DISEASES OF THE UVEA Prof Suhardjo, MD,M Biomed, Ophth

UVEAInflammation UveitisAnatomy classification:Anterior uveitis= iridocyclitisIntermediate uveitisPosterior uveitis=choroiditisPanuveitis=inflammation of the whole uvea

Epidemiology UveitisAdamantiades-Behcets syndrome, and VKH are more common in Japan than in Europe or the United State.Adamantiades-Behcets syndrome seems highly prevalent in Turkey and in China. Tuberculosis remains the main etiology of infectious uveitis in India, Indonesia. Viral uveitis is predominant in the Middle East and in France, followed by Toxoplamosis. Epidemiologic study in northern California: incidence rate 52.4/100,000 person-years.The incidence and prevalence were lowest in the pediatric age groups and highest in those over age 65, women was greater than that man.

Terminology base of: Standardization of Uveitis NomenclatureInactive: grade 0 cells (anterior chamber)Worsening activity: 2-step increase in level of inflammationImproved activity : 2-step decrease or decrease to grade 0Remission: inactive disease for> 3 months after discontinuing all treatments .

Clinical classification:Acute uveitis sudden symptomatic onset and persist for 6 weeks or lessChronic uveitis persists for months or years

Aetiological classificationExogenous uveitis external injury, invasion micro-organisms, other agents to uvea from outsideEndogenous uveitis microorganism, other agents within patient

Endogenous UveitisAssociated with systemic disease (ankylosing spondilitis)Infection bacteria (TB), fungi (candidiasis), viruses (herpes zoster), protozoa (toxoplasma), roundworms (toxocariasis)Idiopathic specific uveitis entities (Fuchs uveitis syndrome)Idiopathic non-spesific uveitis entities

Pathological classificationGranulomatousNon-granulomatous

Clinical Features of UveitisAnterior UveitisSymptomsPhotophobia, pain, redness, decreased vision, lacrimation

Sign: Limbus Ciliary injection

Cornea : Keratic precipitates (KP)Small KP herpes zoster, Fuchs uveitis syndromeMedium KP most types acute and chronic uveitisLarge KP mutton fat granulomatous uveitisFresh KP white and round

Mutton fat KP

Iris nodulesKoeppe nodules Busacca nodules

Koeppe nodulesBusacca nodule

Anterior chamber: Aqueous cellsSign of active inflammationGraded from 0 to +4:5-10 cells = +111-20 cells = +221-50 cells = +3>50 cells = +4

Aqueous flareLeakage of proteins into aqueous humor through damaged iris blood vesselsFaint-just detectable = +1Moderate-iris details clear= +2Marked-iris details hazy= +3Intense-with severe fibrinous exudate= +4

Iris and Pupil : Posterior synechiaeAdhesions between the anterior lens surface and iris

Anterior vitreous cells

Other signs of anterior uveitisHypopyonFibrinPupillary miosisPigment dispersionSynechiaeBand keratopathy (seen in long-standing uveitis)

Intermediate UveitisSymptoms floaters, impairment of visual acuity caused by chronic cystoid macular edema

Sign Cell infiltration of the vitreous (vitritis), with few, if any, cells in the anterior chamber and no focal inflammatory lesion in fundus

Posterior UveitisSymptoms floaters and impairment of visual acuitySignVitreous change cells, flare, opacities and posterior vitreous detachmentChoroiditisRetinitisVasculitisThree main types:Unifocal (toxoplasmosis, onchocerciasis, cysticercus, Masquerade syndromes)Multifocal (ocular histoplasmosis,sypilis, HSV,VZV,CMV,Candida, Sarcoidosis, Masquerade )Geographical (CMV retinitis)

Laboratory and Medical Evaluation Fluorescin angiography; Indocyanine green angiopraphyUSG: vitreous opacities, choroidal thickening, retinal detachment, cyclitic membrane formation.OCT: to measure of uveitic CME.Anterior chamber paracentesis: Goldmann-Witmer coefficient is gold standard for diagnosis of Toxoplasmosis in Europe, PCR is valuable tool in case of viral uveitis or retinitis but less sensitive in diagnosing parasitic infecion.Vitreous biopsyChorioretinal biopsy

Complications of uveitisPosterior synechiae - 30%Cataract -20%Glaucoma due to PAS - 15%Iris atrophy .Band keratopathy - 10%

Therapy for Uveitis Medical : Steroid Immunomodulators: Alkylating agent, antimetabolite, T-lymphocyte modulators,biologic response modifier

Surgical

Uveitis associated with arthritisAnkylosing spondilitisIdiopathic, inflammatory arthritisIgM rematoid factor (-)HLA-B27Acute iritis

Ankylosing spondilitis

Reiters syndromeTriadUrethritisConjunctivitisSeronegative arthritisHLA-B27ConjuncvtivitisAcute iritisKeratitis

ConjunctivitisUrethritis and circinate balanitisKeratodermablenorrhagicaPlantar fasciitis Reiters syndrome

Juvenile Chronic ArthritisChildren before the age 16 yearsPolyarticular onsetArthritis > 5 joints20% 0f casesPaucyarticular onsetArthritis < 4 joints60% of casesAnterior Uveitis, chronic, non-granulomatous, bilateral in 70%

High risk factors for uveitis Girls Paucyarticular onset ANA HLA-DR5 Early onset

Adamantiades-Behcets DiseaseIdiopathic multisystem disorder, typically young men from eastern Mediteranian and Japan. Now many cases have found in Indonesia, Malaysia and China.HLA-B5 as risk factor .Uveitis , with:-Oral ulceration Apthous ulcersGenital ulcerationSkin lesionOther thromboplebitis, arthropathy, gastrointestinal, CNS, cardiovascular lesions

Uveitis in Adamantiades-Behet diseaseAcute iritisRetinitisDiffuse leakageOcclusive periphlebitis

Ocular feature:Recurrent, bilateral, non-granulomatous, intraocular inflammation.Acute recurrent iridocyclitis hypopionPosterior segment involvementDiffuse vascular leakagePeriplebitis RetinitisVitritisAtrophy of the optic nerve head blindness

Vogt-Koyanagi-Harada syndrome

Idiopathic multisystem disorder, typically affects pigmented individuals.Japanese, in whom the disorder is relatively common, increased prevalence of HLA-DR4 and DW15. Many cases have reported in china, Indonesia, Malaysia.Skin and hair change:AlopeciaPoliosisVitiligo

Neurologic feature:VertigoEncephalopathyAuditory symptomsMild meningitis with neck sitffnessOcular featureChronic granulomatous iridocyclitisPosterior segment involvement

Signs of Vogt-Koyanagi syndromeGranulomatous iridocyclitisAlopeciaPoliosisVitiligo

Sympathetic Uveitis

Rare, bilateral, granulomatous panuveitis which occurs after accidental penetrating ocular trauma or intraocular surgeryTraumatized eye exciting eyeDevelops uveitis sympathizing eyeClinical feature:Anterior segment: inflammation become chronic and severe, Koeppe nodule, mutton fat KP, posterior synechia

Posterior segment: small, deep, yellow-white spots corresponding to Dalen-Fuchs nodulesTreatment:EnucleationSteroid therapyImmunosupressive therapy

Sympathetic ophthalmitisBilateral granulomatous panuveitis Typically follows penetrating trauma Granulomatous anterior uveitis Multifocal choroiditis

Treatment of UveitisMydriatic-cycloplegic : sulfas atropine 1% eye drop/hour Steroid : topical, subconjunctival, intra vitreal, systemic.Cytotoxic drugs for chronic uveitis: azathioprin, chlorambucil, cyclosporin, cyclophosphamide

Diseases of the LENS

Eyeball

The Lens is a unique structureTransparent: no blood, no nerveHigher protein contentIt continues to grow throughout life. New fiber from just beneath the capsule, while the older fibers are compressed towards the centre of the lens

Ageing changes in the LensIncrease in hardness presbyopiaIncrease in density more dense (nuclear sclerosis), the power of the lens increases lens induced myopia.Increase in size shallowing of the anterior chamberIncrease in opacity: caused by biochemical damage of the delicate protein structure of the lens cells.

LENS DISORDERSAbnormalities of lens shapeColobomaLenticonusSmall lens

Coloboma Coloboma of iris Coloboma of choroid Giant retinal tearOcular associations

LenticonusPosterior Posterior axial bulge Unilateral - usually sporadic Bilateral - familial or in Lowe syndromeAnterior Anterior axial bulge Associated with Alport syndrome

Small lens Small diameter Small diameter and spherical May be familial (dominant)MicrophakiaMicrospherophakia Systemic association - Lowe syndrome Systemic association - Weill-Marchesani syndrome

Cataract =Opacification of the LensGeneral causes :age, diabetes, chronic renal failure, hypoparathyroidism, Downs syndrome, myotonic dystrophy, steroids, episodes of severe dehydration in early life (osmotic shock, severe dehydrationdamage the lens structure).Local causes: trauma, uveitis, glaucoma,myopia, radiation

Cataract backlog in IndonesiaPrevalence of cataract in Indonesia : 1.02%Incidence of cataract in Indonesia: 0.1%Population in Indonesia: 240.000.000Ophthalmologist surgical rate of cataract in Indonesia =200, should be 500 to avoid backlogTotal ophthalmologist in Indonesia : 1500

Why cataract is so much more common in hot climatesEpisodes of severe dehydration in early life (osmotic shock mechanism)Solar radiation:ultraviolet is absorbed by the lens causing damage to the tissue enzymes and protein molecules. Diet. : The poor people have a higher prevalence of cataract than rich people.Heat: glass-blower

Protective factorsAspirin low dose (100 mg) Vitamin CBendazac lysine

Symptoms of cataractDazzling , when opacity in the centre.Multiple images (ghosting, or polyopia) caused by poor refraction.Haloes, caused by opacity in the lens splitRefractive changes, progressive myopia from nuclear sclerosis .

Signs of cataractCortical lens opacities: the most common type of opacities.Nuclear sclerosis: lens hardens at first yellow, then brown, and finally black.Posterior subcapsular lens opacities: less common, often develop in quite young people.

ECTOPIA LENTIS1. Acquired2. Isolated familial ectopia lentis3. Associated with systemic syndromes Marfan syndrome Weill-Marchesani syndrome Homocystinuria 4. Treatment options

Acquired ectopia lentisTrauma Buphthalmos MegalocorneaAnterior uveal tumoursDegenerate eyeStretched zonules

Isolated familial ectopia lentisAutosomal recessivePupil may be normalPupil may be displaced in opposite direction (ectopia lentis et pupillae)

Autosomal dominantSystemic features of Marfan syndrome Limb-trunk disproportion Arachnodactyly Pectus excavatum High-arched palate Aortic dilatation, dissection and regurgitation Mitral valve prolapse

Homocystinuria Autosomal recessive Defect in cystathio beta-synthaseSystemic features Malar flush and fine, fair hair Marfanoid habaitus Increased platelet stickiness Mental handicapOcular features Downward lens subluxation Disintegration of zonule

CONGENITAL CATARACT In healthy neonates In unwell neonates2. Classification3. Causes1. Important facts

Causes of cataract in healthy neonateHereditary (usually dominant)IdiopathicWith ocular anomalies. PHPV Aniridia Coloboma Microphthalmos Buphthalmos

Causes of cataract in unwell neonateIntrauterine infections Rubella Toxoplasmosis Cytomegalovirus Varicella

Metabolic disorders Galactosaemia Hypoglycaemia Hypocalcaemia Lowe syndrome

Important facts 33% - idiopathic - may be unilateral or bilateral 33% - inherited - usually bilateral 33% - associated with systemic disease - usually bilateral Other ocular anomalies present in 50%

Classification of congenital cataractAnterior polarPosterior polarCoronaryCortical spoke-likeLamellarCentral pulverulentSuturalFocal dots

Anterior polar cataract May be dominant inheritanceCapsularPyramidWith persistent pupillary membraneWith Peters anomaly

ACQUIRED CATARACT Morphological1. Classification of age-related cataract According to maturity Diabetes Myotonic dystrophy Atopic dermatitis Trauma2. Other causes of cataracts3. Surgery Secondary (complicated) Large incision extracapsular extraction Phacoemulsification Drugs

Classification of Age-related Cataract According to Morphology1. Subcapsular Anterior Posterior2. Nuclear3. Cortical4. Christmas tree

Subcapsular cataractAnteriorPosterior

Nuclear cataract Exaggeration of normal nuclear ageing change Causes increasing myopia Increasing nuclear opacification Initially yellow then brownProgression

Cortical cataract Initially vacuoles and cleftsProgressive radial spoke-like opacitiesProgression

Classification according to maturityImmatureMatureHypermatureMorgagnian

Other causes of cataract - diabetesJuvenile White punctate or snowflake posterior or anterior opacities May mature within few daysAdult Cortical and subcapsular opacities May progress more quickly than in non-diabetics

Other causes of cataract - myotonic dystrophy Myotonic facies Frontal balding 90% of patients after age 20 years Stellate posterior subcapsular opacity No visual problem until age 40 years

Other causes of cataract - atopic dermatitis Cataract develops in 10% of cases between 15-30 years

Bilateral in 70% Frequently becomes mature Anterior subcapsular plaque (shield cataract) Wrinkles in anterior capsule

Causes of traumatic cataractPenetrationConcussion Vossius ring from imprinting of iris pigment Flower-shaped Ionizing radiation Electric shock LightningOther causes

DrugsChlorpromazine Long-acting mioticsOther drugs Amiodarone Busulphan- initially posterior subcapsularSystemic or topical steroids- central, anterior capsular granules

Secondary (complicated) cataract Chronic anterior uveitis High myopiaPosterior subcapsular Hereditary fundus dystrophies Central, anterior subcapsular opacitiesGlaukomflecken Follows acute angle-closure glaucoma

The treatment of cataract is SurgeryIntracapsular extraction : not popular now, impossible to intra ocular implantation.Extracapsular : the posterior capsule and suspensory ligament are left intact, IOL can be implanted.Small Incision Cataract Surgery: the most popular in India.Phacoemulsification : the most popular in the World

Complications of cataractAcute angle-closure glaucoma: a lens which is swollen makes anterior chamber more shallow.Phacolytic uveitis and glaucoma. Fluid lens protein leaks out through the capsule into anterior chamberacute uveitislens protein is ingested by macrophages and these block the anterior chamber angle phacolytic glaucoma

CATARACT

Anatomi Mata

Pengertian Katarak

proses kekeruhan lensa mata kebutaan yang bisa ditanggulangi indonesia : - penyebab kebutaan no.1 - 1996 : 1,47% (3 juta penduduk) - tiap tahun tambah 200.000

proses kekeruhan lensa mata kebutaan yang bisa ditanggulangi indonesia : - penyebab kebutaan no.1 - 1996 : 1,47% (3 juta penduduk) - tiap tahun tambah 200.000

pembagian katarakkatarak senilis / ketuaan :- > 40 tahun- karena degenerasi2. katarak kongenital- sejak lahir- virus rubella3. katarak traumatika4. katarak komplikata :infeksi, dm

PENANGANAN KATARAK : Operasi : - Konvensional / Jahitan - Irisan kecil tanpa jahitan PHACOEMULSIFIKASI Setelah Operasi : - Kacamata + 10 dioptri - Langsung pasang lensa tanam Prosedur Operasi : - Bius lokal - Bius umum

PERSIAPAN OPERASI :

Pemeriksaan ahli penyakit dalam : DM, Jantung Pemeriksaan USG mata + ukur lensa Bius lokal : Tidak puasa

KEBERHASILAN OPERASI : Sangat tergantung kondisi kesehatan, kooperatif saat operasi Keadaan : DM, Hipertensi, Paska infeksi, Glaukoma dapat memperburuk Perawatan kebersihan paska operasi, batuk sangat penting

Kelainan Mata yang sering dianggap sebagai katarak oleh masyarakat :

PterygiumKekeruhan di KorneaKelainan Segmen Posterior mata dengan penurunan visus

Pterigium bukan katarakPertumbuhan jaringan fibrovaskular ke dalam kornea Bentuk segitiga pada daerah celah kelopak konjungtiva

Leukoma kornea bukan katarakKekeruhan kornea Mata tenangTerlihat iris koloboma jam 10Pasca iridektomi optik

Katarak ImaturUji bayangan iris Bayangan iris pada lensa keruh Terdapat uji bayangan iris positif pada katarak imatur

Katarak MaturKekeruhan lensa total Mata tenangPupil kecil dan dibesarkan dengan midiriatik

Katarak HipermaturKatarak MorgagniNukleus lensa (warna sedikit coklat) terletak di bagian bawah lensaTerdapat tanda penyulit glaukomaKornea keruhPupil lebar

Katarak HipermaturKatarak hipermatur dengan tanda glaukoma sekunderInjeksi siliarEdema korneaPupil lebarLensa keruh total

Penderita Katarak sering merasa silau siang hari terik atau malam hari bila terkena cahaya lampu dan nyaman pada kondisi remang-remang misalnya sore hari

Tetap mengeluh kabur walau sudah berulang kali ganti kaca mata

Penurunan Ketajaman PenglihatanSehat Katarak

Apa saja yang menyebabkan Katarak, dan bagaimana pencegahannya?Petambahan umurObat-obatan ( Kortikosteroid, Phenotiazine, Myotic, Amiodrarone)Trauma/kecelakaanRadiasi Infra merahSinar Ultra violetGangguan MetabolikNutrisi

Bagaimana Mengobati Katarak?Non OperatifOperatifEkstraksi Katarak Ekstra KapsulerFakoemulsifikasi

UVEITIS

UVEAInflammation UveitisAnatomy classification:Anterior uveitis= iridocyclitisIntermediate uveitisPosterior uveitis=choroiditisPanuveitis=inflammation of the whole uvea

Clinical Features of UveitisAnterior UveitisSymptomsPhotophobia, pain, redness, decreased vision, lacrimation

Sign: Limbus Ciliary injection

Cornea : Keratic precipitates (KP)Small KP herpes zoster, Fuchs uveitis syndromeMedium KP most types acute and chronic uveitisLarge KP mutton fat granulomatous uveitisFresh KP white and round

Mutton fat KP

CORNEAL ULCERS

Keratitis Superfisialis, radang epitel/ sub epitel dapat disebabkan oleh infeksi, keracunan, degenerasi, alergi sebagai titik-titik atau pungtata yang merata, infiltrat dibagian atas pada trakoma, dicelah mata pada keratitis sika, atau akibat sinar u v, dibag bawah pada blefarokonjungtivitis stafilokokus

Ulkus Kornea Bakteri : - Sentral ( stafilokok aureus, streptokokus, pneumokok, pseudomonas, moraxella ), yang karena stafilokok biasanya terlokasi, bila karena pneumokok ulkusnya menggaung disertai hipopion, pseudomonas cepat menimbulkan nekrosis dengan eksudat mukopurulen - Marginalis, biasanya karena stafilokok, ada kemungkinan karena reaksi hipersensivitas, ulkus kornea marginalis harus dibedakan dengan ulkus Mooren

- Pemeriksaan laboratorium dilakukan secara rutin pada ulkus kornea, catnya Gram / Giemsa, mediumnya agar darah, agar coklat atau sabouraud, sensitivity tes perlu dilakukanKeratitis Virus Herpes Simpleksa. Keratitis epitelialis, ( keratitis dendritika, keratitis geografika virus menyerang epitel basal

b. Keratitis metaherpetik atau pasca infeksi bentuk linear tidak teratur sehingga hampir sama dengan keratitis geografika, kesembuhan sangat lambat ( 8-12 minggu)c. Keratitis interstitialis virus putih seperti keju (nekrosis), ada radang limbus, harus dibedakan dengan keratitis krn infeksi sekunder atau jamurd. Keratitis diskiformis, kekeruhan bentuk cakram di parenkim kornea yang udem tanpa nekrosis

Keratitis virus Herpes ZosterInfeksi akut yang mengenai ganglion Gaseri, jarang bilateral, sakit saat awal, timbul vesikula pada kulit dahi, kelopak mata sampai ujung hidung, konjungtiva hiperemi, sensitivitas kornea menurunKeratitis JamurPetani, sukar sembuh, infiltrat abu-abu, kadang ada hipopion, gejala inflamasi berat dimulai dengan ulserai superfisial, disertai infiltrat satelit ditempat lain, ulkus meluas sampai endotel, tepi ulkus tidak teratur ( banyak karena Candida )

ENDOPHTHALMITIS

Endophthalmitis

- An inflammation reaction of intra ocular fluids or tissues caused by infection of microbial organism

Categories :

Post operative endophthalmitis (70%) * Acute onset* Delayed - onsetPost traumatic Endophthalmitis (25%)Endogenous

Incidence :

After ECCE: 0,072 %After Penetrating Keratoplasty: 0,11 %Secondary IOL: 0,3 %Glaucoma filtering surgery: 0,061 %Pars Plana Vitrectomy: 0, 051 % & 0,048%IVTA: 0,5 %Penetrating Trauma: 10,7 % (10FB) & 5,2 % (N10FB)

Spectrum of Causative Organism (AJO 2004; 137:38-42)

Chart3

78

11

8

78, 5%

8, 6%

11, 8%

Sheet1

Gram +Gram -FungiGram +Gram -Fungi

78,511,88,678118

Sheet1

0

0

0

Gram -11, 8%

Gram + 78, 5%

Fungi, 8, 6%

Sheet2

0

0

0

Sheet3

Spectrum of causative Organism (VES, 1995)

Chart1

63

4

18

13

63%

Sheet1

VES

Gram +Gram -No growthEquivocal growth

6341813

Sheet1

0

0

0

0

Sheet2

Sheet3

Spectrum of Causative Organism (AJO 2004; 137:38-42)

Staphylococcus Epidermidis: 27,8 % Streptococcus viridans : 12,8 % Other coagulase-negative staphylococci : 9.3% Staphylococcus aureus : 7.7% Propionibacterium acnes : 7.0%

Most Frequent Causative Organism Among Categories (AJO 2004, 137 : 38-42)

Acute onset post operative: S. Epidermidis (46,9 %)Delayed onset post operative: S. Epidermidis (22,7%)Delayed onset bleb-associated: fastidious gram rodsPost traumatic: S. Epidermidis (20 8%)

Clinical Presentation

Determined by :- Clinical category- The infecting organism- Severity- The duration since initiation of the infection

Prominent Symptoms Ocular discomfort/pain Reduced vision

Sign Marked intraocular inflammation with hypopion Chronic iridolytis Granulomatous KP

Clinical Presentation

Acute Onset Post Operative Typically 2-7 Days After SurgeryOcular discomfort and painMarked intraocular inflammation with hypopion * Lid edema, corneal edema, marked conjungtival congestion, fibrin in the AC

Chronic/delayed onset post operative : Months / years after surgery Chronic iridocylitis Granulomatous appearing KP Hypopion

Diagnosis :

- Clinical recognition- Microbiologic Confirmation

Obtaining specimen for microbiologic examination :

- Sample of aqueous :- Local anesthesia- Partial thickness keratotomy- 25 or 27 G needle attached to a tuberculin syringe- Aspirates 0,1 ml of aqueousVitreous specimen : Needle aspiration Vitrectomy biopsy procedure Part of a full therapeutic vitrectomy

Treatment

Goal: Retention of useful vision Consists of : Intensive antibiotic administrationThe use of anti-inflammatory therapyVitrectomy + antibiotic + anti-inflammatory therapy

Antibiotic Treatment :

Delivery: - Intraocular injection - Systemic administration - Periocular injection - Topical ApplicationAntibiotic Agent

Intravitreal injection of antibiotics

- Achieve high intraocular concentration- Should be performed early (at the time of diagnostic sampling)- Recommended antibiotic agent : * Vancomycin (1 mg in 0,1 ml) * Amikacin 0,4 mg/0,1 ml/gentamycin 0,1 mg in 0,1 cc- Repeated injection is not recommended

Sensitivities of various antibiotics

Gram +Gram -Vancomycin100 %Ciprofloxacin 94,2 %Gentamycin78.4 %Amikacin80,9 %Ciprofloxacin68,3 %Ceftazidime80,0 %Ceftazidime63,6 %Gentamycin75 %Cefazolin66,8 %

Topical antibiotics :

- EVS : - Vancomycin HCL 50 mg/ml - Amikacin 20 mg/ml - Smiddy (2005)- Vancomycin 50 mg/ml- Ceftalzidine50 mg/ml- Tobramycin9/14 mg/ml- Amikacin8 mg/ml- Gentamycin9/14 mg/mlEvery 1-4 hours

Costicosteroid Therapy

- EVS : - Dexamethason 6 mg in 0,5 ml sub conjunctivally - 1 % Predmisolone Acetate Topically - Predmisone, 30 mg 2 x a day orally- Smiddy (2005)- Dexamethason 0,4 m intravitreal- Dexamathason 4 mg sunbconjunctival

Vitrectomy :

-EVS : - Routine immediate vitrectomy not necessary in vision of hand movement or better - Stenberg, 2001- Aggressive immediate vitrectomy for :- Bleb associated endophthalmitis- Delayed onset endophthalmitis- Traumatic endophtahlmitis

Result of therapyDepend on :- Virulence of infecting organism (Pseudomonas, Basillus Sp, Staphylococci)- Severity and rapidity of clinical presentation (include VA)- The pressure of associated ocular damage

Treatment of fungal endophthalmitis :

- No need to inject antimycotics at the time of the initial vitreous sampling- If culture is + for fungal infection : * Amphoterican B 0,005 0,010 mg in 0,1 cc mikonazole 0,025 mg intravitreal * Subconjunctival mikonazole, 10 mg in 1 ml * Avoid the use of corticosteroid

Initial Therapy : Intravitreal antibiotics Antravitreal dexamethason (if onset is not delayed and fungal etiology is not considered) System antibiotics * Vancomycin 0,5 % mg 1 mg and ceftazidine 1 g every 12 hours (intravenous) or * Oral ciprofloxacin, 750 mg every 12 hours, gatifloxacin 400 mg

Orally

Topical

* Vancomycin 50 mg/ml alternatively with gentamycin 14 mg/ml or ceftazidime 50 mg/ml every hours* Topical procedure prednisolone acetate 1 % every 2-3 hours

Conclusion

Standard treatment for endophthalmitis- Intravitreal antibiotics- Systemic antibiotic- Vitrectomy

Endoftalmitis post trauma

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