.0

Single best predictor of imminent opportunistic inf in AIDS

In AIDS ratio reverses [ 0.5-1]

CD4 > 400/cmm

CD8- 200-800 /cmm

2] IMMUNOLOGICAL –

1) RF- Seropositive  arthropathy- rare cause of uveitis

        -Seronegative  -     “     -     - JRA & Anky spond

2) Antinuclear antibodies-

*  Detected by Immunofluorescence / ELISA

*  Positive in- SLE & JRA

3) Anti DNA antibodies- SLE

4)  Antineutrophilic Cytoplasmic antibodies (ANCA)

    - Wegener’s Granul

    -PAN

5)  Angiotensin converting enzyme (ACE)

  Raised in – Sarcoidosis

• DM
• Leprosy
• Hyperthyroidism
• Chr renal dis
• Cirrhosis
• Amyloidosis
• Tb

6. Serum Globulin –Raised in Sarcoidosis
7. Serum Lysozyme-          “
8. Serum C-reactive protein-non-specific

3] SEROLOGICAL TESTS-

For toxoplasmosis-

1. Sabin Feldman dye test
2. Haemagglutination test
3. Indirect Immunofluorescent test
4. ELISA

For Syphiilis

1. FTA-ABS [fluorescent treponemal antibody absorption ]
2. VDRL
3. Rapid plasma reagin

4] RADIOLOGICAL TESTS-

*  X-ray skull- Congenital Toxoplasmosis

*  Chest- Sarcoidosis- Bil Hilar LNpathy

            -Tb

            -Malignancy

* Sacro-iliac & spinal- Anky spond

* Gallium scan- Sarcoidosis

5] HLA typing-

*  Behcet- HLA B5

*  Ank spond- HLA B27

*  Reiter’s – HLA B27

*  Birdshot retinochoroidopathy- HLA A29

* Sympathetic oph- HLA A11

* VKH –HLA DR4 & HLA DW15

6] SKIN TEST-

1. Tb – Mantoux

2. Histoplasmosis- Histoplasmin test

3. Sarcoidosis- Kweim test

4. Behcet- pathergy test & dermatographism

7] USG-

-To  reveal retinochoroidal thickening & exud RD in-

*  VKH

*  sympathetic oph

-To rule out longstanding RD ,IO tum or coat’s dis

-useful in parsplanitis

8] FFA

*  To confirm diagnosis of chorioretinitis

* Detect- cystoid / non-cystoid macular edema

            - dye leakage

            -SRNV

*  Any case of ant uveitis / intermed uveitis with unexplained visual loss must be investigated with FA to r/o CME

*  assess response to t/t

8] DIAGNOSTIC INVASIVE PROCEDURES-

1. paracentesis-

-To detect org by direct exam or culture

-Microscopic study to r/o-RB

                                       - leukemia

-Biological enzyme- aqueous ACE is more sensitive than ser ACE in sarcoidosis

--PCR in Herpes

2. Vitreous aspiration /biopsy

Ind- Uveitis not responding to t/t

     -Infection

     -Ocular reticulum cell sarcoma

     -Phacoanaphylactic uveitis

3. Retinal /retinochoroidal biopsy-

Ind- Bil lesion threatening ARN

    -No response to t/t in retinochoroidal lesion

Complication-

• Choroidal h’age
• RD
• PVR
• Inf

KERATIC PRECIPITATES-

• Def- Cellular deposits on the cor endothelium
• Nutrition of the cornea affected→ cells become sticky & desquamate at places.Exud tends to stick here forming KPs
• Derived from the uvea
• Wander in the aqueous by convection current & stick to cor endothelium
• Mutton fat KPs- Granul uveitis
• Fine KPs- Fuch’s uveitis

                       -herpes zoster uveitis

* Fresh KPs-white,round & dome shaped

* Old KPs-Flatter, smaller,crenated & pigmented.Ground-glass appear

Arlt’s triangle-KPs are arranged in a base down triangular area at the lower part of the cor

AQUEOUS CELLS-[2mm height,1mm width] by Hogan

GRADE	CELLS PER FIELD
0	0
1+	5- 10 cells
2+	10-20 cells
3+	20-50cells
4+	> 50cells

AQUEOUS FLARE-

GRADE	FLARE
0	Absent
1+ [faint]	Barely detectable
2+[mild]	Iris & lens details visible
3+[mod]	Iris & lens details hazy
4+[intense]	Fibrinous aqueous

Aq flare is d/t scattering of light [Tyndall effect] by proteins that have leaked into the aq hum thru the damaged iris BVs.

In the absence of cells,aq flare is not indicative of active inflamn

IRIS NODULES-

KOEPPE’S NODULES- pupillary border

BUSSACA NODULES-away from pupil

Juvenile chronic arthritis + Acute anterior uveitis→

• RF- Neg
• ANA- Neg
• HLA-B 27 – positive

Juvenile chronic arthritis + Chronic anterior uveitis→

• RF- Neg
• ANA- Positive
• HLA-B27- low incidence

VIVA- Why do you get sluggish pupillary reaction in iritis?

1. Exudation → Iris becomes a water-logged sponge full of sticky fluid→ Impaired iris movts→ so sluggish / abolished reac
2. Irritants in the extravasated fluid cause the muscle fibres to contract→ sphincter overcomes the dilator→ pupil constricts

In acute iritis ,pain is typically worse at night

Inv oph div of V n

Refers to forehead & scalp,cheeks,malar bone,nose & teeth

PLASMOID AQUEOUS-

Aqueous contains leucocytes , flakes of coagulated protein & fibrin

PLASTIC IRITIS-

Exudates poured out by iris & CB cover  the iris surface as a thin film & also the pupil.When this becomes profuse,iritis is k/as plastic

                MASQUERADE SYNDROME

DEF-Simulation of an inflame condition by a neoplastic process

Conditions that prod MS-

1} Primary central nervous system lymphoma-

 *  vitreitis

*    Creamy yellow retinal,subretinal & subRPE infiltrates

*    cranial n palsies

2} B cell lymphoma-

-vitreitis

-retinal vasculitis

-necrotizing retinitis

-diffuse choroiditis

-hypopyon

3} T cell lymphoma-

-Ant uveitis

Vitreitis

-chorioretinitis

4} Mycosis fungoides-

-Ant uveitis

-vitreitis

-papilloedema

5} HTLV-I lymphoma-

-ret vasculitis

-CW spots

-vitreitis

-subreyt infilt

-CME

6}Hodgkin’s lymphoma

-AU

-CR

-papill

-periphlebitis

7] leukemia-

-IR H’age

-CWS

-Roth’s spots

-MA

-peripheral NV

-Exud RD

8] Uveal melanoma

-episcleritis

-AU

-PU

-Endophthalmitis

-Panophthalmitis

9]RB

-Lack of calcification

-AU

-Shifting white hypopyon

10]Juvenile xanthogranuloma

-Yellowish iris nodules

-heterochromia

-spontaneous hyphaema

11]Metastatic tum

-MC prim site-lung & breast

-Plateau shaped yellow posterior seg lesion with SRF

-iris nodules

                               CMV RETINITIS [d-05]

• MC opportunistic inf in AIDS
• Agent-ds DNA Herpes virus
• Transmission-inf body flds

-bld

-transplacental

-transplanted organ

C /F-

SYMPTOMS-

• Blurring of vision
• Floaters
• Scotoma
• Photophobia

INDOLENT RETINITIS-

• starts in the periphery
• progresses slowly
• mild granular opacification

FULMINATING RETINITIS-

• Dense ,white, geographical area of opacification
• Vasculitis
• Mild vitritis
• ‘Brushfire-like’ extension along ret BVs
• RD / consecutive OA

REGRESSION-

• Few h’ages
• Less opacification
• Diffuse atrophic & pigmentary changes

FACTORS AFFECTING VISION-

• Optic neuropathy
• Direct ON inv
• Retinitis at macula
• RD

FACTOR PREDICTING CMV DEVELOPMENT  IN AIDS-

Falling CD- 4 Count- 50 cells / ml

T/T     -[D-05]

1 .Ganciclovir-

A]  IV 10mg/kg BD for 14 days [induction]

          5mg/kg every 24 hrs          [ maintenance]

           S/E- neutropenia.[Rx-G-CSF ]

B]  oral 300mg daily

     Advantage- less neutropenia

                      -no central line sepsis

C] .Intravitreal Ganciclovir-

     Inj. 200-2000µg in 0.05-0.1ml once/ twice wkly

     Implant[vitrasert]- 1µg/hr

     Complication- VH

                           -RD

                           -Endophthalmitis

2 .Foscarnet-Iv Induction→ 90mg/kg BD for 2wks

                   -Maintainence→ 90mg/kg OD

S/E-1. Nephrotoxic

      2. Neurotoxic

3.Cidofovir- 5mg/kg once wkly for 2 wks &then every 2wks.

  S/E- nephrotoxic

  Given along with probenecid

PROGRESSIVE OUTER RETINAL NECROSIS            [D-04]

• 2nd MC inf in aids
• Varicella Zoster
• C/F- rapidly prog visual loss
• Initially UL ,later BL
• SIGNS-Multifocal, deep, yellow white ret infiltrates

               -Outer & peripheral ret

               -Min vitritis

               -Rapid confluence

               -Full thickness ret necrosis

               -Early macular inv

* Inv-PCR of vitreous

T/T-1) IV Ganciclovir 10mg/kg  BD for 14 days [induction]

                                  5mg/kg 24hrs [maintenance]

     2) –Foscarnet-90 mg/kg BD for 2wks [Induct]

                           -90mg/kg  OD

* Blindness d/t macular necrosis&Rd

3)-Vitrectomy + silicone oil tamponade & Relaxing retinotomy

        ACUTE RETINAL NECROSIS

• Necrotizing retinitis
• Biphasic-< 15 yrs- HSV 2

-older-HZV & HSV 1

  * twice MC in Males

C/F- Painful visual impairment

     -  floaters

SIGNS

• Ant granulomatous uveitis & vitritis-universal
• Peripheral periarteritis
• Multifocal, deep,yellow white ret infiltrates
• Gradual confluence→ full thickness ret necrosis
• Post pole spared.Therefore good vision
• Disc edema,choroidal thickness & ret h’ages

INV-

• Inv-PCR assay of aq & vit
• Complications- RD

                          -AION

                          -Ret vascular occlusion

T/T* Acyclovir Iv 10mg/kg for 14 days

Orally 800mg 5 times daily for 5 days

           * famciclovir 500mg Tds for 3 mo

           * Sys steroid

           * Aspirin for vas occln

           *argon laser for RD

           *silicone oil tamponade

                TOXOPLASMA   RETINITIS

• Obligate intracellular parasite
• Definitive host- cat
• Intermediate host- man & mice
• 3 forms- Sporocysts[oocysts]

-Bradyzoites

-Tachyzoites

* Toxon means a crescent

* LIFE-CYCLE-

Cat’s intestine→ Male + Female Gametocyte →Zygote→zygote becomes surrounded by an oocyst wall→oocyst gets excreted in cat’s faeces→infective form-contaminated hands→

                                            -undercooked inf meat→

                                            -bld transfusion/organ transpl→      

                                            -transplacental→        Human inf

                                            -raw milk→

Human intestine→oocyst wall digested by gastric enzymes→release of tachyzoites→proliferative form→multiply intracellularly→If good host response→tachyzoites transform into bradyzoites-predilection for-heart,ms,neural tiss& ret.

CLASSN-

1] Congenital

2] Acquired

3] Toxo in immunocompromised

CONGENITAL TOXO-

Classic triad- Retinochoroiditis

                   -cerebral calcification

                   -convulsions

Others-

-hydrocephalus

-microcephaly

-organomegaly

-Jaundice

-MR

-Incidence is more if acqd in III trim

-severity is more in I trim

ACQUIRED TOXO-

-subclinical & asymptomatic

-Fever

-LNpathy

-malaise

-maculopapular rash [spares palms & soles]

TOXO IN IMMUNOCOMPROMISED-

-Pneumonitis

-Myocarditis

-Encephalitis

-Necrotizing retinochoroiditis-sight threatening

OCULAR FEATURES-

SIGNS-

1. QUIESCENT- Healed lesion-Foci of chorioret atrophy &        scarring with pigmented borders.

                         -Bil

2.FOCAL RETINITIS-

- Satellite lesion- A solitary inflame focus with overlying vitreous haze adjacent to an old pigmented scar.

-‘Headlight in fog’-sev vitritis impairing fundus visualization

-vasculitis

-Detached post hyaloid face becomes covered with inflame ppts

-Jensen choroiditis-Papillitis [inflame of optic n hd] sec to juxtapapillary retinitis.

-Atypical lesions-immunocompromised indiv

                             -Bilateral

                             -multifocal

                             -Discrete foci/confluent areas of retinitis

                             -Pre-existing scars –nt [means newly acqd inf or dissemination from EO sites.]

INV-

1. Indirect immunofluorescent antibody test
2. Haemagglutination test
3. ELISA[Enzyme linked Immunosorbent Assay]
4. Sabin Feldman dye test-titer.1:16
5. Serial tests for immunoglobulins-IgG & IgM
6. Western Blot analysis
7. PCR
8. X ray skull-calcification
9. CT SCAN & MRI- lesions in corticomedullary junction & basal ganglia

10. FFA- early- hypofluorescence & late-hyperfluorescence

T/T-

INDICATIONS-

Immunocompetant –

• Lesion threatening the macula,PM bundle,ONH or major BV
• Very sev vitritis→vit fibrosis→ tractional RD

Immunocompromised-All lesions

Rx- C2 A2 PS

1. Clindamycin 300mg Qid for 3 wks
2. Sulphadiazine –loading dose-2g→1g Qid for 3 wks [S/E-stevenjohnson syn]
3. Pyrimethamine-loading dose-50mg→25-50mg daily for 4wks.[ shud not be used in AIDS ]
4. Co-trimoxazole- Trimethoprim-160mg + Sulphamethoxazole 800mg [960mg] Bd orally for 4-6 wks
5. Atovaquone 750mg TDS
6. Azithromycin 500mg daily on 3 successive days
7. Topical steroids
8. topical cycloplegics
9. Photo & cryo
10. PPV –for RD sec to vit traction

        FUCH’S UVEITIS SYNDROME

• Also k/as Fuch’s Heterochromic cyclitis

DEF-

• Chronic,
• Non-granulomatous
• Ant uveitis

EPID-

• Insidious onset
• Typically unilateral
• M=F
• 3rd -4th decade

• Symptoms-Gradual blurring d/t cataract

-Floaters

                        -Colour diff bet 2 eyes

* Signs-KPs-small,round , scattered,grey-white [Stellate KPs]

           -Faint flare

          -cells +2

          -vitritis & stringy opacities

          -Gonio-Amsler’s sign-fine ,radial ,twig like Vs in the angle                                                            

           Responsible for filiform h’age which dev on AC paracentesis opp the puncture site.

          -PAS

Iris signs-

• No post synechiae
• Diffuse stromal iris atrophy
• Loss of iris crypts
• Washed out appear
• Prominent radial iris BVs
• Post iris pigment layer atrophy-transillumn def
• Iris nodules
• Rubeosis iridis
• Mydriasis
•  Heterochromia iridis-affected eye is hypochromic & d/t disturbance of symp n supply which controls chromatophores

COMPLICATIONS-

• cataract
• glaucoma

T/T-

   1. Topical steroids

2.Post subtenon inj of triamcinolone acetonide

3.vitrectomy

4.Topical steroid & mydriatics are ineffective

Q- what are the complications of cataract surgery in Fuch’s ?

A-Pre-oper-Pupil does not dilate well d/t iris atrophy.

  -Peri-oper-Hyphaema d/t abnml iris Vs. [ Amsler’s sign ]

               PARS PLANITIS [j-07]

DEF- IO inflamn centered around ant vit, peripheral ret &pars plana

EPIDEM-

• Bimodal –young-5-15 yrs &old-20-40yrs
• M=F

AETIO  ( association)-

1. Sarcoidosis
2. MS
3. Lyme’s dis
4. Peripheral toxocariasis
5. Syphillis
6. Tb
7. Human T cell lymphoma virus

C/F-

• insidious &gradual
• Bil asymmetric
• Symp- blurring of vision

             -floaters

             -mild pain

             -photophobia

-red eye

SIGNS-

• Aq flare+2
• “spill –over” ant uveitis
• Post synechiae
• Vitritis-sine qua non
• Vit snowballs[ exud ]-inferior vit
• “snow Bank”-inflam exud accumulate over pars plana
• Periphlebitis
• CW spots & h’age rare
• CME d/t inflam & vit  traction
• NV-NVE,NVD,NVI
• Papillitis
• Subret exud adjacent to snowbank→serous RD
• Ret traction→ret tear→rheg RD/ retinoschisis
• RET traction→PVR or cyclitic memb formn

COMPLICATIONS-

• Band KP
• Post subcapsular cataract
• Sec glaucoma
• CME

INV-

1. complete bld count
2. Tests for sarcoidoses-

• chest x-ray-hilar LNpathy
• Raised ACE
• Ser lysozyme
• Ser Ca++
• Inorganic phosphorous
• Gallium scan-increased uptake

    3.Tests for Lyme,s dis-

    * Indirect immunofluorescence

    * ELISA

     4. Tests for syphyllis-

       -FTA ABS

       -VDRL

       -Rapid plasma reagin antibody test

     5.Tests for Tb-

        -montoux test

        -X ray chest

        -Sputum exam for AFB

     6. Tests for multiple sclerosis

         -MRI –periventricular plaques

    7..FA-CME- petalloid

            -dye leakage from inflamed Vs

            -Optic n hd staining

    8 .UBM- Exud / memb over pars plana

    9 .Pathology-

      * snowball opacities- epitheloid cell granuloma

       Snowbank-condensed vit,hyperplastic non-pigmented epith of    pars plana

10  .Immunopathological study-CD4/CD8

T/T-KAPLAN’ 4 STEP APPROACH- [j-07]

STEP 1→Post sub-tenon inj of methyl prednisone/triamcinolone acetonide 40 mg 0.1ml

If active & sev parsplanitis- oral steroids

STEP 2→Cryopexy

-Eliminates NV & ischaemic tiss

-Double freeze & Thaw tech

STEP 3→PPV

-Removes vit antigen,inflame cells & mediators

-Removes vit opacities

-Eliminates vit traction

STEP 4→Immunosuppressive therapy

-cyclophosphamide 1-2mg/kg before meals

-chlorambucil 2mg/ day orally

-azathioprine 1-3mg/kg/d orally

Cataract extraction in pars planitis-

• eye shud be quiet 3-6 mo prior to surg
• Topical steroid + periocular steroid + oral steroid→ ECCE+ PCIOL+PPV

D/Ds-1. Coat’s dis-UL

                             -intra-retinal angiomatosis

                             -Exud RD

                             -Vit flare is striking

2.Tumours- RB, MM

 These can disemínate into the vit & simulate PP

3. Fuch’s heterochromic iridocyclitis-vitris

                                                          -CME

                                                          -no snowbank

                                                          -stellate KPs

4. IOFB
5. Chr RD
6. Sarcoidosis
7. Lyme’s dis
8. Retinal vasculitis ( weg gr,behcet’)

                     RUBEOSIS IRIDIS   -viva

           [ IRIS NEOVASCULARIZATION-]

1. DR
2. CRVO
3. BRVO
4. RD
5. RB
6. Eale’s dis
7. Sickle cell RP
8. Coat’s Dis
9. Giant cell Arteritis

10.Aortic arch syn

11.Carotid A occlusion

12.CRAO

13.Retrolental fibroplasias

14.Carotid cavernous fistula

15.PHPV

16.Choroidal melanoma

17.Endophthalmitis

18.Open angle glaucoma

19.Trauma

20.Iris tumours

-Tiny tufts of BVs are seen over the papillary margin

-Complication- NVG

-T/T- PRP

MALIGNANT  MELANOMA-patho

EPIDEM-

• Light skinned
• Age-50 yrs
• Choroid-85%
• CB-9%
• Iris-6%
• Usually UL [L>R]
• Choroid-post pole-temporal

              MALIGNANT MELANOMA-CHOROID

MC prim IO malign in adults

STAGES-

1. symptomless
2. EO extension
3. Glaucoma
4. Metastasis

C/F-

• Asymptomatic-detected as a mass on routine o’scopy
• Circumscribed,elevated,round masses protruding into vit cavity
• Shape indicates extent-

• Choroid- globular/elliptical
• Bruch’s membrane-mushroom shaped/ collar-button

After Bruch’s memb has been perforated→Exud RD

• visual field defect- localized
• Intractable sec UL glauc

PATHOLOGY-            [D-05]

* origin-some say-neural crest cell

           -others say-mature melanocytes in the stroma of iris,CB -

& choroids

• Callender,s class-

1. Spindle A cell-Slender spindle shaped

                          -flattened nuclei

                          -devoid of nucleolus

                          -best prognosis

2.Spindle B cell-larger cells

                         -round/oval nuclei [plump nuclei]

                         -prominent nucleolus

                         -2nd best prognosis

3.Epitheloid cell-same as spindle B cell

                         -Eosinophilic cyto

                         -increased mitotic fig

                         -worst prognosis

4. Mixed cell-spindle + epitheloid

                     -intermed prog

5.Fascicular cell-‘Palisading’ / ribbon like arrangement in parallel rows

                         -spindle A/B cells

6.Necrotic-insufficient bld supply/autoimmune mech→necrosis→actual cell type cannot be recogonised

MODE OF SPREAD-

1. EO spread by perforating Vs & Ns
2. IO spread –rare
3. sys metastasis- liver & lungs

INV-

1. Medical-chest x-ray & LFT
2. Exam of other eye- PRIM MM ARE ALMOST ALWAYS UL
3. Indirect O’scopy-diff flat[ naevus] from elevated lesion

-melanomas>3mm can be diagnosed

                                   -shifting SRF-hallmark of exud RD

    

   4.3-mirror contact lens-

     * surface changes over tum-pigment

     * SRF

     *cystoid changes over sensory ret

      * dilated Vs within the tum

5.Transillumination-

   Dark shadow-pigmented tum

                        -dense h’age

   Transmit light-non-pigmented tum

                          -exud RD

                          -Solid Rd

6.Visual field defect-localised-

7.fundus photo-

  Serial photo-whether the lesion is enlarging

Stereoscopic photo-flat/elevated lesion

8.FFA-pinpoint foci of hyperfluorescence→depicts site of future break thru bruch’s memb

-‘Double circulation’-simultaneous visibility of choroidal & ret Vs in melanomas that hav perforated bruch’s memb

9. USG

* A-scan-location of mass

             -Ant surf spike-double peaked-1st peak-Ant ret surf

                                                             -2nd peak-Ant surf of mass

             -Jagged post surf spike-scleral infiltrtn

             -Increase in tum thickness by 0.5mm suggests tum growth

Diagnostic triad-low reflectivity

                         -solid consistency with no after-movt

                         -vascularity with fast spontaneous vertical spike motion

• B-scan-Dome shaped mass

              -mushroom if breaks BM

              -strong sound attenuation

              -acoustic hollowing[ quiet zone]

10.Radioactive P32 uptake test

Principle- Malignant cells b/o their higher metabolic activity will incorporate & utilize more of radioactive element than nml cells

-Used only once per pt

-C/I-preg

     -childn

     -polycythemia vera

11.CT Scan-

    * well-circumscribed lesion

    *hyperdense

    *extends into vitreous

    *extrascleral extn

     *size & extent of lesion

12.Colour coded Doppler

13.Carcinoembryonic antigen-increased in metastatic tum but not in prim choroidal tum

14.FNAB-C/I ed unless diag is clearly establd by other ancilliary test

T/T-

1. PHOTOCOAGULATION-

IND-

1. Small active tum located > 3mm from foveola,not overhanging disc margin
2. Active juxtapapillary tum 2-3mm thick located sup,inf or nasal to disc

TECH-

• 2 confluent rows around tum margin
• Spot 200-500µ
• Power-500-1000mW
• Time-0.5-1sec

COMPLICATION-

• sudden intraret/subret h’age
• Bruch’s memb perforation with melanin release

2.RADIOTHERAPY-

Gold radon seeds,co-60 plaques,Ru-196,radon gas encapsulated in gold,I-125,iridium-192

IND-

1.small melanomas which are growing or show activity

2.med & large tum with some salvageable vision

3.only useful eye

C/I→ 10mm thickness

    →15mm dia

• Enucleation shud be done

TECH-

1. Episcleral plaque RT-

35000cGy- tum base

800-10,000 cGy –apex

2. Charged particle RT-

  _Proton beam/Helium ion method

  -Beam encompasses the lesion plus 1.5mm of nml fundus

3. External beam RT

3.LOCAL RESECTION-

Penetrating partial sclerouveoretinovitrectomy [SURV]

OR partial lamellar sclerouveactomy

IND-

1.Ciliochoroidal melanoma < 4 clock hours of pars plicata

2.Choroidal mel < 15mm dia, centered near equator & growing

COMPLICATIONS-

1. Blding
2. cataract
3. ant seg ischaemia
4. Pre-ret /subret fibrosis
5. expulsive h’age
6. CME
7. RD

3. ENUCLEATION-

IND-

1.Tum producing visual loss,but is too large for local resection/RT.

2.Total RD/sec glauc

3.Tum invading ON

4. ORBITAL EXENTERATION-

IND-

1. Extensive EO inv
2. No sys metastasis
3. Orbital recurrence after enucleation

COMPLICATIONS-

1. Blding
2. # ethmoid bone
3. PO inf
4. sloughing of skin graft

   POOR PROGNOSIS-

1. Big size
2. Anteriorly situated
3. EO inv

                  COLOBOMA [J-07]-case

DEF- Developmental imperfect closure of the foetal fissure

Coloboma→Typical

                →Atypical

Typical- coloboma in inferonasal dirn

           -Genesis-overgrowth of inner layer of optic cup→eversion of lips of fetal fissure→obstrn of natural union bet the lips→failure of dev of retina & other struc

Typical C→. Complete

               →Incomplete

Complete-extends from pupil to ON

                 -Sector shaped defect occupying 1/8th of the circumference of ret & choroids,Cb & iris & causing a corresponding indentation of the lens where the zonules are missing.

Incomplete-When it stops short of ON or iris.

Typical col of iris-Pear shaped pupil

                           -Broad base towards pupil

                           -Extends upto CB

Atypical coloboma of iris-Foetal fissure closes before iris forms

                                       -occurs at any meridian

- - - - - - - - - - - - - ---- - - - -  - - - - - - - - - - - - - - - -  - - - - - - - - - -

HETEROCHROMIA IRIDUM-

Two irides show diff in colour

HETEROCHROMIA IRIDIS-

Part of the same iris shows diff in colour.

Heterochromia iridum may be –

HYPOCHROMIC-

1.Congenital

2.Horner’s [ IMP]

3.fuch’s uveitis [IMP]

4.Glaucomatocyclitic crisis

5.Amelanotic tum of iris

6.iris atrophy

HYPERCHROMIC-

1. Retained IO FB [siderosis][IMP]
2. Malignant melanoma of iris
3. Haemosiderosis [foll hyphaema]
4. Latanoprost

IRIDODONESIS-

1. Aphakia
2. Subluxated / dislocated lens
3. buphthalmos

PHTHISIS BULBI	ATROPHIC BULBI
Irregular shape	Quadrilateral
Foll-penetrating inj,panophthalm,endophthlm	Foll-iridocyclitis,absolute glaucoma
Ocular struc cannot be distinguished	Can be distinguished
Calcification/malignancy may be +nt	No such chance

                    STEROIDS

ACTIONS-

Reduce inflamn by-

• Decreasing capillary permeability
• Limiting exud
• Inhibiting NVs & granulation formn

ROUTES OF ADMINISTRATION-

1.Topical-

*  Dexamethasone acetate 0.1%

*   Betamethasone 0.1%

*   Prednisolone acetate 1%

2.Periocular inj-

Adv over topical-

-Therapeutic conc behind lens

-Water sol drugs incapable of penetrating the cor can enter trans-sclerally

-longlasting effect with depot prep [triamcinolone acetonide,methylpred acetate]

A] Ant subtenon’s-

-1ml steroid drawn up into a 2ml syringe

-ask pt to look away from the site of inj

Grasp the conj & tenon’s capsule with a non-toothed forcep

-with the bevel away from the globe,needle is passed thru conj & tenon’s

-0.5ml inj

B] Post-sub-tenon

-1.5ml is drawn into a 2ml syr with 26 G needle

-Ask the pt to look inferonasally wen inj is being given superotemporally

-Bulbar conj is penetrated with the tip of the needle,bevel towards the globe,along the contour of the globe with wide side to side motions & limbus is watched

-Movt of limbus means that sclera is engaged

-When the needle has been advanced up to the hub & cannot be inserted any further,inj 1ml

3] Intra-vitreal-Triamcinolone acetonide [2mg in 0.5ml]

                      -For resistant uveitic chronic CME

4] Systemic-

  Oral-T prednisolone 1mg/kg in tapering dose

  PULSED STEROID

  -This is high dose intra-venous steroid T/T

  -T- cells are affected to a greater extent than B- cells with a relatively greater depletion of helper / inducer sub-population

- Concn of lymphocytes returns to nml after 48 hrs

- A pulse steroid possibly resets an aberrant immune response by the simultaneous inhibition of the proliferating zone & temporary removal of recirculating T-cells from the bld &eye.

-Dose- 250mg QID [ 1gm] daily for 3 days-IV methyl pred f/b

          1mg/kg oral pred for 11days

-Ind- ocular- 1. Optic neuritis

                    2. Symp oph

                    3. VKH

                    4. TED

                    5. Pseudotum

                    6. Scleritis

Non-ocular-graft rejection-renal

5] Sustained release steroid implant-currently posurdex implant containing dexamethasone is under clinical trial.DOA-6wks

INDICATIONS OF STEROIDS-

1. Sterile ocular inflamn-

1] Disciform keratitis

2] episcleritis

3] scleritis

4] uveitis

5] optic neuritis

2. Allergic-

1] phlycten

2] VKC

3]allergic blepharoconjunctivitis

3. Post-oper

1] cat

2]KP

3] vitrectomy

4] trab

4. misc-endo exophthalmos

           -pseudotum

           -temporal arteritis

           -post-herpetic neuralgia

COMPLICATIONS-

A] LOCAL-

1] risk of superinfection

2]steroid induced glaucoma

3]steroid induced cat

4] delayed wound healing

5]corneal melting [d/t increased collagenase activity]

6]transient ptosis

7]transient myopia

8] mydriasis

9] papilloedema

B]SYSTEMIC

1] peptic ulcer

2] cushingoid facies

3] severity of diab

4] osteoporosis

5] electrolyte imbalance

6]mental changes

7] benign ICT

INTRAVITREAL STEROIDS-

IND-

1. DR
2. DME
3. venous occlusions
4. CME
5. PVR
6. endophthalmitis

Dose- 2mg/0.1ml

            IMMUNOSUPPRESSIVE AGENTS [D-02,j-07]-read from notes

A]  ANTIMETABOLITES-

1  AZATHIOPRINE-

*  Purine analogue

* Pro-drug of 6 mercaptopurine

*  affects the synthesis of nucleic acid & proteins

* Selective toxicity to T-helper/ inducer cells

IND-  Behcet’s

• SLE
• VKH
• Pars planitis
• Sympathetic oph

DOSE-  1-3mg/kg/day OD orally

S/E-1. BM suppression

2. GI disturb
3. Hepatotoxicity
4. Neutropenia
5. Sev nausea & vomiting
6. Infections
7. Stomatitis

Monitoring-1] Hematological parameters weekly for 1 mo,bimonthly for 3 mo & monthly thereafter

2]Ser transaminase & bilirubin

C/I- Preg & lactation

2.  METHOTREXATE-

*  Folic acid antagonist

*  Inhibits dihydrofolate reductase

* Both T & B cells are suppressed

*  Folinic acid is given concurrently

IND-1. Steroid resistant uveitis

2. Retinal vasculitis
3. Sympathetic oph
4. Cyclitis
5. Necrotizing scleritis
6. Iridocyclitis asstd with JRA

DOSE- 7.5-25mg single dose once wkly

S/E-1.BM toxicity.

2. GI sym
3. Pulmonary fibrosis

7. Hepatotoxicity
8. Pneumonitis
9. Stomatitis

10.Ocular-photophobia,tearing & irritatn

C/I-Preg ,lact,children

Monitor-

1. LFT every 6-8 wks

2. liver biopsy after an accumulative dose of 1.5gm is reached

3. Chest X-ray

3. MYCOPHENOLATE MOFETIL

DOSE- 1gm BD

S/E- 1. BM Tx

4. GI dist

B] T-CELL INHIBITORS

CYCLOSPORIN-

IND- 1. Behcet’s

        2. Parsplanitis

       3.  VKH syn

         4. Birdshot retinochoroidopathy

         5. Sympathetic oph

         6. Retinal vasculitis

DOSE-2-5mg/kg/d

S/E-1. HT

      2.  Nephrotoxicity

      3. Hirsutism

       4. Hepatotxicity

       5. Gingival hyperplasia

TACROLIMUS-

DOSE- 0.05-0.15mg/kg/d

S/E-1. Hyperglycaemia

5. neurotoxicity

CYCLOPHOSPHAMIDE-

• nitrogen mustard
• Interferes with cross-linking of cellular DNA→ Inhibits proliferation & replication of cells
• Suppresses only T- suppresser cell activity & enhances cellular immunity
• IND-Symp oph

          -Parsplanitis

          -Behcet’s

          -PAN

          -Weg gran

        

*  DOSE- 1-2mg/kg  before meal

C/I- Preg & lact

    -cautious in child

*  S/E-

1.myelosuppression

2. Sterility

3.Hemorrhagic cystitis

4. Risk of infection & neoplasia

5. Bladder fibrosis & carcinoma

6. Dry eyes

7. Rise in IOP

Monitor-Blood count

            -Urine analysis

CHLORAMBUCIL-

• Nitrogen mustard
• Slowest acting & least toxic of all nitrogen mustards
• Highly carcinogenic
• IND- Behcet [ DOC]

          -Sym oph

          -JRA

*  Dose- 2mg /day oral→ Increase 2mg/day every week

*  S/E-

1. Myelosuppression

2. sterility

3.alopecia

4.pulmonary fibrosis

5. seizures

C/I-preg & lact

Cautious in child

CYCLOSPORIN-

• Affects T-cell mediated responses & selectively inhibits T helper cell activation
• Inhibits interleukin 2-4 ,TNF & gamma interferon
• Available as a white crystalline powder,insoluble in aqueous.so dissolved in castor oil or olive oil with ethanol
• Dose- 5mg/kg`.Must be diluted with milk or orange juice before using orally
• Stored below 30deg C Do not refrigerate
• C/I preg & lact
• Caution in child & epilepsy
• IND-

1. Behcet
2. sym op
3. Birdshot retinochoroidopathy
4. Parsplanitis

5-FLUORORACIL-

*  Pyrimidine analogue

* Inhibits thymidilate synthetase & cell div

* Antiproliferative

IND-

Glauc filtering surg

DOSE-

-S/C  0.5ml of 10mg/ml

-cellolose sponge-50mg/ml

S/E-

1. Cor  epith defect
2. Wound leak

6.MITOMYCIN –C

MOA- Inhibits DNA ,cellular RNA & protein synthesis

IND-

1. Filtering surg -0.2mg/ml
2. pterygium excision-0.02% BD for 5 days

S/E

1. Scleral necrosis
2. hypotony
3. shallow AC
4. Choroidal detachment

   BROMOCRIPTINE-

Ind- Ant uveitis

Dose- 2.5mg 4 times /day oral

S/E- postural hypotension

COLCHICINE-

Ind- Behcet

Dose- 0.5-0.6 mg 2-3 times/ day oral

S/E- BM suppression

DAPSONE-

Ind-Cicatricial pemphigoid

Dose- 25-50mg 2-3 times /day oral

S/E- Haemolytic anaemia

          UVEITIS  IN JUVENILE RHEUMATOID ARTHRITIS

• Childhood arthritis [< 16 years]
• 3 mo duration
• 3 types-

	SYSTEMIC ONSET JRA[STILL’S DIS]	PAUCIARTICULAR JRA	POLYARTICUALR JRA
Systemic features	+	Mild / -	-nt
uveitis	Very rare	uncommon	Very common
RF	-	-	-
ANA	-	+	+
Joints	Rare	> 5	< 4

Uveitis-

• Chronic
• Unilat/BL
• Band keratopathy
• Fine KPs
• Flare & cells
• Posterior synechiae
• Cataract [Rx-lensectomy & ant Vtomy]
• Glaucoma

Joints inv- knee→ wrist→ ankle