Kanski’s

Clinical Ophthalmology
Sebuah rangkuman oleh seorang calon PPDS
Table of Contents
Index.........................................................................................................................................................................................................4
Color Coding........................................................................................................................................................................................4
Abbreviation.........................................................................................................................................................................................4
Examination Technique............................................................................................................................................................................5
Psychophysical test...............................................................................................................................................................................5
Perimetry..............................................................................................................................................................................................6
Eyelids......................................................................................................................................................................................................7
Anatomy...............................................................................................................................................................................................7
Non neoplastic lesion...........................................................................................................................................................................7
Benign epidermal tumours...................................................................................................................................................................7
Benign pigmented lesions....................................................................................................................................................................7
Benign adnexal tumours.......................................................................................................................................................................7
Miscellaneous benign tumours.............................................................................................................................................................7
Malignant tumours...............................................................................................................................................................................7
Disorders of the eyelashes....................................................................................................................................................................7
Allergic disorders.................................................................................................................................................................................7
Immune related inflammation..............................................................................................................................................................7
Bacterial infection................................................................................................................................................................................7
Viral infections.....................................................................................................................................................................................8
Blepharitis............................................................................................................................................................................................8
Ptosis....................................................................................................................................................................................................9
Ectropion..............................................................................................................................................................................................9
Entropion..............................................................................................................................................................................................9
Miscellaneous acquired disorders......................................................................................................................................................10
Cosmetic eyelid and periorbital surgery.............................................................................................................................................10
Congenital malformation....................................................................................................................................................................10
Lacrimal Drainage System.....................................................................................................................................................................11
Anatomy.............................................................................................................................................................................................11
Physiology..........................................................................................................................................................................................11
Causes of a watering eye (Epiphora)..................................................................................................................................................11
Evaluation...........................................................................................................................................................................................11
Acquired obstruction..........................................................................................................................................................................12
Congenital Obstruction.......................................................................................................................................................................12
Chronic Canaliculitis..........................................................................................................................................................................13
Dacryocystitis.....................................................................................................................................................................................13
Dry eye...................................................................................................................................................................................................14
Mechanism of disease........................................................................................................................................................................14
Classification......................................................................................................................................................................................14
Clinical Features.................................................................................................................................................................................15
Investigation.......................................................................................................................................................................................15
Treatment............................................................................................................................................................................................16
Sjögren disease...................................................................................................................................................................................17
Conjunctiva............................................................................................................................................................................................18
 Anatomy.............................................................................................................................................................................................18
Histology............................................................................................................................................................................................18
Glaucoma................................................................................................................................................................................................19
Aqueous production...........................................................................................................................................................................19
Aqueous outflow................................................................................................................................................................................19
Intraocular pressure............................................................................................................................................................................19
Ocular hypertension...........................................................................................................................................................................19
Glaucoma............................................................................................................................................................................................19
Secondary glaucoma...........................................................................................................................................................................24
Uveitis....................................................................................................................................................................................................26
Classification......................................................................................................................................................................................26
Clinical Feature..................................................................................................................................................................................26
Investigation.......................................................................................................................................................................................26
Treatment............................................................................................................................................................................................26
Immunomodulatory therapy for non infectious uveitis......................................................................................................................26
Fuchs Uveitis Syndrome....................................................................................................................................................................26
Uveitis in Juvenile Idiopathic Arthritis..............................................................................................................................................26
Uveitis in Bowel Disease...................................................................................................................................................................26
Uveitis in Renal Disease.....................................................................................................................................................................26
Vogt-Koyanagi-Harada (VKH) Syndrome........................................................................................................................................26
Sympathetic Ophthalmitis..................................................................................................................................................................26
Lens induced Uveitis..........................................................................................................................................................................26
Sarcoidosis..........................................................................................................................................................................................26
Behçet disease....................................................................................................................................................................................26
Parasitic Uveitis..................................................................................................................................................................................26
Viral Uveitis.......................................................................................................................................................................................26
Fungal Uveitis....................................................................................................................................................................................26
Bacterial Uveitis.................................................................................................................................................................................26
Misc. Idiopathic Chorioretinopathies.................................................................................................................................................26
Retinal Detachment................................................................................................................................................................................27
Introduction........................................................................................................................................................................................27
Innocuous peripheral retinal degeneration.........................................................................................................................................27
Definitions..........................................................................................................................................................................................28
Ultrasonography.................................................................................................................................................................................28
Peripheral lesions predisposing to retinal detachment.......................................................................................................................28
Posterior vitreous detachment............................................................................................................................................................30
Retinal break.......................................................................................................................................................................................31
Rhematogenous retinal detachment....................................................................................................................................................32
Tractional retinal detachment.............................................................................................................................................................35
Vitreous opacity.....................................................................................................................................................................................36
Introduction........................................................................................................................................................................................36
Perdarahan vitreous............................................................................................................................................................................36
Asteroid Hyalosis...............................................................................................................................................................................36
Synchesis scintillans...........................................................................................................................................................................36
Amyloidosis........................................................................................................................................................................................37
Vitreous cyst.......................................................................................................................................................................................37
Persistent fetal vasculature.................................................................................................................................................................37
Index
Color Coding
Orange: Sub-bab
Yellow : Penting
Green: Do
Blue: Don’t

Abbreviation
AC: Anterior Chamber
Ant.: Anterior
Conj/konj.: Conjunctiva
DD: Disc Diameter
Degen.: Degenerative
Det: detachment
Hmrrg: haemorrhage
HSx: Herpes simplex
IO: Intra Ocular
Inj: Injeksi
IVit: Intra Vitreous
LD: Lattice Degeneration
NSR: Neurosensory Retina
NRR: Neuro retinal rim
ON: Optic Neuropathy
PAS: Peripheral Anterior Synechiae
PB: Pupillary block
PEE: Punctate Epithelial Erosion
Post: Posterior
PHM: Posterior Hyaloid Membrane
PVD: Posterior Vitreous Detachment
Ret: Retina/Retinal
RD: Retinal Detachment
RPE: Retinal Pigmented Epithelium
RRD: Rhematogenous Retinal Detachment
RS: Retinoschisis
SNQ: Superonasal Quadrant
SRF: Subretinal Fluid
VA: Visual Acuity
Vitr.: Vitreous

↓↑←→
Examination Technique
Psychophysical test
1. Snellen Visual Acquity > visus jauh digambarkan dg minimun angle of
separation yang membuat 2 objek distinct
a. Normal monoocular VA
b. Best-corrected VA
c. Pinhole VA
d. Binocular VA
2. Very poor visual acquity
a. Counting fingers
b. Hand movement
c. Perception of light
3. LogMAR acuity > standart
a. Acronym dari base-10 logarithm of Minimum Angle of
Resolution
b. Tiap letter size berkontribusi 0.1, tiap huruf 0.02. LogMAR. 6/6
= 0.00. < 6/6 = negative value
4. LogMAR Chart
a. The Bailey Lovie
b. The Early Treatment Diabetic Retinopathy Study
c. Computer
5. Near Visual acquity > pada comfortable reading distance.
Kacamatanya pake. Ukur masing2 mata lalu kedua mata
6. Contrast sensitivity > kemampuan mata membedakan objek dari latar.
Cek terutama di pasien dengan good VA tapi ada visual sympt
(terutama low light). Cth testnya: The Pelli-Robson, Sinusoidal
gratings, Spaeth Richman Contrast Sensitivity Test.
7. Amsler grid > evaluasi 20˚center visual field on fixation. Untuk
screening dan monitoring macular disese dan central visual defect non
macular. Ada 7 charts
8. Light brightness comparison test > berkurang pada optic neuropathy
9. Photostress test > untuk dark adaptation. Habis kena cahaya ada fase
retinal insensitivity temporer spt skotoma. Untuk cek maculopathy saat
ophthalmoscope ambigu. Misalnya pd mild cystoid macular edema, central serous retinopahy, dan untuk membedakan vision loss krn
macular disease dan optic nerve lesion
10. Colour vision testing > evaluasi optic nerve disease dan congenital anomalous colour defect
Dyschromatopsia > retinal dystrophies prior to impairment of other visual parameter
3 populations of retinal cones:
- Blue (tritan) > 414-424 nm Deficient -omaly
- Green (deutran) > 522-539 nm Absent -opia
- Red (protan) > 549-570 nm Trichromats > posses all cones (gk hrss semuanya normal
Dichromats (absent 1) / Monochromat (absent 2)
Tests > ishihara, the city university test, the gardy-rand-rittler test, the farnsworth-munsell 100-hue test
11. Plus lens (+1.00D) test > temporary hypermetropic shift bisa terjadi kalau ada elevasi sensory retina – eg. CSR
Perimetry
 Visual field
Harry Moss Traquair - “a island hill of vision in the sea of darkness”
Superior – 50˚
Nasal – 60˚
Inferior – 70˚
Termporal – 90˚

 Isopter> visual field tp yg same sensitivity dipetakan

 Scotoma > area of reduced (Relative)/total(absolute) loss of vision
surrounded by a seeing area
 Luminance > intensitas stimulus cahaya (satuan asb). Bertolak belakang
dengan sensitivity
 Differential light sensitivity > derajat saat luminance target harus lebih dari
luminance background (cahaya dari sekitar) supaya bisa di tangkap.
Rod lebih sensitive di dim light drpd cones jadi lebih banyak di perifer retina.
 Threshold > brightness stimulus yg dapat ditangkap subjek. ‘the luminance of
a given fixed location stimulus at which it is seen on 50% of the occasions it
is presented’
 Static perimety > lokasi fixed, intensity nya dinaikkan sampe subjek bisa
lihat atau sebaliknya
 Kinetic perimetry (lbh common) > intensity constant, bergerak dari non-
seeing area ke seeing area dg kecepatan yg terstandar sampai tertangkap oleh
subyek. Manual (Goldmann) or automated ( Humphrey field analyser , the
octopus, medmont, Henson, dicon)
Selalu hubungkan hasil VF dengan klinis
Algorithm
- Threshold > biasa untuk monitor glaukoma
- Suprathreshold > screening
- Fast algorithm
Testing pattern
 Glaucoma
o Central! Defek di 30˚ radius dari fixation point paling sering
o 24-2/30-2 pattern
o 10-2 pattern
 Peripheral field > neurological. Eg. FF-120
 Binocular field testing > assess statutory driving entitlement in many juridictions. Eg.
Esterman strategy
Analysis
Eyelids
Anatomy
Epidermis: 4 layers keratinocytes + melanocytes + langerhans + merkel cells
Dermis: connective tissue (inc. orbital muscle) and blood vessels, lymphatics & nerve fibers. +macrophages, fibroblats and mast cells
- Sebaceous > caruncle & w/i eyebrow hairs.
- Meibomian glands(modified sebaceous) > @ tarsal plates. 1 row or 20-30 orifices lid. Consist of central duct w/ multiple acini (produce lipid)
- Gland of Zeis > modified sebacous ass. w/ lash follicles
- Glans of Moll > apocrine sweat glands either into lash folicle / ant. lid margin antara lash. Banyak di lower eyelid
- Eccrine sweat glands > distributed di eyelid, ga cuma di lid margin
- Pilosebaceous unit > hair follicles and sebaceous glands
Non neoplastic lesion
Chalazion
Pathogenesis> sterile chronic granulomatous inflammatory lesion
(lipogranuloma) of meibomian, sometimes zeis, ec retained sebaceous
secretion. Blepharitis common. Multiple & recurrent > rosacea.
Bortezomib>proteasome inhibitor>chalazia w/i 3months.
Recurrent>biopsy to exclude malignancy
Symptoms:
- Subacute/chronic: gradually enlarging painless rounded nodule.
- Acute: sterile inflammation / bacterial inf w/ localized cellulitis. 2˚
infected meibomian > internal hordeolum
Signs:
- Nodule w/I tarsal plate w/w/o inflammation
- Bulging inspissated secretion di orifice
- May be conj. granuloma
- Lesion di anterior lid margin bisa connected ke chalazion di dalem
(lebih sering) atau isolated involevent Zeis
Tx:
- Oral AB kalo ada bacterial inf
- Konservatif: 1/3 spontan hny observe,jkkeliatan membaik
- Hot compress several times/day.Mmbantu esp early lesion
- Expression: tekan dg 2 cotton bud klo lesi dekat margo lid
- Steroid inj.=insisi kuretase.Dipilih kl marginal lesion/dekat
struktur (eg punctum lakrimal). 0.2-2ml triamcinolone acetonide
aqueous suspension + lidocaine s/d 5mg/cc. & 0.1-0.2ml of
40mg/ml dg gauge 27. Srg depigmentation & fat atrophy. Retinal
vascular occlusion rare complication
- Surgery: gambar. Gausah jahit. Topical AB tid 5 hari.
Prophylaxis: Tx blepharitis. Systemic tetracycline pada reccurent
chalazia, terutama ass w/ rosacea

Benign epidermal tumours

Benign pigmented lesions
Benign adnexal tumours
Miscellaneous benign tumours
Malignant tumours
Disorders of the eyelashes
Allergic disorders
Acute allergic oedema
Exposure to pollen / insect bite. Sudden bilateral boggy periocular oedema + chemosis. Tx ga perlu/antihistamin sistemik
Contact dermatitis
Inflame response ↑ sering krn eye drops/ cosmetics/metal. Bisa toxic dermatitis jg. 1 st expose = sensitisasi exposure berikut jadi immune reaction
(type IV). SnS lid skin scaling, angular fissure, oedema & tightness. Chemosis, redness, papillary conjitis. Corneal>punctate epithelial erosion. Tx.
Avoidance,cold compress. Kdg steroid/antihistamin topikal
Atopic dermatitis
Idiopatic, common, sering bareng asma/hay fever. Thickening, crusting, fissuring. Staph blepharitis, vernal / atopic keratoconjitis sering ada.
Herpetic blepharitis & keratoconjitis lebih sering dan lebih parah di px atopi. Tx:emollient + judious use of mild topical steroid. Jarang2 bisa
keratoconus, cataract & ret. detach

Immune related inflammation

Bacterial infection
External hordeolum (stye)
Acute staph. absc di lash follicle, ass w/ Zeis. ↑ anak & dws muda. Tender swelling lid marging, nonjol keluar, dg lash di apex. gak harus tunggal.
Tx: topical(/oral)AB, hot compresses & epilasi lash yang terlibat
Impetigo
Superficial skin infection krn staph aureus / strep pyogenes. Sering di anak. Nyeri, eritema, macules dg cpat>thin walled blister>ruptur>golden
yellow crust.demam,malaise, local lympdnpthy.Tx:topical (kdg oral) AB. Mudah menular terutama ke neonatus!
Erysipelas (St. Anthony’s fire)
Jarang akut, bisa severe, dermal & superficial lymphatic inf. krn S pyogenes. DM, obese & alcohol abuse. Erythematous plague inflammed, raised
border (beda sama selulitis). Komplikasi=metastatic inf(rare). Tx: oral AB (tapi sering kambuh)
Necrotizing fasciitis
Rare, tapi very severe inf. krn rapid progressive necrosis. Sering S. pyogenes, kadang S aureus. Paling sering di ekstrimitas, trunk, perineum &
luka operasi. Bisa fatal kalo gak early debridement & high dose IV AB. Redness+edem diikuti large bullae & nekrosis

Viral infections
Molluscum contagiosum
Transmisi dr kontak dan autoinokulasi. Immunocompromised: multiple+confluent. ≥1 pale, waxy, umbilicated nodules. White
cheesy material (infected degenerated cell) bisa di express. Lesi di lid margin>pindah lewat tear film>chronic follicular conjitis. Tx:
spontan. Kalo perlu, shave excision, kuretm, cauter, chemical ablation, cryo, pulsed dye laser.
Herpes simplex
Bisa primer/reaktivasi viral dormant di ganglion trigeminal. Prodromal (tingling) 24h>vesikel di eyelid&periocular pecah dalam 48h. biasanya 1
dermatome. Bisa bareng papillary conjitis, discharge & lid swelling. Dendritic corneal ulcers sering di px atopic. Tx: ilang sndiri dlm 1 mggu. Bila
perlu, topical aciclovir cr 5x/d / oral aciclovir, famciclovir, valaciclovir. 2˚bac. inf = AB (↑ eczema herpeticum)

Blepharitis
Chronic blepharitis (chronic marginal blepharitis)
Sering ocular discomfort+iritasi. Sns, etiologi&mekanisme ga jelas>susah
ditangani. Anterior lbh gampang sembuh drpd posterior. Staph blepharitis > abn
cell mediated response ke cell wallnya S aureus > red eye, peripheral corneal
infiltrate. Posterior blepharitis krn meibon dysfunction, dan alteration of
meibom secretion. Bacterial lipase > free fatty acids > ↑ melting point
meibum>gak keexpress dari glands >surface irritation> S aureus growth. Loss
of tear film phospholipids (as surfactants)> ↑ tear osmolarity & unstable tear
film. Bisa juga disebabkan o/ demodex > overpopulation / hypersensitivity
>symptoms.
- lid hygiene 2x1 (warm compress beberapa menit u/ soften crust, lid
cleaning, scrub lid margin dg buds/kain+baby shampoo/ baking soda,
epress accumulated maibum),
- AB: o Topical: Fusidic acid, erythromycin, bacitracin, azithromycin or
chloramphenicol (ditaro setelah lid hygiene)
1. Oral AB (doycycline (2x50-100mg 1mggu lanjut 1x/d 6-24 weeks.Tetra (posterior), azithro (anterior) 1x500mg 3 hari,
3 cycles of 1 week intervals) erithhromycin 1-2x250mg bisa jadi alternatif
- Bisa tambah plants/fish oil (suplemen), tear subs bisa bermanfaat, topical steroid low potency pada px inflamm aktif. Papilary
conjitis>higher potency. Tea tree oil/permethrinu/ demodex + high temp cleaning of bedding, pake tea tree shampoo/facial
wash u/ cegah rekuren
- Novel: topical ciclosporin, pulsed light di post ds

Phthiriasis palpebrarum
Bisanya di pubic hair tapi sering di bg berambut lain. Sympt: iritasi kronik, kdg kremu lice nya. Tx: removal of lice w/ fine forceps.
Yellow mercuric oxide 1% / petroleum jelly bid 10 hari. Cek keluarga dan bersihin cloth dan ranjang
Tick infestation of the eyelid
Cabut secepat mungkin u/ cegah lyme ds, rocky mt fever, african tick bite fever (rickettsial inf, sympts 4-10hari stlh kegigit)or
tularemia. Kalo agak jauh, bisa di spray dg yg mengantung (pyrethrine/pyrethroid) 2x selang 1 menit. Permethrine cream bisa.
Detach ticknya se-dekat mungin spy kepala & mulutnya ga ketinggalan. Kalau perlu, diidentifikasi tick apa. Kalo endemik lyme,
AB profilaksis dg doxycycline. (u/ jd tick, perlu attach at least 36jam)
Angular blepharitis
Krn moraxella lacunata / S aureus, kdg bakteri lain / HSx juga bisa. Symps: red scaly fissured skin di lat/med canthi. Lat srg skin
chafing 2˚tear overflow. Bisa papillary&follicular conjitis Rx: topical chloram, bacitracin / eritro
Childhood blepharokeratoconjunctivitis
Tends lebih severe di asian & middle eastern. Presentation +/- 6yo dg recurent ant/post blepharitis, stye/chalazia. Eye rubbing bs
misdiagnose jadi allergic eye. Conj change: diffuse hyperemia, bulbar phlyctens & follicular/papillary hyperplasia. Corneal:
superficial punctate keratopathy, marginal keratitis, peripheral vascztion&axial subepithelial haze. Tx: lid hygiene&topical
antibiotic ointment@bedtime. Bisa topical lowdose steroid (prednisone 0.1%)&erythromycine syr 12mg/d 4-6mggu.

Ptosis
Classification:
- Neurogenic > ec nerve innervation defect (eg CN III palsy & horner syndrome)
- Myogenic > myopathy m. levator, impaired impulse neuromuscular juction.
- Aponeurotic > involutional ptosis krn defek levator aponeurosis
- Mechanical > krn efek gravitasi / massa / scar
Age at onset! Bandingin sama foto lama, dan cari systemic disease (diplopia, time of day)
Clinical Evaluation
Pseudoptosis
- Lack of support>orbital volume deficit
- Contralateral lid retraction
- Ipsilateral hypotropia>upper lid follows globe downward
- Brow ptosis>excessive skin on the brow/CN VII palsy
- Dermatochalasis>overhanging skin on upper lids (bisa mechanical
ptosis juga
Measurement:
- Margin reflex distance - Upper lid crease
- Palpebral fissure height - Pretarsal show
- Levator function
Associated signs:
- The pupils > exclude horner syndrome&CN III palsy
- ↑innervation > naikin proptotic lid>cari drooping opposite lid !surg>lower opposite lid
- Fagitability> look up 30-60secs ga kedip
- Ocular motility defects
- Jaw-winking
- Bell phonomenon>weak=risiko postop exposure keratopathy
- The tear film

Simple congenital ptosis

Marcus Gunn Jaw-winking syndrome
Third nerve misdirection syndromes
Involutional ptosis
Mechanical ptosis
Surgery

Ectropion
Involutional ectropion
Cicatricial ectopion
Paralytic ectropion / facial nerve palsy
Mechanical ectropion

Entropion
Involutional entropion
Cicatricial entropion
Miscellaneous acquired disorders
Varix
Floppy eyelid syndrome
Blepharochalasis
Eyelid imbrication synd
Upper lid retraction
Lower lid retraction:
Cosmetic eyelid and periorbital surgery
Involutional changes
- ↓cutaneous elasticity & thickness>loose wrinkled skin
- Weakening of orbital septum>orbital fat prolapse
- Atrophy orbital&brow fad pads>enophlmos&brow sagging
- Thinning&stretching of midfacial>descent w/ tear
formation through depression&exacerbation of lower
eyelid changes
- Thinning& resorption of periorbital bone krn appearance of
surplus overlying tissue
Non-surgical technique > botox, fillers, skin resurfacing
Surgical technique > Upper eyelid blepharoplasty, lower eyelid blepharoplasty, brow ptosis correction
Congenital malformation
Epicanthic folds: bilateral vertical fold dari lid ke medial canthi. Bisa pseudoesotropia. Tx: V-Y / Zplasy
Telecanthus: bisa sndiri/ass w/ blepharophimosis&syst synd.
Blepharophimosis, ptosis and epicanthus inversus syndrome: mod-sev symm ptosis w/ poor levator fx, telecanthus, epicanthus
inversus, small palpebral fissure. minor facial anomalies commonly present.
Epiblepharon: extra horizontal fold of skin, stretch spjng ant. lid margin, srg di eastern asian. Biasa sembuh pas gede/surg.
Congenital entropion: 2˚ to mechanical effects of microphthalmos. Lower lid ec maldevelopment of the inf retractor aponeurosis.
Tx: eksisistrip of skin & muscle & fixation of skin crease ke tarsal plate (Hotz procedure)
Coloboma: uncommon, unilateral or bilateral, partial / full thickness. Eyelid development is incomplete krn either failure of
migration lid ectoderm to fuse the lid folds atau mechanical forces (amniotic bands). Mesti cek bagian lain ada yg coloboma
juga. Tx: small: primary closure, large: skin grafts & rotation flap
Upper lid: junct of mid&inner thirds. Strong ass w/ cryptophthalmos, facial abn & gold-enhar synd
Lower lid: @ junc of mid & outer thirds, sering ass w/ systemic cond.
Treacher collins synd (mandibulofacial dysostosis): genetic heterogenous cond w/ malformation of 1 st&2nd branchial arches
(terutama mandicular&ear anomalies) lower eyelid coloboma is a feature. Lainnya: slanted palpebral apertures,
cataract, microphthalmos & lacrimal atresia
Cryptophthalmos:
Complete: microthalmic covered w/ fused layer w/no separation between lid
Incomplete: rudimentary lids & microphthalmos
Fraser synd: inherited, sering disertai cryptophthalmos, syndactyly, urogenital & craniofacial anomalies
Euryblepharon: horizontal enlargement of palpebral fissure w/ ass lateral canthal malposition & lat ectropion> lagophthalmos &
exposure keratopathy.
Microblepharon: small eyelid, sering anophthalmos
Ablepharon: defisiensi anterior lamellae of eyelid. Tx: recon skin grafting. Ablepharone-macrostomia synd > enlarged fish-like
mouth, ear skin & genital anomaly.
Congenital upper lid eversion: sering pada afro-caribbean origin, down synd & conj inchthyosis. Bilateral & symmetrical.
Ankyloblepharon filiforme adnatum: upper and lower eyelids joined by thin tags. Transection w/ scissors (bisa tanpa anestesi
Lacrimal Drainage System
Anatomy
Structure:
- Puncta: @post. edge of the lid margin @ junc of lash bearing lateral 5/6 & med. Non
ciliated 1/6
- Canaliculi: vertical dr lid margin 2mm belok ke medial yg turun horizontal 8mm
sampe lacrimal sac. 90% sup & inf canaliculi bersatu jadi common cannaliculus.
Rosenmüller valve (mucosa) cegah reflux air mata
- Lacrimal sac > p: 10-12mm
- Nasolacrimal duct: P: 12-18mm laterally * posteriorly open to inf. nasal meatus.
Valve of Hasner (mucosa) tutupin bukaan duct
Physiology

Causes of a watering eye (Epiphora)

- Hypersecretion: dry eye, inflammation
- Defective drainage: malposition of puncta, onsbtruction along drainage system & lacrimal pump failure
Evaluation
 Drainage failure: cold & windy environment, tears overflowing to cheek
 Puncta & eyelids (slitlamps)
o High meniscus (≥0.6mm)
o Tears commonly overflow from medial canthal. Mucopurulent:nasolacrimal obstruction>more proximal block
o Punctal stenosis mostly asymptomatic. Paling sering di small child. Congenital glaucoma!
o Conturion synd.: ant. Malposisi med. lid+displacement puncta dr lacus lacrimalus ec prominent nasal bridge
o Obstruction of puncta by conjunctiva (conjunctivochalasis), eyelash lodge
o Ectropion and lid laxity o Canaliculitis > pouting punctum
o Large caruncle displace punctum from globe o Chronic epiphora > scaly & erythematous skin
 Lacrimal Sac: palpasi. Puncal reflux mucopurulent>mucocele.
 Fluorescein disappearance test (done before any manipulation and instillation). Fluorescein 1%/2% drop ke both conj fornices. normally
5-10 little / no dye masih tersisa.

 Lacrimal Irrigation: cek punctal patency. CI: acute infection. Anesthesia

punctum dilator(insert vertical-exert lateral tension ke lid sambil tilt horizontal)
 gauge 26-27 curved blunted tip + 3ml saline sambil gentle stretch lateral
eyelid, naikkin beberapa mm sambil ikutin kontur kanalikuli.
Hard stop> kalau kena rigid lacrimal bone = excludes complete obstruction. Bila
saline kerasa oleh pasien = patent, ga kerasa = total onstruction.
Soft stop (spongy feeling)> occlusion / crimpped
Saline reflux from lower + soft stop = lower canalicular obstruction
Reflux from upper punctum = upper and lower canaliculi patent, obstruction of
common canaliculus
 Jones Dye
  Contrast dacryocystography
 Nuclear lacrimal scintigraphy
 CT & MRI > paranasal sinus/susp lacrimal sac pathology
 Internal nasal examination > polyps or deviated septum
Acquired obstruction
Conjunctivochalasis
Folds of redundant conj prolamps over lover eyelid margin > dry eye & epiphora
Loss of adhesion of underlyting Tenon capsu &episclera. May be analogous to conj abn  superior
limbic keratoconjitis
Chronic low grade inflammation (dry eye, blepharitis) may also cause. Severe exposes redundant fold
Tx: Obs/lubes(mild).Topical steroid/anti inflm.&surgical(a)suture to secure(eg polyglactin6-0)6-8mm dr
limbus,(b) excision crescent shaped excess bulb conj, (limit6mm dr limbus).(c)suture edges of
excised/replace w/amniotic membrane
Primary punctal stenosis
Absence of punctal eversion. Ec chronic blepharitis & idiopatic, herpes, local radiotx, cicatrizing conitis,
chronic topical glau tx, systemic cytotoxic, porphyria
Tx. Dilatation (rarely sustained), punctoplasty 1/2/3 snip enlrgement w/ removal of post ampulla wall,
mechanical punch, laser/ microsurg, temporary stent
Secondary punctal stenosis
Punctal eversion cause failure tear entry. Tx. Punctoplasty+correction of punctal eversion
-Retropunctal cautery (Ziegler) u/ pure punctal eversion. 5mm bawah punctum di cauter shrinkage
-Medial conjtivoplasty u/ medial ectropion if no substantial laxity. Diamond cut T:4mm L:8mm parallel
dg inferolateral dari canaliculus & punctum + aproksimasi sup & inf margin luka.
-Lower lid tightening dg tarsal strip. Bisa kombinasi dg conjtivoplasty
Canalicular obstruction
Cause: congenital, trauma, HSV, drug irradiation. Chronic dacryocystitis  membrane@common
canaliculus. Partial obstruction=intubation dg silicone stent 6weeks–6mos. Total individual canalicular
obs.=canalicular trephination dg sisler+intubation or dg IV cath dg tetracted introducer needle as stent.
Balloon canaliculoplasty & endoscopic laser tech. kalau panjang yang patent dari puntum sampe
obstruction ada 6-8mm, anastomosis dg intubation bisa dicoba. Kalau
severe=conjunctivodacryocystorhinostomy dg masukin lester jones tube (bisa untuk pump failure juga)
Nasolacrimal duct obstruction
Cos: idiopathic, naso-orbital trauma, granulomatous ds, infiltration by
nasopharyngelal tumour.Tx: conventional DCR (anastomosis lacrimal
sac ke mid nasal meatus under hypotensive GA) if obst distal to media
openingl.Success rate ≥90%, failure bs krn inadequate size&position of
ostium, unrecognized common canalicular obstruction, scaring & sump
syndrome (surg opening in lacrimal bone is too small & too high).
Endoscopic DCR probing, intubation, stent insertion & balloon
dacryosytoplasty

Dacryolithiasis
Common in males, late adulthood. Mgkn krn tear stagnation 2˚ to
inflammatory obstruction. Kdg krn squamous metaplasia of epitel
lacrimal sac. Sympt: intermitent epiphora, recurrent acte dacryocystitis &
lacrimal sac distension (firm, not inflammed, tender). Mucus reflux on
pressure bisa +/-. Tx: DCR
Congenital Obstruction
Nasolacrimal duct obstruction
Region of Hasner is the last portion to canalize. Complete patency soon after birth. 25% neonates = epiphora, 80% spontan resolve in 1 st year.
Signs: constant/intermitten epihora & matting eyelash, esp URTI. Superimposed bact. inf  BS topical AB. Gentle press  mucopurulent reflux.
Rarely acute dacryocystitis. Confirm normal vision+ant segment ass. Fluorescein disapperance test (highly specific), 1 fine line should remain at 5-
10mins w/ blue light in darkened room
Dd/ punctal atresia, cong. glaucoma, chron conjitis, keratitis & uveitis.
Tx: massage lacrimal sac > hydrostatic pressure > rubture membranous obstruction.. probing & intubation with silastic tubing (w/w/o balloon
dilatation), endoscopic or DCR if probing fail.
Congenital dacryocoele
Collection of amniotic fluid/mucus ec imperforated Hasner valve. Bluish cystic swelling below medial
cantus+epiphora. Intranasal component bisa respiratory distress. Dd/ encephalocoele (pulsatile swelling diatas medial
canthal tendon. Bisa konservatif, tapi kalo gagal  probing
Chronic Canaliculitis
Uncommon condition. Sering krn Actinomyces israelii (Gram+ anaerob). Bisa scaring & canalicular obstr. Unilateral
epiphora, w/ chronic mucopurulent conjitis, refakter sama conventional tx. Pericanalicular redness, edema &
mucopurulent discharge saat kanalikulus ditekan. Pouting punctum = diagnostic clue. Actinomyces menghasilkan
sulfur granules (concretion)  pas canaliculus ditekan bisa keluar/.
Ddx/ Giant fornix synd, dacryolithiasis & larimal diverticulum bisa gejala serupa. Kalo akut > krn HSx.
Tx: fluoroquinolon qid 10d rarely curative kalo ga combine dg canaliculotomy&kuret concretionnya.
Dacryocystitis
Acute dacryocystitis
Subacute onset of pain di medial canthal area+epiphora. Very tender tense red swelling di medial cantus. Sering jadi abses & preseptal cellulitis.
Tx. Warm compress & oral AB. No irigasi&probing. Insisi dan drainase kalo abses bisa drain spontan, ada risiko persistent sac fistula. DCR saat
sudah tdk akut, ↓rekurensi&promotes fistula closure

Chronic dacryocystitis
Chronic epiphora+chronic/recurrent unilateral conj. Mucocele bisa ada (walau ga ada,
pas canalicular ditekan > mucopurulent reflux). Tx: DCR.
Dry eye
Physiology
Constituents:
1. Lipid layer: o/ meibomian glands
tear instability
Komposisi:
a) Luar: polar> phase phospholipids + aquoeous mucin phase
dan non polar>wax, cholesterol esters & trigliserid
b) Polar lipid terikat pd lipocalins (bs bind ke molekul
hidrofobik, berperan pd tear viscocity) pd lapisan aqueous.
c) Saat mata mengedip kuat, lapisan ini lebih tebal
Fungsi:
d) Mencegah evaporasi lap. Aqueous dan menjaga ketebalan ocular surface
damage tear hyperosmolarit

tear film
e) Surfaktan untuk penyebaran tear film
f) Kalo defisiensi > evaporative dry eye
2. Aqueous layer: o/ lacrimal glands
Sekresi:
a) 95% oleh lacrimal gland, 5% o/ Krause dan Wolfring gland
b) Merespon pada stimulasi corneal dan conjunctival. Bisa s/d inflammation
500% pada injuri
c) Berkurang pada anestesi topikal dan tidur.
Komposisi:
a) Air, elektrolit, dissolved mucins dan protein
b) Derivat growth factors dari kelenjar lakrimal Faktor agar resurfacing of the tear film efektif:
c) Pro-inflammatory interleukin cytokines yang mengumpul 1. Normal blink reflex
pada saat tidur (produksi air mata menurun) 2. Contact between external ocular surface dan eye lid
Fungsi: 3. Normal corneal epithelium
a) Menyediakan atmospheric oxygen ke epitel kornea
b) Efek antibakterial (IgA, lysozyme dan lactoferin) Classification
c) Mencuci debris dan noxious stimuli, dan menggerakkan
leukosit setelah injuri Aqueous-deficient Evaporative
d) Membantu optik dengan menghilangkan iregularitas korena
kecil
3. Mucous layer: o/ conjuctival goblet
Intrinsic
Komposisi: Sjögren syndrome
meibomian gland defect
a) Terdiri dari mucin yang disekresi oleh conjuctival goblet, disorders of lid aperture
sedikit o/ lacrimal gland low blink rate
drug action
b) Sel epitel superficial kornea dan conjuctiva produksi Non sjogren syndrome
transmembrane mucin yg membentuk gycocalyx lacrimal deficiency
Function: lacrimal gland obstruction
c) Wetting dengan melapisi epitel kornea dari lapisan reflex hyposecretion
hidropobik Extrinsic
d) Lubrikasi Vit A def.
Topical drug w/ preservatives
4. Regulasi: contact lens
Hormonal ocular surface ds
a) Diatur oleh androgen dan hormon primal
b) Reseptor estrogen dan progresteron di konjungtiva dan
kelenjar lakrimal bantu menjaga Environmental factors
Internal:
a) Umur
b) Status hormonal
c) Kebiasaan
External:
a) Low relative humidity cause exacerbation of evaporative
factors

Mechanism of disease
4 core inter-related
Clinical Features
Gejala pada mata (lihat gambar): Post. seborrhoic blepharitis, konj. merah+keratinisasi+conjunctivochalasis, kelainan tear film, kelainan kornea.

Posterior blepharitis inflammed meibomian gland

Lipid contaminated mucin thin marginal tear meniscus

Komplikasi bisa vision treatening (epitelial breakdown, melting, perforation dan bacterial keratitis)

l
Melting (panah) perforasi dg iris mencuat infeksi bakterial

Investigation
Kolerasi gejala dan hasil penunjang rendah
tear production (schimer, fluorescein, ocular surface disease (corneal
stability of the tear film (BUT)
tear osmolality stain&impression citology
Urutan pemeriksaan
1. Tear film break up time > Abnormal pada aqueous tear deficiency dan meibomian gland disorder
Fluorescein 2% or an impregnated fluorescein strip moistened with non-preserved
saline is instilled into the lower fornix. The patient is asked to blink several times.
The tear film is examined at the slit lamp with a broad beam using the cobalt blue
filter. After an interval, black spots or lines appear in the fluorescein-stained film,
indicating the formation of dry areas.
The BUT is the interval between the last blink and the appearance of the first
randomly distributed dry spot. A BUT of less than 10 seconds is suspicious.
numerous dryspots are present in a
fluorescein-stained tear film

Kalau dry spot nya selalu di tempat yang sama, mungkin ada local corneal surface abnormality rather than intrinsic instability tear film
2. Schirmer test > Aqueous tear production
Excess tears are delicately dried. If topical anaesthesia is applied the excess should be removed from
the inferior fornix with filter paper.
The filter paper is folded 5 mm from one end and inserted at the junction of the middle and outer
third of the lower lid, taking care not to touch the cornea or lashes
The patient is asked to keep the eyes gently closed.
After 5 minutes the filter paper is removed and the amount of wetting from the fold measured.
Less than 10 mm of wetting after 5 minutes without anaesthesia or less than 6mm with anaesthesia is
considered abnormal
! “increased tear fluid production as a compensatory response of Meibomian gland”
 Schirmer test

Diagnosis ga boleh dengan sekali schirmer, tapi kalo berulang kali abnormal=highly supportive
3. Ocular surface staining > bikin stinging up to a day, terutama pada severe KCS
a) Fluorescein > untuk epitel kornea dan konjungtiva
b) Rose bengal > untuk sel epitel yang dead / devitalized. Lebih jelas untuk filaments dan plagues. Pakai very small drop rose bengal
1% / moistened imprenated strip + topical anesthetic lalu lihat pakai red-free filter. Wash out with saline

Filaments mild and severe mucous plague

c) Lisamine green > kayak rose bengal, tapi less irritation (preferred)
Patterns:
d) Interpalpebral staining of cornea & conj. > sering di aqueous tear deficiency
e) Superior conj. stain > superior limbic keratoconjunctivitis
f) Inferior corneal and conj. stain > blepharitis / exposure
Lainnya (yang jarang)
a. Fluorescein clearance test c. Tear constituent e. Tear meniscometry
b. Tear film osmolarity d. Phenol red thread test f. Impression cytology

Treatment  Prinsipnya, biasanya causatifnya irreversible, terapi hny u/ manage symptoms & cegah surface damage.
Level 1 3. Tetracyclines > untuk mibomianitis, rosacea
1. Edukasi dan modifikasi lingkungan / dietary 4. Punctal plugs
Pentingnya compliance dan jelaskan expectationnya Temporary > collagen plugs ke canaliculi. Disolves dalam hitungan
Lifestyle review(pentingnya kedip saat aktivitas khusus and the minggu. U/ tes permanent plugs bs ga.
management of contact lens wear) Reversible > pake silicon/long acting (2-6 bln) collagen plugs.
Environmental review, e.g. ↓suhu&jaga kelembaban Problems: extution, granuloma, distal migration
Caution the patient that laser refractive surgery can exacerbate dry Permanent > pada KCS berat, dan udah coba temporary plug tanpa
eye. epiphora. jgn keempat puncta sekaligus
2. Systematic medication review > hentikan toxic/preserved
topical medication
3. Artificial eyetear substitutes > kalo level 1 boleh yg
preserved. Mucolytic agents bisa dikasih juga
Drop and gels
Cellulose derivatives (e.g. hypromellose, methylcellulose) > mild
cases.
Carbomer gels adhere to the ocular surface and so are longer-lasting,
but some patients are troubled by slight blurring. Insertion Plug inserted
Lainnya: Polyvinyl alcohol (meningkatkan persistensi tear film. Bagus 5. Mucin secretagogues > jgn kalo ada mucous plug
untuk mucin deficiency), sodium hyaluronate, povidone, 6. Moisture chamber specs & specs side shields
glycerine, propylene glycol, polysorbate dll Level 3
Diquafosol is a newer agent that works as a topical secretagogue.
Ointments containing petrolatum (paraffin) mineral oil untuk pas 1. Serum Eye drops (autologous / umbilical cord serum)
tidur, kalo siang blur Haemoderivative treatment has been used to manage severe
Eyelid sprays semprot saat mata tertutup. Isinya lisosome based, ocular surface disease including GvH related dry eye disease,
stabilize tear film & ↓penguapan Sjögren syndrome, post-LASIK dry eye persistent epithelial
Artificial tear inserts extended duration defects and recurrent erosions.
Mucolytic agents. Acetylcysteine 5% drops u/ corneal 2. Contact lenses > bs dipakai u/ reservoir effect dr cairan di
filaments and mucous plaques. Manual debridement of balik lensnya. Efektif untuk gejala krn secondary cornal
filaments jg bs
changes. Musal silicon hydrogel bisa untuk 12-16jam, single
4. Eyelid therapy > kompres hangat dan lid hygiene untuk
use. Occlusive gas permeable juga bisa
blepharitis. Reparative lid surgery bagi yang butuh, nocturnal
3. Permanent punctal occlusion
lagophthalmos di tape. Kalo extreme bisa di lateral
tarsorraphy
Level 4
Level 2
1. Systemic anti-inflammatory agents
1. Non-preserved tear substitutes > Pengawet jadi sumber
2. Surgery
toksik, especially after punctal occlusion. Eyelid surgery (misal tarsorrhaphy)
2. Anti-inflammatory agents > topical steroids, oral omega fatty Salivary gland auto-transplantation
acids dan lainnya (misalnya topical ciclosporin)
 Mucous membrane/amniotic membrane transplantation for corneal Lainnya
complications Botulinum toxin injection to the orbicularis muscle
Oral cholinergic agonists untuk Sjögren

Sjögren disease
Kelainan autoimun > inflamasi limfositik dan rusaknya kelenjar lakrimal, saliva dan organ exocrin lain
Primary kalau berdiri sendiri, secondary kalo bareng sistemik lain (paling sering RA / SLE)
Kriteria diagnosis
1. Positivity for anti-SSA or anti-SSB antibodies, or positive rheumatoid factor together with significantly positive antinuclear antibody
2. Ocular surface staining above a certain grade
3. Focal lymphocytic sialadenitis to a specified extent on salivary gland biopsy
Classic triad
1. Dry eyes
2. Dry mouth
3. Parotid enlargement
Conjunctiva
Anatomy Histology
Mucous membrane, transparent. Epitelium
Supply: anterior ciliary & palpebral arteries Stoma
Drainage: preauricula & submandibula Conjunctiva-associated lymphoid tissue (CALT) > ocular surface
immune response
Discharge
1. Watery: serous exudate & tears. Acute viral / acute allergic conjungtivitis
2. Mucoid chronic allergic conjunctivitis & dry eyes
3. Mucopurulent: chlamydial / acute bacterial conj.itis
4. Moderately purulent: acute bacterial conjunctivitis
5. Severely purulent: gonnococcal
Pseudomembranes: coagulated exudate. Can be peeled
True membrane: membrane attached to conjunctiva
Both pseudomembrane & true membrane can cause scarring after resolution
Glaucoma
Aqueous production
Diproduksi dari plasma oleh ciliary epithelium of the ciliary body pars plicata
Aqueous outflow
Anatomy
1. Trabecular meshwork. Tdd: Uveal, corneoscleral dan juxtacanalicular meshwork
2. Schlemn canal
Physiology Trabecular outflow 90%, uveoscleral drainage 10%, iris sedikit

Intraocular pressure
IOP = Production banding Outflow, berfluktuasi dengan diurnal variation, heartbeat, BP dan RR
Tiap periksa IOP harus catat jam

Ocular hypertension
IOP normal biasanya 16mmHg, ranging 11-21mmHg.
CCT ≥555µm & C/D ratio >0.5 paling berisiko
Faktor2:
- African ethnic
- Males
- Heart disease
- single nucleotide polymorphism in TMC01

Management > pilih2 pasien yang perlu. Target: turun ≥20% atau sampe ≥24mmHg
Terapinya sama seperti POAG, tapi less aggressive. Monitor baik2
Glaucoma
Definisi> chronic progressive optic neuropathy yg mengakibatkan perubahan morfologi optic nerve head dan ret.nerve fibre layer yang khas yang
mengakibatkan progressive ganglion cell death dan visual field loss
Klasifikasi > congenital (developmental) vs acquired, open-angle vs angle-closure, primary vs secondary
Primary Open-Angle Glaucoma
Majority: responder (topical steroid↑ IOP )
Definisi> chronic progressive optic neuropathy adult onset
1. Ret. nerve fibre layer thinning. 4. An open anterior chamber angle.
2. Glaucomatous optic nerve damage. 5. 2˚ glaucoma or a non-glaucomatous ON
3. Characteristic VF loss as damage progresses. 6. IOP is a key modifiable risk factor.
Paling sering di European dan African. 70 tahun ke atas 6% di white, 16% di black, 3% asian. Ga terpengaruh gender
Risk Factors:
1. IOP > makin ↑, makin ! kalo asimetri ≥4mmHg 6. Anti-VEGF > risk ↑ after 6x inj 10. Optic disc area > lbh rentan disc yg besar
harus tiati 7. Contraceptive pill > yg long term, krn hambat 11. Ocular perfussion pressure (OPP) > perbedaan
2. Age protective effect nya estrogen BP dg IOP
3. Race 8. Vascular disease > mgkn krn poor ocular (Baca file Ocular perfusion pressure and glaucoma)
4. Family history perfusion
5. Myopia 9. Translaminar pressure gradient
Gens: setidaknya ada 20 loci, tapi mutasi cuma MTOC gene > coding u/ protein myocilin di trab. meshw. dan OPTN gene > coding u/ optineurin
Patogenesis: ret. ganglion cell death paling banyak terjadi karena apoptosis (vs necrosis)

- calcium ion influx ke dalam sel - astrocyte dan glial cel

proliferasi optic nerve
- ↑ intracell NO
- terganggunya extracell
matrix lamina cribosa remodelling
One of both of the following mechanism may be involved:
1. Direct mechanical > optic nerve keteken langsung, kemungkinan saat melewati lamina cribosa
2. Ischemic damage > kompresi pembuluh darah yang suplai optic nerve head.. OPP ngaruh di sini
3. Common pathway of damage > 1&2   axoplasmic flow, terganggunya pasokan nutrisi atau pembuangan metabolic products,  neuronal
growth factors, oxidative injury, dan mulainya immune-mediated damages
Screening
1. Older individuals 3. African racial background
2. >40 dengan riwayat POAG di kerabat dekat Ga bisa hanya tonometri aja, harus cek cupping & visual field

Diagnosis
History
1. Visual simptoms biasanya ga ada, kecuali udah advance banget
2. Previous ophthalmic history: refractive status dan kemungkinan secondary.
3. Family history, baik terkait glaucoma atau gangguan mata lainnya
4. Past medical history > asthma (ß-blocker kontraindikasi), head injury/intracranial pathology, vasospasm, DM, systemic HT dan
cardiovascular ds, KB oral
5. Current meds > steroid, oral ß-blocker, smoke/alcohol, allergies
Exam > VA, pupils, colour vision (singkirin ON lain), slit lamp (singkirin secondary pigmentary&PEX), tonometry sebelum pachymetri(catat
jam), goniosopy dan optic disc exam
Optic nerve evaluation
Normal:
- Neuro retinal rim di tepi luar cup & optic disc margin, warna orange pink. Mengikuti ISNT rule sen 81%, spe 32%
- C/D ratio > pake yg vertical. Sedikit banget yg >0.7, kalo asimetris ≥0.2 antar mata, tiati
- Optic disc size > large disc lebih prone, terutama di NTG. Normal medial verical diameter = 1.5-1.7mm in white population

ISNT rule Normal optic disc

Changes in glaucoma: optic nerve head, peripapillary area and retinal nerve fibre layer
- Optic nerve head > pathological cupping krn hilangnya jumlah serat syaraf, glial cells
dan pembuluh darah yang ireversibel
- Subtypes of glaucomatous damage
1. Focal ischemia disc > localized superior &/or inferior notching + localized field
defects w/ early threat to fixation
2. Myopic disc with glaucoma > tilted (obliquely inserted) shallow disc dg temporal
crescent krn parapapillary atrophy + glaucomatous damage. Dense superior/inf
scotomas threatening fixation sering. ↑ Pria muda
3. Sclerotic disc > shallow saucerized cup & gently slopping NRR, peripapillary
atrophy + VF loss. Ass w/ systemic vasc ds.
4. Concentrically enlarging disc > serial monitor > uniform NRR thinning+diffuse
VF loss + ↑↑ IOP
- Non-specific signs
1. Disc hemmrg dr NRR  retina (↑ inferotemporal). Kalo ada>RF develop/progress ke
glaucoma. Sering di NTG&healthy px w/ syst vasc ds. ¾ ga jadi glaucoma
2. Baring of circumlinear BV > early thinning of NRR. Ada space antara NRR dan
superficial BV
3. Bayoneting: double angulation BV. Krn NRR loss, vessel yg masuk ke disk dari
retina angle sharply backward ke disc lalu turn towards original directionnya u/
lewat lamina cribrosa
4. Collateral antara 2 veins di disc (kyk CRVO). Uncommon. Ec chronic low grade circ obstruction. Bisa tortuous juga
5. Laminar dot sign: advance. Grey dot-like fenestration of lamina cribrosa jd keliatan krn NRR recedes. Tapi bisa di normal eye juga
6. Sharpened edge/rim: advance. NRR lost di samping edge, jadi ada margin contour. Sering ada bayonet
7. Peripapillary changes (atrophy) di sekitar optic nerve head
a) Alpha (outer) zone: superficial retinal pigment epithelial
changes.
b) Beta (inner) zone: chorioretinal atrophy
- Retinal nerve fiber layer
Fibre dari fundus perifer lie deep di retinal nerve fibre layer, yg dari
deket optic nerve lie superficially
Di glaucoma, RNFL subtle defects duluan muncul, sering stlh disc
hemmrg.
a) Pattern 1: localized wedge shapped
b) Pattern 2: Diffuse defect dg batas ga jelas

Visual field defects

1. Early changes > slight asymmetry
2. Small paracentral depression (A). Sering superonasal. Sering di NTG
 3. Nasal step & temboral wedge (B)
4. Arcuate defects (C,D,E)
5. Ring scotoma (F)
6. End stage > sisa central (tunnel) vision, dan ada temporal island
TX goal
1. Target presure Initially: >18mmHg (every ↓ 1 mmHg = ↓ 10% progression)
2. Kalo target udh tercapai tapi terus damage > surgery
Medical tx
Commencing med tx:
- Harus ↓est concentration w/ desired effect, as infrequent as possible, least side effect
- Paling sering protagrandin analogue / ß-blocker
Review usually tiap 4-8minggu, kalo memuaskan jadwalin 2-6bulan.
Kalo dikit/no response> ganti . kalo incomplete response > tambah atau kombinasi
Kalo kombinasl, jedain 5 menit. Pilih2 kapan mesti tambah/ganti/tunggu
Perimetri tiap 6-12 bulan. Gonioscopy tiap tahun
Optic disc exam harus tiap kunjungan: kalo disc hemmrg>ongoing damage. Foto/gambar!
Penyebab tx gagal:
- Target pressure nya salah - Flutuasi IOP yang lebar - Impaired ocular perfusion
- Compliance buruk - Diurnal variation - Other compressive lesion
Selective Laser Trabeculoplasty > sering jadi first line tx
Surgery: trabeculectomy
Prognosis: rata2 POAG ga buta (buta both eyes, pd white: 5-10%), tapi tgt compliance thdp tx.

Normal/low Tension//Normal-pressure Glaucoma

Definisi: POAG dengan IOP dalam variasi normal scr epidemiologi
1. IOP ≤21mmHg pada diurnal test 4. Open anterior chamber
2. Optic nerve damage sesuai glaukom 5. 2˚ glaucoma or a non-glaucomatous ON
3. VF loss sesuai dengan optic nerve

Pathogenesis > masih ? overall CCT di NTG < POAG. Low CCT cause? Some has marked nocturnal spike, kadang only pas supine
Risk factor
1. Age 5. CCT: lower 10. Translaminar pressure gradient
2. Gender: ♀> ♂  6. Abn vasoregulation: migraine, Raynaud 11. Ocular perfusion pressure
3. Race: Japanese 7. Systemic hypotension 12. Myopia
4. FH(OPTN gene coding mutation) 8. OSA 13. Thyroid disease?
9. Autoantibody levels: higher
DD/
1. Angle closure 7. Progressive RNF defect yg bkn krn 10. Previous AION (sering 2˚ temporal
2. Low CCT> underestimated IOP glaukom arteritis) sering bikin disc abn dan VF loss
3. POAG (krn diurnal jd dikira NTG) 8. Congenital disc anomaly mirim claucoma
4. Riw ↑ IOP (krn trauma, steroid dll) 9. Neurological (lesi>kompresi>kirain 11. Previous ON insult
5. Masking (eg. oral ß bloker) glaukom) 12. Misc optic neuropathies (inflamasi,
6. Pigment glaucom yg spontan resolved infiltrative, drug induced)
Clinical features
History: migraine, Raynaud, episodes of shock, head/eye injury, headache/oth neurosympt, medication
IOP biasanya di high teens, tapi ga selalu
Optic nerve:
- Familiar cupping pattern - Splinter hemrhg di margin: NTG> POAG.
- Peripapillary athropy lebih prevalent Risk progresi! FOTO!
- Pallor tapi disproporsi dengan cuppingnya
VF defect mirip POAG, tapi closer to fixation, deeper, steeper dan lebih localized. >50% tidak ada progresi. Seringkali VF loss lebih parah drpd
POAG at presentation. Kalo defisit pattern > curiga lesi di belakang ON
Investigasi:
- Systemic vascular risk factor - Cek penyebab non glaucomatous ON (defisiensi B12, FBC,
- Cek BP > u/ cek OPP ESR/CRP, treponemal serology, serung ACE level, plasma protein
- Duplex Carotid electrophoresis & cek autoantibody
- Ocular blood glow assessment

Treatment
50%, dalam 5-7 tahun ga deteriorate. Cek dulu progresi sebelom start treatment
Start kalo advance glaucomatous damage, terutama kalo central vision kena
- Non specific: reg exercise, avoid head stand :D - Antihypotensive measure kalo ↓ BP nocturnal
- Meds: protaglandines. Brimonidine ada neuroprotective juga. - Tidur head up 30˚
Topical ßblocker tiati (esp bedtime) krn ↓BP signifikan pas tidur - Neuroprotective agents
- Laser trabeculoplasty: SLT
- progress terus > Surgery. Sering butuh antimetabolite
- Kontrol syst vasc ds
- Syst CCB

Primary angle closure glaucoma

Definisi: ada oklusi di TM oleh iris perifer (iridotrabecular contact).
Bisa primary & secondary. Biasanya narrowest angle di superior.
Shaffer system:
- Grade 4 (35-45˚) widest angle. Pada myopia & pseudophakia. Ciliary body keliatan tanpa tilt lensa
- Grade 3 (25-30˚) open angle, scleral supur keliatan
- Grade 2 (20˚) scleral spur keliatan tapi trabeculum masih keliatan
- Grade 1 (10˚) very narrow angle, Cuma schwalbe line yg keliatan (atasnya trabeculum masih mungkin keliatan)
- Slit angle: no iridocorneal contact tp ga ada struktur angle yg keliatan
- Grade 0 (0˚) closed (iridocorneal contact)
Van Heric method: (baca proc di kanski hal 371, pojok kanan atas)

System lain: Speath, scheie

Classification
1. Primary angle closure suspect
a. Axial anterior chamber depth < normal: ada crescentic
shadow di nasal iris waktu disinar dari temporal (eclipse
sign)
b. Gonioscopy: ITC di posterior meshwork @≥3quadrants
tapi ga ada peripheral anterior synechiae
c. Kalo 2 quadrants ITC dan ada tanda intermitten closure
(pigment smuge) > bisa jadi PACS
d. Normal IOP, OD dan VF. No PAS
e. Risk rendah: 8/1000 untreated. 4.2/1000 kalo yang di
laser PI
2. Primary angle closure (PAC)
a. Gonioscopy: ITC di ≥3q+ ↑IOP&// PAS
b. OD dan VF normal
c. Bisa di classify ke ischemic (ada iris changes /
glaukomflecken) dan non ischemic
3. Primary angle-closure glaucoma (PACG)
a. ITC di ≥3q+glaucomatous optic neuropathy
b. Optic nerve damage ec episode of severe IOP elevation (eg acute angle closure) bisa ga tipical glaucomatous cupping
Mechanism
1. Relative pupillary block: aqueous gagal keluar dari pupil  perbedaan tekanan antara ant & post
chamber (11.34)
Peripheral iridectomy often useful. Kecuali kalo ada PAS / TM damage
Large lens vault (jarak antar anterior pole lens ke garis horizontal
sejajar scleral spur
2. Non pupillary block (sering di asian px) deeper AC.
a. Plateau iris: di younger px. Flat / only slight convex central
iris plane  normal / only slight shallow central ant chamber.
Anatomical causative: plateau iris 2˚ to ant positioned/rotated
ciliary processes & thicker/>ant positioned iris. Some says
thick peripheral iris (esp di Asian)
Not fully relieved by iridotomy (plateau iris syndrome).
b. Angle recess
3. Lens-induced angle closure:
a. Sudden change in lens volume
b. Rapid progression of lens intumescence (phacomorphic
glaucoma / ant lens subluxation
c. All cases of pupillary block = phacomorphic element (krn ↑
usia = lensa nebel)

4. Retrolenticular
a. Malignant glaucoma (ciliolenticular block)
b. Post segment  2˚ angle closure
5. Combined: ada elemen angle closure DAN open angle
6. Reduced aqueous outflow
a. Obstruksi o/ iris
b. Degeneratif (krn chronic / intermitent contact dengan iris krn ↑ IOP)
c. Permanent oklusi TM krn PAS
Risk factors:
1. Age (PB: 62yo), NPB ↑ younger 4. FH
2. Gender ♀> ♂  5. Refraction: pure PB usually hypermetropic. NPB usually myopic.
3. Race: far eastern & indian asian > NPB 1/6 ≥1D hypermetropic = PACS. Rutin gonioscopy!
6. Axial length: shorter length > shallow AC (esp nanophthalmos)
Diagnosis
Precipitation factor:
- watching TV in darkened room - acute emotional stress
- pharmacological mydriasis & rarely miosi - syst meds: symphatetic agonist / parasymphathetic antagonists
- adoption of semi-prone position
Keluhan:
- Intermittent blurring (smoke filled room) & haloes ec corneal oedema
- Acutely / marked ↓ vision, redness dan ocular / periocular pain & headache. Bisa ada GI symptoms
- Sering asimptomatik
APAC: - Makin lama attack dan PAS post APAC > makin susah dikontrol
- VA 6/60 – HM dgn obat
- IOP sangat tinggi (50-80mmHg) Sub acute angle closure: intermitent episodes of mild/moderate APAC
- Conj hyperemia + violaceous circumcorneal injection yang sembuh spontan. Seringkali pada px PB
- Corneal epithelial oedema Chronic presentation
- AC shallow, aqueous flare - VA normal kecuali kalo dh parah bngt
- Non reactive mid dilated vertically oval pupil - AC shallower di RPB dibanding NPB
- Fellow eye = occludable angle (kalo gak, cari 2˚ cause) - IOP ↑ intermittent
Resolved APAC: - Creeping angle closure: gradual band-like anterior advance of the
- Early: low IOP (ciliary body shutdown krn obat)+descemet fold apparent insertion of the iris
kl IOP ↓ rapidly, ON head congestion, choroidal folds - Intermittent ITC > discrete PAS (pyramidal / saw-tooth
- Late: iris atrophy dg spiral like configuration, glaukomflecken appearance)
(white foci of necrosis di superficial lens) & katarak, pupil - Kerusakan ON variatif
iregular krn spinchter rusak, posterior synechiae. ON bisa aja
normal/pallor/cupping dll
DDx/
- Lens-induced (swollen/subluxed lens) - Scleritis
- Malignant glaucoma (aqueous misdirection) - Pigment dispersion
- 2˚ cause - Pseudoexfoliation
- Neovascular glaucoma - Orbital/retro-orbital lesion
- Hypertensive uveitis
Tx
APAC
- Initial tx: 3. Early laser iridotomy / iridoplasty stlh corneal edema
1. Supine position > lens gerak ke posterior 4. Paracentesis bisa, tapi takut rusak lens (jarang)
2. Acetazolamide 500mg (IOP >50mmHg: IV, <50 = oral). 5. Surgical: PI, lens extraction, goniosynechialysis,
CI: alergi sulfa, angle closure krn topiramate dan sulfa trabeculectomy, dan cyclodiode laser tx
lainnya - Subsequent med-tx
3. Simgle dose apraclonidine 0.5/1%, timolol 0.5% dan 1. Pilocarpine 2% 4x1 ke mata sakit & 1% ke mata sehat
prednisolone 1% (atau dexa 0.1%) tetes mata. Jeda 3- 2. Topical steroid (prednisolone 1% atau dexa 0.1%) 4dd1
5menit kalau acutely inflamed
4. Pilocarpine 1% 1 tetes ke mata yang sakit. Bisa diulang 3. Tergantung respon: timolol 0.5% 2dd1, apraclonidine 1%
setelh ½ jam disertai 1 tetes ke mata yg satunya. Kalau 3dd1, oral acetazolamide 4x250mg
udah <40mmHg jangan diulang - Bilateral laser iridotomy setelah attack broken (clear cornea &
5. Analgesia dan anti emetic kalau diperlukan kurleb normal IOP. Topical steroid≥ 1 mggu
- Resistant case: - Gonioscopy ulang untuk pastiin angle kebuka
1. Central cornea indentation degan squint hook / goniolens > - Subsequent management  kyk post iridotomy chronic
u/ dorong aqueous ke angle. Epitel edem >50% topical PAC/PACG. Low treshhold u/ cataract surgery terutama kalo ada
glycerol supaya visual membaik & hindari abrasi elemen phacomorphic. Trabeculectomy penting untuk persistent
2. Mannitol 20% 1-2g/kg IV selama 1 jam. oral glycerol 50% IOP tinggi walau angle open
1g/kg (cek kontra indikasi dulu)
PACS:
- Laser iridotomy > untuk yg risiko jd PACG aja
- Kalau significant ITC netep setelah iridotomy > observe, laser iridoplasty & long term pilocarpine prophylaxis. Kalau ada symptomatic
cataract = lens extraction
PAC & PACG
- Management sama kayak PACS tapi lebih agresif.
- Review urgensi dan intensiti treatment tergantung pasien. Pertimbangkan IOP,closure,& glaucomatous damage kalau ada
- Med tx: kalau ada synechia atau persistent elevated IOP walau angle kebuka
- Trabeculectomy dengan mitomycin C. hati2 risiko malignant glaucoma
- Phacoemulsification w/ IOL > mengurangi hypermetrop dan anterior chamber deepens & buka angle

Secondary glaucoma
Open angle
Pretrabecular > ada membrane cover TM - Macrophages & lens proteins (phacolytic)
- Fibrovascular tissue - Proteins (eg hypertensive uveitis)
- Endothelial cellular membranous proliferation (ICE syndr) - PEX material
- Epithelial cellular membranous proliferation - Altered trabecular fibres klo edema TM ( trabeculitis di HT
Trabecular > obstruction  clogging TM & 2˚ degenerative changes uveitis)/ scarring (post traumatic angle recession
- Pigment particles (pigmentary glaucoma) Post trabecular > TM normal tapi aqueous terganggu krn episcleral
- RBC (red cell glaucoma)/Degenerate red cells (ghost cell) venous pressure
 - Carotid-cavernous fistula - Obstruksi SVC↑
- Sturge weber syndrome
Close angle
- Dengan PB - Tanpa PB
1. Seclusio pupillae (360˚ post-synechiae) 1. 2˚ cause of PAS (advance neovasc glaucoma, chronic
2. Subluxated lens ant uveitis)
3. Phacomorphic glaucoma 2. Cilio-choroidal effusion.
4. Capsular block syndrome dg 360˚ iris-capsule adhesion 3. Capsular block syndr w/o iris–capsule adhesion.
pada pseudophakic 4. Ciliary body/iris/post seg cyst/tumour
5. Aphakic PB 5. Contraction of retrolenticular fibrovascular tissue (eg.
6. Ant-chamber lens implant tanpa patent iridotomy proliferative vitreoretinopathy/ROP
6. Malignant glaucoma (ciliolenticular block).

Pseudoexfoliation syndrome
Systemic disorder, sering bikin 2˚ open angle glaucoma
Jarang dibawah 50tahun, 75-85 tahun 5%, 2/3 one eye
Pathogenesis
PE material = grey white fibrillary dari abn extracell matrix metabolism>deposit di mana2
PE +>sering pada high tone hearing loss dan cardio ds
Gene: Single nucleotide polymorphism di LOXL1, chomosome 15 (fx:cross link tropoelasti dan colagen>maintain elastic fibre&extracell matrix.
Gak semua jadi PXS > sering ↓ homocysteine (aqueous&plasma)< ↓ folate intake ?
PE obstruct trabecular + liberated iris pigment(degenerative outflow dysfx> PEG open glaucoma
Clinical features
- Cornea: deposit di endotel, srg ada scatter pigment deposit juga. kdg ada krukenberg spindle. Low density endotel kdg
- Ant chamber: PE kdg keliatan. Mild aqueous flare krn impaired blood aqueous barrier
- Iris:granular PE material deposit, pupillary ruff loss &patchy transillumination defect di margin pupil
- Lens: anterior capsul central and sekeliling perifer indent o/ PE material (dilate pupil). Sering bikin katarak (mgkn krn ↓ ascorbate level di
aqueous). Phacodenesis krn zonular weakness (jrg bikin subluxi)
- Ant chamber angle:
1. Patch trabecular & schwalbe line hyperpigmentation (paling banyak di inf)
2. Sampaolesi line > irrglr band pigment di anterior Schwalbe (patognomonic)
3. Dandruff-like PE material
4. Zonular laxity > risiko close angle
- IOP>glaucomatous damage < chronic open angle glaucoma
Prognosis lebih jelek dari POAG, krn IOP ↑ &marked fluktuasi. Seringkali dh severe damage. Tiati Visua loss. Monitor!
TX:
- Medikamentosa>kyk POAG (tp lebih sering gagal dari POAG)
- Laser trabeculoplasty lebih sering berhasil drpd POAG. Rata2 ↓30%. !jgn terlalu hi power > trabecular pigmentation > ↑absorbsion >
transient IOP spike
- Phaco: kmbinasi dengan trabeculectomy. High complication krn poor mydriasis, zonule fragile, dan defisiensy kapsul lensa dan endotel. Ada
risk spike OP, corneal edema, inflammation, capsular opacities, capsulorhexis contraction (phimosis) & late IOP descentration / dislocation
- Filtration surgery sama efektif dg POAG
- Trabecular aspiration : sementara aja, harus bareng prosedur lain

Pigment dispersion synd&pgmentary glaucoma

Karena granul pigment iris lepas dan deposit ke ant seg. Sering jadi 2˚ glaucoma. ↑cowok (young myopic white), kec di afrika (jaragn PDS, tapi ↑
old hypermetropia woman). 15% dari PDS ↑ IOP/jd glaucoma dalam 15 tahun
AD inheritance. ↑ myopia > earlier & more severe glaucoma
Bisa 2˚dispersion krn trauma , IO tumor, malpositioned IOL menggesek
Pathogenesis
Primary PDS/PG > pigment shedding krn rubbing post pigment layer ke zonule < post mid perifer iris bowing
↓ ant>post chamber pressure reverse PB (terbukti dari peripheral iridotomy > iris flatten, ↓ zonular contact)
↑ IOP :
- Acute krn direct obstruction oleh pigment
- Chronic ↑ IOP krn obstruksi pigment+damage trabecular krn denudation, collapse & sclerosis. Sering kali steroid responsive

Dx
- Presentation:seringkali ktemu pas routine exam. Biasanya bilateral tapi subtle
- Cornea: vertical spindle shape. Makin kronik makin gajelas, ga pathogomonic
- AC: deep+ada melanin granules di aqueous
- Iris: transillumination radial spoke-like, lebih sering di lighter iris
- Gonioscopy: angle wide open, iris bow backward di mid perifer (sering). Pigmen ↑ @trabec & di schwalbe line
- Lens: deposit di ant lens. Bentuk garis (scheie stripe) atau Zentmayer (ring di perifer sekitar zonule insertion)
- IOP: volatile, sebagian px lebih IOP lebih tinggi dan fluktiatif dibanding POAG. Seirin erjalan waktu > turun/jadi normal. Sering kayak NTG
krn IOP normal
- Post seg: peripheral retinal pigmentation&lattice degeneration. RD ↑. Glaucomatous damage sering markedly assymetrical.
Tx:
Review tiap tahun u/c ek glaucomatous damage. Kalo ada, jadi 4-6 bulan sekali
- Lifestye measures: exercise > bikin iris pigment dispersion dg acute sympt.
- Medical: kyk POAG. Miotics (↓ iridozonular contact)!eksaserbasi myopia dan ↑ RD.
- Laser trabeculoplasty: efektif. Over treat! Pake low laser dan max 2 quadrants
- Laser iridotomy dan filtration surg
Acute bilateral iris pigment loss w/ raised IOP
Bilateral Acute Depigmentation of the Iris (BADI) > - Asal: iris stroma
 - Less severe dan less resistant - Asal: iris pigment epithelium
- Less transillumination defect & less irrgeular mydrasis - More severe dan more resistant
Bilateral Acute Iris Trasillumination (BAIT) - more transillumination defect & more irreular mydrasis
Sering di young – mid age woman, spontan setelah flu-like illness (possibly juga post AB, esp moxifloxacin)
Diduga krn phototoxicity setelah sensitisasi pada individu yg predisposed.
Gejala: acute bilateral ocular redness & photophobia+↑IOP(more severe dan resistant di BAIT

Neovascular glaucoma
Pathogenesis> aggressive iris neovascularization (rubeosis iris)>progressive angle closure + rapid glaucomatous atrophy
Etiology: severe, diffuse and chronic retinal ischemia > ↓ angogenic. ! VEGF untuk ↓ angiogenesis
Cause
- Ischemic central retinal vein occlusion (35-50%). VA <6/60, RAPD, extensive peripheral retinal capillary non-perfusion (Fluorescein
angiography). Glaucoma in 3months (100-day glaucoma) (interval 1mgu-2thn)
- DM (10-15%): ↓ dg panretinal coagulopaty & anti VEGF. Pars plana vitrectomy precipitate NVG jika angle neovasc + preop
- Arterial retinal vascular disease (CRAO, ocular ischemic syd, dll)
- Misc: IO tumours, long standing RD &chronic IO inlammation
Clinical features
- Sympt: none – seveere pain, ↓ vision, redness & photophobia
- Cornea: ↑ IOP (khususya substantial & acute) > corneal edema
- IOP: awalnya normal, lalu jadi extreme high. Ant seg congestion. Hypotony di advance case
- Pupillary margin: ada vessels (may be subtle!)
- Iris surface: new vessels tumbuh radial>kdg joining dilated vessel yg collarette.
- Gonioscopy: non mydriatic gonioscopy
- Cataract: common once ischaemia is established
- Posterior segment: Glaucomatous optic neuropathy
- Investigation: FA, B-scan
TX
! address the cause. Poor visual outcome: youing, VA <6/60, IOP >35 at presentation
- Review: frequent @hi risk period: 1st few months post CRVO & 1st few weeks post DM vitrectomy
- Medical tx u/ IOP,, spt POAG tp miotic.
1. Atropine 1% 2dd1 spy synechiae &↑ uveoscleral outflow
2. Topical steroid @ acute stage
3. Topical apraclonidine& acetazolamide (hati2 di DMt1 dg renal dysfx) temporary
- Panretinal photocoagulopathy: ↑ regresi neovasc, kalo early bs prevent glaucoma
- IO VEGF inhibitors: Bevacizumab (Avastin) 1.25mg in 0.05ml bisa sambil PRP. Terutama kalo fibrovasc angle closure belom.
- Retinal repair stlh IOP controlled
- Ciliary body ablation (cyclodiode) kalo med IOP control
- Filtration surg kalo VA Hm/better. Post op anti inflammation harus agresif (termasuk oral steroid)
- Pars plana vitrectomypada early stage > ↓ hemorrage (terutama pd CRVO)
- Retrobulbar alcohol inj: relieve pain. Tapi bisa permanen ptosis & ↓ congestion
Prognosis
Bukan ga buta tapi confortable eye (prevalensi buta 25-50%. ↓ 50% life expectancy

Inflammatory glaucoma
↑ IOP bisa transient dan innocuous/persistent dan severely damaging
Paling sering Fusc uveitis synd & chronic ant uveitis (post uveitis jarang block outflow)
Dx dilemma: IOP fluctuation, cilliary body shutdown, butuh pake topical steroid, iris vessel (neovasc?)
Tx
-Med: bagus kalo angle competely open, target IOP rendah pada px dengan glaucomatous optic neuropathy.
1. Long acting depot steroid kalo dianggap steroid responsive
2. DOC: ß blocker
3. Hati2 prostaglandin derivates> edem makula & ↑ inflamasi
4. Ga boleh miotics
5. Lainnya sesuai kondisi
-Laser iridotomy:hati2 occluded pada on going uveitis. ! intensive topical steroid
-Surgery
1. Preop prep: control chronic uveitis at least 3 cln sblm op, pre op steroid, dan kalo labile inflammatory ds: oral prednisolon
2. Trabeculecomy +mitomycin/long tube. Combine cataract & glaucoma surg, tp bisa ditimbang2 u/ goniosynechialysis / cataract surg aja.
Most case cataract surg 6 bulan stlh trabeculectomy. !!!Post op hypotony. Taper steroid pelan2
3. Cyclodestructive hati2, krn bisa ↑ inflamasi
Posner schlossman syndrome
Recurrent attacks unilateral acute raised IOP+mild ant uveitis.spekulasi: cute trabeculitis & ada bukti kaitan infeksi (CMV/H.pylori)
PGE meningkat seiring IOP naik. HLA- Bw54 haplotype. Usually di young adult-mid age. Males >. 50% pindah2 mata. Intervals bervariasi tapi
biasanya becomes longer w/ time. Review berkala walau udh ga attack krn bisa ↑ IOP kronis, termasuk fellow eye
Dx:
- Presentation: mild discomfort, haloes, slight bluring, kadang redness. One eye
- Slit lamp: few ant chamber cells, white keratic precipitate (s). inj / mnimal. Sering mild corneal epithelial oedema
- Mydriasis w/o post synechiae
- IOP typically ≥ 40mmHg. Ga proposional dg iritis. klo untreated, terus sampe hours-weeks. ↑ IOP precede inflammatory sign
- Gonioscopy: open angle tanpa PAS
- Glaucomatous optic neuropathy jarang. Biasanya cuppingnya reversible
Tx
Topical steroid (pas serangan. Profilaksis)+ aqueous supressants. Topical/oral NSAID bisa di coba. Antiviral masih ?
Steroid-induced glaucoma
1/3 ↑ IOP krn potent topical steroid (responder) > more likely untuk develop POAG, vice versa. (2/3 non responder)
Uveitis
Classification
Clinical Feature
Investigation
Treatment
Immunomodulatory therapy for non infectious uveitis
Fuchs Uveitis Syndrome
Uveitis in Juvenile Idiopathic Arthritis
Uveitis in Bowel Disease
Uveitis in Renal Disease
Vogt-Koyanagi-Harada (VKH) Syndrome
Sympathetic Ophthalmitis
Lens induced Uveitis
Sarcoidosis
Behçet disease
Parasitic Uveitis
Toxoplasmosis
Cause: Toxoplasma Gondii (obligate intracell protozoan).
Systemic features:
o Congenital toxoplasmosis
o Postnatal Childhood acquistition
o Acquired toxoplasmosis in immunocompetent adults
o Toxoplasmosis in immunocompromised patients
Ocular Features
o

Viral Uveitis
Fungal Uveitis
Bacterial Uveitis
Misc. Idiopathic Chorioretinopathies
Retinal Detachment
Introduction
Anatomy
1. Pars plana > Ciliary body dari 1mm dari limbus sampai 6mm ke arah posterior. 2mm anterior = pars plicata, 4mm = flattened PP. Supaya gak
kena lensa / retina, insisi / intravet. inj. Ambil 3.5 dan 4mm posterior dari limbus pada phakic dan pseudophakic. Di mid pars plana, bisanya
anterior dari vitreous base.
2. Ora serrata > Junction antara retina dan cilliary body. Pada RD, persatuan antara retina sensori dg RPE dan choroid limits forward extension
of SRF pada ora.

Ora serrata dan normal anatomical landmarks

-Dentate processes>tapering extensions of retina ke pars plana. Marked nasally drpd temporally dan tdpt variasi
kontur
-Oral bays> scalloped edges of epitel PP
-Meredional folds(A)> small radial folds of thickened retinal tissue sejajar dg dentate, plg srg di SNQ.
- Enclosed oral bay (B) >small islands of PP dikelilingi retina krn persatuan antara 2 dentate processes.
3. Vitreous base > 3-4mm bagiannya melekat kan cortical vitreous ke ora serrata.
Innocuous peripheral retinal degeneration
1. Microcystoid (peripheral cystoid)
degeneration > vesikel kecil2 dg batas tdk
tegas dan latar greyish-white. Retina tampak
menebal dan krg transparent. Mulai dari ora
serrata bergerak melingkar ke posterior
smooth undulating post. border. Hmpr smua
orang ada. Biasanya ga bikin RD tp bs bikin
typical degen. retinoschisis
2. Paving stone degeneration > discrete yellow-white
patches of focal chorioretinal atrophy yg ad
pigmented margins. Biasanya ada di equator dan ora,
terutama inf. fundus. Ada di +/- 25% normal eye
3. Reticular (honeycomb) degeneration > fine network of
perivascular pigmentation. Kdg nerus sampe post.
equator.
Innocuous peripheral retinal degeneration
4. Peripheral drusen> clustered / scattered small pale
discrete lesion, kdg hyperpigmented borders.
5. Pars plana cyst> clear walled cyst, biasanya kecil.
Muncul dari non-pigmented ciliary epithelium. 5-
10%, biasanya di temporal. Biasanya ga bikin RD.

Sites of vitreous adhesion

Physiological> Vitr. Peripheral cortical loosely attached ke internal Pathological > abn adhesions bisa bikin retinal tear formation lalu PVD
limiting membrannya sensory retina. atau vitreomacular interface ds.
1. Vitreous base (sgt kuat) 1. Lattice degeneration
2. Optic disc (cukup kuat) 2. Retinal pigment clumps
3. Perifoveal (cukup lemah 3. Cystic retinal tufts
4. Peripheral blood vessels (biasany lemah) 4. Vitreous base anomalies
5. “white w/ pressure” & “white w/o pressure”
6. Zonular traction tufts
7. Vitreomacular traction
8. Preretinal new vessels
Definitions
1. Retinal detachment> perpisahan NSR dr RPE. Akibatnya terjadi akumulasi SRF dipotential space tsb
 2. Rhegmatogenous> RD full thickness defect di sensory retina, jd cairan dari synchytic (liquefied) vitreous ke subretina. RRD artinya fluid
masuk further than 1 optic disc diameter dari pinggir robekan
3. Tractional RD> NSR ketarik dr RPE krn contracting vitreoretinal membranes tanpa ada retinal break
4. Exudative (serous, secondary) RD> SRF muncul dari pembuluh NSR dan/atau choroid
5. Combined trational-rhematogenous RD> retinal break krn traksi dari daerah dekat fibrovascular proliferation
6. Subclinical RD> asymptomatic break dan sedikit SRF, 1 disc diameter dari robekan, tapi gak sampe 2 disc diameters posterior dari equator.
(Atau semua asymptomatic RD juga dibilang gini)
Ultrasonography
Terutama kalo medianya opaque (misalnya ada severe vitreous hemmorage
Technique
• Methylcellulose or an ophthalmic gel is placed on the tip of the probe to act as a coupling agent.
• Sesuaikan Bscan probe ke pentunjuk di layar, usually to the left.
• Vertical scanning> marker ke atas, Horizontal scanning > marker ke hidung
• Mata pasien liat straight ahead, up, down, left and right. Tiap posisi liat horizontal dan vertikalnya
• Probe gerak berlawanan arah mata pasien. Dynamic scanning dgn pasiennya gerakin mata, probenya diem

B scan shows retinal detachment

Peripheral lesions predisposing to retinal detachment
Lattice degeneration (LD)
Occurs in 80% of the population, probably develops early in life, peaks in 20s-30s. Common
in moderate myopes
Lifetime risk in RD 1%. 40% patient with RD has LD, because of premature PVD and
tractional tears
Discontinuity of the ILM w/ variable atrophy of the underlying NSR. Vitreous sekeliling
lattice synchytic, tp vitreous attachmentnya tetep nempel.
Signs: Biasanya bilateral, temporal dan superior
1. Spindle shapped areas of penipisan retina, biasanya antara equator dan batas posterior
vvitreous base
2. Pembuluh yg sklerotik membentuk jaring putih berantakan yg khas
3. Beberapa kasus bisa sisaan dr sel müller yg degenerasi ‘snowflakes’
4. Berhubungan dengan hiperplasia RPE
5. Sering ada lubang kecil
Complication (gak terjadi di semua dg LD):
6. Retinal tears krn PVD
7. Atrophic holes (2%). Lebih sering di young myopes, biasanya tanpa acute
symptoms of PVD dan SRF spread slowly (diagnosis lama)
Management
Kalo asymptomatik > edukasi baik2 ttg RD
Kalo ada U-tear, tatalaksana sesuai U-tear

Snailtrack degeneration
Bands berbatas tegas of tightly packed ‘snowflakes’. Dianggap sebagai precursor
of lattice degeneration. Traksinya kecil jadi jarang sobek, walau holes sering. Gak
perlu treatment profilaksis.

Cystic retinal tuft

Granular patch / retinal rosette adalah congenital abnormality terdiri dari kecil bulat atau oval, whitish lesion, biasanya di equatorial / retina
perifer, lebih sering di temporal. Berhubungan dengan pigmentasi pada dasarnya, terdiri dari glial tissue. Adhesi vitreoretinal kuat, biasanya ada
small round holes dan robekan horseshoe. CRT ada pada 5% populasi, 20%nya bilateral dan menjadi RD 5-10%.
Snail track degeneration islands of snailtrack degeneration cystic tuft with small round hole

Degenerative retinoschisis (RS)

RS terjadi pada 5% populasi pada populasi di atas 20tahun dan sering
hipermetropia. 80% bilateral
Berawal dari microcystoid degeneration berasal dari dari lubang degeneratif
yang perlahan menyatu, hasil dari separatiom / splitting of NSR jadi lapisan
luar dan dalam dengan memotong neuron dan hilangnya penglihatan
sepenuhnya pada area yang terkena.
No photopsia dan floaters, rarly shows symptoms walau spread posteriorly
kecuali ada vit hmrrg/ RD
Early RS > extreme inferotemporal perifer pada kedua fundus, seperti
microcystoid degen. yg berat dg convex, smooth, thin, relatively immobile
dome shaped elevation of retina, may progress circumferentially sampai kena
semua perifer, biasanya gak sampai lewat dari equator. Kalo ada pigmented
Retinoschisis early large outer break
demarcation kemungkinan besar jd RD. Permukaannya inner layer bs kayak snowflakes,
whitish remnants of müller cell footplates dan pembuluh sklerotik dan rongga schisis
dihubungkan grey-white tissue strands. Microaneurysma/telangiectatic sering, terutama
reticular type. Jarang2 bikin RD, kalopun jadi, hampir selalu asymptomatic, jrg progresif
dan butuh op. Posterior extension ke fovea dan perdarahan vitreous jarang.
Penanganan > diskusikan dg pasien, terutama yg double layer break. Kalo kecil, ga perlu
review rutin. Kalo besar, terutama kl both layer dan sampe belakang equator, observasi
berkala dg foto dan test visual field. Kalo posterior extention, OCT. Retinopexy or surgical
kalo progress ke arah fovea. Vithem rekuren mesti di vitrectomy.

Zonular traction tuft OCT > seperation  pd outer plexiform layer

Fenomena akibat zonular fibre aberrant (15%) meluas posterior dan melekat ke retina dekat
ora serata dan menanggung traksi retina ke base nya. Biasanya lokasi di nasal. Risiko jadi RD 2%

White with pressure (WWP) and White without pressure (WWOP)

WWP > area di retina putih-keabuan jernih yg dicetuskan o/ indentasi sklera. Tiap area dh fixed jd WWP ny gk gerak klo indentasinya gerak. Bs
ad di post. bordernya islands of LD, snailtrack degen & outer layer acquired RS. Srg ad di (n) eyes & associated dg abnormally strong attachment
of vitreous gel, walo ga selalu berarti  risk sobekan retina.
WWOP > mirip WWP tapi tanpa scleral indentation. WWOP mirip dg area yg adhesi condensed vitreousnya cukup kuat. Kalo ga teliti, retina
normal di sekitar WWOP sering dikira flat retinal hole. Robekan retina biasanya terjadi di batas posterior WWOP. Klo ada WWOP dg mata
satunya riwayat robek retina, saran profilaksis. Pemeriksaan reguler penting

(A) WWP (B) WWOP dgn retinal tear (panah pseudo-break) Myopic choroidal atrophy

Myopic choroidal atrophy

Choroidal depigmentation difus /sirkumskript, biasanya krn penipisan retina & muncul biasanya pd pole posterior dan equator high myopic eyes.
Retinal hole krn atrophic retina kdg bs jd RD. Krn kontras yg buruk, lubang kecil susah terlihat.
Posterior vitreous detachment
PVD adalah perpisahan antara cortical vitreous+delineating PHM. PVD
terjadi krn synchysis dan syneresis dg akses ke ruang preretinal oleh
dehiscence pada cortical gel &/atau PHM. <50 10%, ↑2/3x usia 70thn.
Biasanya spontan, tapi bisa dicetus oleh tindakan. Perifoveal hyaloid
detachement diikuti foveal separation > detachment dr posterior retina -
equator, attachment di OD akan tetap. Baru complete detachment dari
vitreous kortikal keanterior sampai vitreous base.
Clinical features:
Symptoms:
1. Photopsia hampir selalu di temporal.
2. Myedesopsia (ga selalu patologis, tapi bisa aja vitreous blood).
Weiss ring retina tepi optic yang detached > ga ada≠ga RD, ada
≠RD
3. Blurred vitreous > may due to dispersed hmrrg.
Signs:
1. Di slit lamp kayak crumpled translucent membrane di rongga mid-
vitreous
2. Perdarahan> RBC di anterior vitreous/focal intra gel/preretina (🌙).
Kalo ada, hrs cari retinal break (40-90% ada), tend to be posterior
3. Pigment granules anterior vitr. (Shafer sign/tobacco dust) 95% ada
retinal break krn nunjukin ada loss of continuity antara RPE dan
vitreous
4. Vitreous cell> kalo banyak signify presence of break
5. Retinal breaks (lihat di bawah) \

Crumpled membrane. Schafer sign

Investigation> ß-scan uUSG > demonstrate extent of PVD. OCT> separasi post. vitr. face and retina

B scan USG OCT

Management
Harus diperiksa segera (dlm 24-48jam)! Lebih urgent yg myopia, riw. RD keluarga (+), high risk synd (misal Stickler, pseudophakia & gejala VF
defect), ↓penglihatan / floaters heboh. Tanya RPD (terutama DM) kalo cm ada 1 floater kecil tanpa photopsia, gak urgent.
 Anterior vitr. harus diperiksa adanya darah/pigment. Periksa 360˚ sampe ora serrata. Fellow eye walau asymptomatik harus priksa. Kalau
≥10 vitr. cell dalam 1mm slit lamp >30% fellow eyes juga robek.
Subsequent management> kalau ga ada suspicior finding, ga usah periksa lagi. Kalo ada yg aneh2, periksa interval 1-6minggu. Prominent
floater/hazy vision harus FU. Pasien harus pulang dg KIE jelas ttg kapan harus balik. Kalau ada area di fundus yg ga keliatan krn darah > weekly
FU. Fundus-obscuring vitr. hmrrg. difus (tanpa faktor risiko non-PVD hmrrg)> retinal break (60-90%) dan RD (40%). RAPD harus di ekslusi
dan B-scan USG rutin sampe resolve u/ exclude detachment/identifiable break. Coba very low treshold / vitrectomy, terutama kalau ada risk factor
(apalagi ada riw RD di fellow eye)
Retinal break
Paling sering karena traksi adhesi vitroretinal. Terjadi di 1/5 px symptomatic PVD. Kalo ada break, retrohyaloid fluid masuk ke subretinal space.
Asymptomatic retinal break > 8%
Clinical feature
- Timing > biasany at / soon stlh onset gejala PVD. 5% bs delayed beberapa mggu
- Location > biasanya upper retina, temporal > nasal. Macular breaks jarang, biasany 🌑 pd myopic eye.
- Morphology > bisa flat / cuff krn SRF. Kalo extend >1 DD dari tepi break = RD
o U-tear (horseshoe) > flap dg apex tertarik ke anterior o/ vitr.
Basenya tetap nempel ke retina
o Operculated tears> Flap tersobek semua o/ vitr. yg detach jd
sobekanny bulat/oval.
o Retinal holes> Bulat/oval. Lbh kecil dari breaks+lbh jarang
jd RD, adany progress lambat shallow RD pd young female
myope. PVD jarang, tp kalo ada, opperculum (retinal patch
yg lepas dan nempel ke vitr.) biasa ada di dekat sana.
Retinal holes bulat bisa ada di LD. Atrophic retinal hold yg
jadi RD harus di-distinct dr atrophic retinal holes variant dr
paving stone degen. (lower risk)
o Dialysis>circumferential tear sepanjang ora biasanya krn
blunt trauma. Vitreous harus tetap nempel! Seringi spt
peripheral break yg besar dg regular rolled edge. Seringkali
jadi RD w/o PVD
o Giant retinal tear> Variasi U-tear. ≥90˚ dari retina
circumferance sobek. Beda sama dialysis, vitreous ttp
nempel ke margin anterior sobekan. Paling sering tepat post-
oral retina & pada equator(lebih jarang)
Management
Penanganan bervariasi. Pasien haru di KIE dengan jelas terutama u/
kontrol kalo ada gejala baru.
- Faktor risiko jadi detach:
1. Riw RD di fellow eye, pernah op katarak (terutama kalo ada vitr. loss)
myopia, riw RD keluarga & systemic terkait
(Marfan,Stickler&Ehlers-Danlos synd.). Saran profilaksis sblm op.
katatak, laser capsulotomy & IVitreal inj.
2. Symptomatic breaks terkait acute PVD>asympt breaks yg ga sengaja
ketemu
3. Size> robekan besar lebih mungkin progress
4. Persistent vitreoretinal traction&shape> kyk U-tear=ada ongoing
traction. Round hole jarang ada ongoing traction
5. Location> superior breaks lebih mungkin progress. Equatorial breaks
> oral breaks. 6. Pigmentation di sekitar breaks indicates chronicity dan degree of
stability
7. Aphakia
- U-tears symptomatic akut 90% jadi RD. Tx ↓ jadi 5% >> urgent! U-tear asymptomatic 5% jd RD> observasi.
- Operculated tears> terutama kalo asymptomatic, jarang jadi RD. FU 2-4mggu, 1-3months, 6-12 bulan lalu tiap tahun. Intact briging vessels
overlying the break = vitreoretinal traction > bisa bikin vitr. hmrrg. > consider u/ tx
- Traumatic retinal breaks (termasuk acute dialysis) selalu harus di tx
- Asymptomatic subclinical RD 10% jd gejala dlm 2-3tahun. Tx case by case, tgt risiko. KIE baik2. Kl progress> terapi
- Asymptomatic flat round holes ga perlu profilaksis. Review tiap 1-2 thn.
Treatment technique > tanpa RD, pake laser(via slit/BIO)/cryo.
Laser lebih precise, retina berdekatan aman, risiko jd epiretinal membrane rendah.
Kl yg di perifer bgt>pake BIO/cryo. Kalo contiguous/extensive lesion/eyes w/ hazy media/small pupil> mending cryo
After tx> avoid strenuous physical exertion 1mggu (adesi sudah cukup). FU 1-2 minggu.
(detil laser/cryo baca di buku lgsg)
Rhematogenous retinal detachment
Pathogenesis
1:10.000 populasi / tahun. 10% bilateral. Akumulasi liquefied vitreous di bawah neurosensory
retina. Kalo vitreous gak liquefied dan ga ada traksi, hampir ga pernah jd RD. 40% RD muncul di
myopic eyes (makin ↑myopia=↑ risiko). High myope at risk krn small round holes in chorioretinal
atrophy dan dr macular holes. Visual loss saat op katarak dan laser capsulotomy ~ ↑ risiko RD di
high myope.
Identification of retinal breaks

!! ~50% >1 break,

biasanya dalam 90˚ of
each other
Konfigurasi SRF spread
governed by:
- Gravity
- Anatomical limit (ora serrata, optic nerve)
- Lokasi primary retinal break, kalo di superior biasanya
ke inferior, same side baru ke superior opposite side.

Modified Lincoff’s rule

(A)
Shallow inferior RD yg SRF lbh tinggi di temporal
= primary break di inferior sisi sama
(B) Primary break di arah jam 6 = equal fluid level
(C) Bullous inferior RD = primary break di atas meredian horizontal
(D) Primary break di upper nasal > SRF muter kelilingin optic disc lalu naik di
temporal sampe level primary break
(E) Subtotal RD dg ruperior wedge of attached retina = primary di perifer
dekat highest border.
(F) SRF crosses vertical midline above = primary break dekat jam 12, bawas
bawah SRF = side of the break
Symptoms
60% premonitory sympt:flashes & floaters (+) (krn acute PVD) ada curtain
like VF field defect>bs smp central vision. Sebagian ga ada, pada pagi krn
keserap waktu inactive saat tidur. VF defect bawah lbh cepat terasa dibanding
atas. Kuadran VF defect pertama berguna u/ bantu cari lokasi primary break.
Loss of central vision bisa krn fovea kemasukan SRF/visual axis ketutup large
bullouw RD.
Sign
General
- RAPD (+) kalo RD extensif. - Retinal breaks terlihat spt diskontinuitas permukaan retina. Biasa
- IOP ↓ 5mmHg dibanding mata sebelah. Biasanya berhubungan dg merah krn kontras sensory retina dg underlying choroid. Kalo
choroidal detachment. IOP bisa ↑ di Schwatz-Matsuo synd, choroidnya hipopigmentasi (misalnya pada high myope) colour
dimana RDD+mild uveitis ant. yg berkaitan dg dialisis krn blunt contrasnya berkurang, small break sering overlooked
trauma pada pria muda. Displaced photoreceptor outer segment di - Tobacco dust
aqueous yg nyumbat trabecular outflow.
- Retinal signs depend pd durasi RD dan ada tidaknya proliverative
vitreoretinopathy
- Iritis sering(mild) (jgn kirain Schwartz-Matsuo). Kdg kalo berat >
posterior synechiae > RD jadi overlooked.
Fresh retinal detachment
- RD bentuk convex agak opak dan bergerigi krn retinal oedema. Loss of choroidal pattern dan pembuluh terlihat lbh gelap dibanding flat
retina
- SRF melebar s/d ora serrata, kec klo penyebabnya macular hole fluid initially confined to posterior pole (rare)
- Macular pseudohole klo posterior pole detached kesannya ada lubang makula krn retina fovea tipis. Tiati overdx
- B-scan USG menunjukan good mobility of retina & vitreous

-------------------Retinal detachment---------------------- SRF

Longstanding retinal detachment
- Retinal thining krn atropi. Tiati jgn kirain RS.
- Intraretinal cysts krn RD udh +/-1tahun. Kalo reattached biasanya hilang
 - Subretinal demarcation lines (high water / tide marks) krn proliferasi of RPE di junction of flat & detached retina. terbentuk dlm 3 bulan.
Pigmentation makin hilang dg waktu.

---------------------------------Retinal cyst----------------------USG--------------- Demarcation lines

Proliferative vitreoretinopathy
Krn epiretinal & surretinal membrane formation, kontraksi bikin tangential retinal
traction & fixed retinal fold formation. Sering setelah op RRD atau penetrating
injury (walau bias aja tanpa riwayat) retinal folds dan rigidity  retinal mobility
krn gerakan mata / scleral indentation berkurang
- Grade A (minimal) diffuse vitreous haze & tobacco dust. Pigmented clumps
di inferior retina.
- Grade B (moderate) wrinkling of inter retinal surface, mobilitar vitreous
berkurang, rolled edge of retinal breaks, tortuosity pembuluh darah &
kekakuan retina. Penyebabnya krn epiretinal membrane (srg ga muncul scr
klinis)
- Grade C (marked) rigid full-thickness retinal fold (sering star shaped)
+vitreous condensation dan strands berat. Note ant/post. Catat lokasi dg arah
jarum jam, biasa gak contiguous
- Advance disease > gross reduction of retinal mobility dg retinal shortening
dan kyk funnel like triangular formation

Grade A Grade B Grade C

Differential diagnosis
- Degenerative RS
- Choroidal det. ec hypotony (biasa stlh op glaucom drainage), sulfonamide, uveitis, post. scleritis,
choroidal tumours & cyclodialysis cleft krn trauma / surg. Kadang 2˚ to RD jg.
o Ga ada photopsia dan floaters krn ga ada traksi vitreoretinal. VF defect bias (+) kalo luas
o Low IOP krn sering ciliary body detachment. Anterior chamber dangkal bs jd non pupillary
block glaucoma. The elevation warna coklat, convex, licin dan relatively immobile. 4 lobes
are present (temporal & nasal choroidal effusion ec hypotony
biasa paling prominent). Large kissing choroidal detachment bias obscure the view of fundus.
Elevasi tidak meluas ke posterior pole krn dibatasi o/ vortex vein yg msk ke scleral canals. Tp
bs meluas lewat dr ora (beda dr RD)
o Rx: sesuai penyebab. Biasanya perlu drainage via partial thickness sclerotomies.
- Uveal effusion synd. Rare, idiopathic, biasa bilateral. Di middle aged hypermetropic men. Bs jg di
nanophthalmos. Disebabkan gangguan drainage fluid normal dari choroid ke sclera / vortex veins.
o Inflammasi ringan / absent, ciliochoroidal detachment + exudative RD, setelah penyembuhan
residunya bentuk ‘leopard spot’ (high concentration of protein di SRF di RPE jadinya
degeneratif)
o Ddx: UFS secondary to other cause, choroidal hemorrhage & ring melanoma of the anterior
choroid
o Tx: full thickness sclerectomy, terutama di nanophthalmos
Uveal effusion syndrome
Surgery
Indication of urgent surgery
- Acutely symptomatic RD terutama kalo macula is not involved
- Superior atau large brea, krn SRF cepet bgt nyebar
- Advanced syneresis di high myope
- Fresh vitr. hmrrg. + B scan RD (+)
 Lgsg puasa, kurangi aktivitas, bed rest w/ head turned sedemikan rupa jd detachmentnya ke tindih dan SRF berkurang
Threatened macula

Pars plana vitrectomy

Pneumatic retinopexy
Outpatient> masukin gas bubble IVitreal+cryo/laser tanpa scleral buckling. Pake SF 6 atau C3F8 (lebih long-acting)
Outcomenya lebih jelek dr scleral buckling. Biasanya untuk small break / breaks yg lbih kecil dari 2 jarum jam di 2/3 atas retina perifer.

Cryo-gas inj-gas sealed-gas absorbed Reflection seen on disc ‘fish eggs’ ec gas bubble breakup
Principles of scleral buckling > conventional / external RD surgery
Tujuannya u/ tutup sobekan dg bikin RPE nempel ke sensory retina & mengurangi dynamic vitreoretinal traction. harus slalu dilakukan pd
pasien dg RD ec post traumatic dialysis
- Explants pake soft/hard silicone. Ukurannya +2mm dari tepi robkean dan kena ke vitreous base anterior dari tear supaya jgn reopening &
bocor anterior SRF.
- Buckle configuration > radial/segmental/circumferential/encircling, tgt uk, conf &jumlah sobekan
- Technq> konj. di peritomy  retinal breaks localized  cryo  explant dijahit ke sklera  cek posisi thdp sobekan
Drainase SRF via sklera (eg. D-ACE) > spy cepet attach pada SRF yg dlm / long standing viscous SRF, tp tiati retinal perforation/inkarserata di
drainage site/choroidal hmrrg. Prefered kklalo dilakukan sbg pars plana vitrectomy
Komplikasi:
- Diplopia (kadang hialng sendiri
- Cystoid macular edema (25%) > responds to tx. Bisa epiretinal membrane (15%)
persistent subfoveal fluid dan foveal structural disruption (biasanya di macula-off
detachment)
- Anterior segment ischemia, krn vascular compromise. ↑ pada encircling band & w/
syst. cond.
- Buckle extrusion, intrusion or infection. Segera lepas + AB tx k/p
- ↑ IOP. Seringan turun sndiri, tapi kadang butuh terapi
- Choroidal detachment, bisa sembuh sendiri saat edema sklera mereda dan fungsi
vortex vein membaik
- Surgical failure:
o Missed breaks
o Buckle failure, inadequate size, incorrect positioning or inadequate height.
Fish mouthing biasanya large superior U-tear di bullous RD kebuka lebar
setelah scleral buckling.
o Proliferative vitreoretinopathy (PVR) (late). Tractional forces w/ PVR bia
bikin robekan baru, biasanya berapa mggu w/re-detachment
o Reopening w/o PVR. Bs krn inadequare cryo / buckling / ↓ buckle height krn
waktu / late surgical removal

Tractional retinal detachment

Karena progressive contraction of fibrovascular membranes pada are yg luas of vitreoretinal adhesion
Vitreous opacity
Introduction
- Definisi: gel extracell transparan yang terdiri dari kolagen, - Fungsi: structural support bola mata, memberikan jalan masuk
protein terlarut asam hyaluronic dan air. cahaya yang jernih ke retina
- Total volume: 4.0ml - Tidak memiliki kemampuan regenerasi

Muscae Volitantes
Biasa disebut floaters. Pesien mengeluhkan benang2, jaring laba2, atau benda kehitaman dan paling terlihat di latar pucat. Kadang bisa sisa
embriologi. Kalau tiba2, curiga perdarahan vitreous atau perubahan struktur vitreous misalnya posterior viterous detachment

Perdarahan vitreous

- Gejala bervariasi tergantung beratnya

 Mild: floaters mendadak dan buram keseluruhan, tapi pengaruh ke VA
 Severe: severe vision loss

Perdarahan vitreous ringan Perdarahan vitreous Berat

- Penunjang
B-scan USG: penting untuk menyingkirkan adanya ret. tear atau det. dan choroidal melanoma
- Penanganan tgt berat dan penyebab. Pada dense hemrrg disarankan untuk early vitrectomy
TERSON SYNDROME>IO hmrrg+ICH/TTIK/TBI
Biasanya bilateral, tipikalny intraretunal/preretinal, tp bs subhyaloid blood keluar ke vitrous. Diduga krn statis darah ec  tekanan sinus
cavernosus. Prognosis baik.
Asteroid Hyalosis
Penyakit degenerative krn penumpukan calcium pyrophosphate di vitreous gel. Gerak saat mata bergerak tapi tdk mengendap. 75% unilateral,

kebanyakan asimptomatik. Man>woman

Asteroid hylalosis ringan Asteroid hyalosis berat
Synchesis scintillans
Diakibatkan perdarahan vitrous kronik, paling sering pada mata buta. Ditemukan saat perdarahan massif berkurang. Kristal terdiri dari kolesterol
dan terbentuk dari sel plasma dan hasil degradasi eritrosit. Flat golden-brown refractile, seringkali mengendap saat mata immobile. Kadang bisa
masuk ke AC.
Synchysis scintillans
Amyloidosis
Kondisi deposit fibrillary protein extracell, sistemik atau lokal. Di mata: polyneuropathy, nprominent corneal nerves dan pupillary near dissociation

Amyloidosis Menempel di posterior lensa o/ thck

foot plates
Vitreous cyst
Kongenital: awalnya dari ciliary body pigment epithelium. Bisa pigmented/non pigmented (typically attached to disc)
Acquired ec trauma atau inflamasi.
Kalau terganggu: laser cystotomy atau vitrectomy

Vitreous cyst

Persistent fetal vasculature

Selain non pigment, hylaoid vessles yg persisten bs jd:
- Bermeister papilla> Keliatan spt benang2 di opt disc

Bermeister papilla
- Mittendorf dot>di posterior lens surface
- Congenital vitreous veil>extremely rare. Tx ga perlu
Congenital vitreous veil