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Figure 2-13 Inflammation of the corneal stroma.

A

Suppurative kerati ti

s. B

Nonsuppurative,

non necrotizing disciform) stromal

kera

t i t i

s.

Table 2-3 Common Causes of Corneal Inflammation

Finding

Punctate epi

the

l a l e ros i ons

P unc ta te ep i t he l a l k e ra t i t is

Stromal

kerati t is,

suppur

ative

S t roma l k e ra t i t i s , nons uppura t i v e

Periphera l kerat

it

is

E

xa

mples

D ry -ey e s y

ndr

o m e

Toxic

it

y

At

op

i c k e ra toc on j

unctivitis

A denov i rus k e ra t

oconjuncti

vi t is

Herpes sim

pl

ex virus epi thel ial

ke

rati t is

T

hy

ges on s up

erf

ic ial punctate kerati t is

Bac

ter

ial kerati t is

Fungal kerati t is

Herpes

simp

lex

virus

s t roma l k e ra t i t is

Varicel la-zoster

virus

s t roma l k e ra t i t i s

S

yphilit

ic interst i t ial kerati t is

Blephari t is-associated

marginal

inf i l trates

Peripheral ulcerative kerati t is caused

by

c onnec t i v e t i s s ue

diseases

Mo

oren ulcer

MATA MERAH VISUS NORMAL

&

MATA MERAH VISUS TURUN


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MATA MERAHVISUS NORMAL

KonjungtivitisPingueculaPterygium

MATA MERAHVISUS TURUN

Keratitis

Glaukoma AkutEndophthalmitis

EpiscleritisScleritisUveitis

Hyphema


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CONJUNCTIVITIS

Features of conjungtival inflammation

SYMPTOMSLacrimationGritty irritation

StingingBurningItchingPain

PhotophobiaForeign body sensation


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CONJUNCTIVITIS

Features of conjungtival inflammation

Discharge

- watery

- mucoid

- mucopurlent

- purulent

Conjunctival reaction- conjunctival injection

- haemorrhagic conjunctivitis

- chemosis

- membranes

- infiltration- scarring

- follicular reaction

- Papillary reaction


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CONJUNCTIVITISBacterial Allergic Viral Chlamidya

Pain Minimal No pain Minimal Minimal

Itching Occasional Common Common Occasional

Discharge Mucopurulent Watery/Mucoid Watery Mucopurulent

CausesSaph, Strep,

GonnococcusAllergen

AdenoviralHerpes Simplex

C. Trachomatis

Investigation Gram PCR- Immunofluorescence

-PCR- Inclussion bodies


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CONJUNCTIVITISBacterial Allergic Viral Chlamidya

Treatment

- 60% resolve without treatment

- Broad spectrum antibiotic

- drops - ointment - systemic

- Mast cell stabilizers(sodiumcromoglycate

lodoxamide- Steroid- Antihistamines- Artificial tears

symptomatically- cold compress- artificial tears- spontaneous

resolution within 3weeks

Topical- Erythromicyn EO- Tetracyclin EO

Systemic- Doxixycline 2x100mg- Azythromicyne 1 grsingle dose


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PTERYGIUM

- Triangular fibrovascular subepithelial ingrowth of

degenerative bulbar conjuctival tissue over the limbus

onto the cornea

- Hot climates

- Chronic dryness

- Ultraviolet exposure


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PTERYGIUM

Type I

Extends less than2 mm onto the

Cornea

Type II

-

Involve up to4 mm of the

cornea

- Induce astigmatism

Type III

-

Invade more than

4 mm of the cornea- Involve Visual Axis


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PTERYGIUM

Differential Diagnosis

Pseudopterygium- adhesion of a fold of conjuctiva to a pefipheral corneal

ulcer/ thinning

- only in the apex of cornea


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PTERYGIUM

Treatment

Medical

- symptomatic patients (tear subtitutes, topical steroidultraviolet sunglasses)

Surgery

- type 2 n 3- technique

bare sclera

amnion graft

conjuctival limbal graft and or MMC

pterygioplasty


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PTERYGIUM392 E

xt

ernal Disease and Cornea

A

J

B

c

o E

Figure 14 Surgical wound closures following pterygium excision. A,

Bare

sclera although

sutures can be placed to tack down conjunctival wound edges. B, Simple closure with fine,

absorbable sutures. C, Sliding flap that

is

closed wit interrupted and/or running suture.

D,

Ro-

tational flap from the superior bulbar conjunctiva. E Conjunctival autograft that is secured

wit

interrupted and/or running suture. Reproduced

wit

permission from Gans LA.Surg ica l trea tment of

pteryg ium. Focal PO nt S Cl in ica l Modu les fo r Ophtha lmolog ists. San Francisco. American Acade my of Ophrha lmology;

1996, modu le

12

lI1usrration by Christine Gralapp.)


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PINGUECULA

- Extremely common, innocuous, usually bilateral,assymptomatic

-

SignsYellow white deposit on the bulbar conjunctiva adjacentto the nasal or temporal limbus

- Treatment

Usually not necessary

!inflamed cases!weak steroid


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KERATITIS

Bacterial Keratitis

- Very uncommon in a normal eye (only develop when ocularsurface have been compromised)- Bacteria that can penetrate an normal corneal epithelium :

N.gonnorhoeae, N.meningitides, C.diphtheriaea, H.influenza

- The most common pathogen : P.aeruginosa, S.aureus, S.pyogenes, S.pneumoniae


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KERATITIS

Risk Factor :1. Contact lens wear2. Trauma3. Ocular surface disease4. Systemic immunosuppression5. Diabetes6. Vitamin A deficiency


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KERATITISDiagnosis

Clinical features1. History (particular attention paid to risk factors)2. Presenting symptoms (pain, photophobia, blurred vision, and

discharge)3. Signs

- infiltrate with ciliary injection- epithelial defect associated with infiltrate around the margin- enlargement of the infiltrate associated with stromal oedema andsmall hypopyon- severe infiltration- progressive ulceration corneal perforation endophthalmitis


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KERATITIS

peripheral infiltration enlargement of infiltrate

hypopyon advance keratitis


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KERATITIS

Diagnosis

Microbiology- Gram staining

Differentiated bacterial species into Gram positive and Gram negative- Culture media

Blood agar, Chocolate agar- Sensitivity report

Susceptible, Intermediate, or Resistant


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KERATITISTreatment

General principles1. Decision

Treatment should be initiated even gram stain is negative and before theresult of culture are available2. Antibiotics

- topical antibiotics- oral antibiotics- subconjunctival

3. Mydriatics- prevent the formation of posterior synechiae- reduce pain from ciliary spasm

4. Topical steroids- only in some cases with special attention


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KERATITIS


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KERATITIS

Causes of failure1. Incorrect diagnosis

2. Inappropriate choice of antibiotics3. Drug toxicity4. Gram negative ulcers

Ciprofloxacin corneal precipitates


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KERATITIS

Visual rehabilitation

1. Lamelar keratoplasty2. Rigid contact lenses3. Cataract surgery


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KERATITIS

Fungal Keratitis

- Fungi are microorganism that have rigid walls and multiple

chromosomes containing both DNA and RNA.- The main types

1. Filamentous (Aspergillus spp, Fusarium solani,Scedosporium spp)

2. Yeasts (candida spp)


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KERATITIS

Clinical features1. Presenting symptoms

- foreign body sensation, photophobia, blurred vision, discharge.

- history of trauma or chronic ocular surface diseases2. Signs

a. Filamentous keratitis- grey yellow stromal infiltrate with indistinct margins- satellite lesions- hypopyon- feathery edge

b. Candida keratitis- yellow white infiltrate associated with dense suppuration

CHAPTER : Infectious Diseases/Externa l Eye: Microbial and Parasitic

Infections.

165

aregardeners who use weedtrimmers or other similar motorized lawncare equipment

without wearing protective eyewear Trauma reated to contact ens wear is another com

mon risk factor forthe develop ment of ungal keratitis. Topical corticosteroids are a major

risk factor

as

\ve

as

they appear to activate and increase the virulence of ungal

ismsbyreducing the cornea s resistance to infection. Candida species cause ocular

tions in immunocompromised hosts and in corneas with chronic ulceration from

other

causesThe increasing use of opical corticosteroids during the past 4 decades has been

implicated as a major cause forthe rising incidence of ungal keratitis during his period.

Furthermo re, systemic corticosteroid usage may suppress the host s immune response,

thereby predisposing to fungal keratitis.

Othe

r common rsk factors include corneal sur-

gery (eg PK, radial keratotomy) and chronic keratitis (egherpes simplex [HS V] herpes

loster

or vernal/allergic conjunctivitis).

In early 2006 an outbreak of contact lens-associated fungal keratitis wasobserved,

f rst inSingapore and the Pacific Rim and then in the United Sa es The epidemic oc-

curred in association with the use ofRenu wi h MoistureLoc solution (Bausch and Lomb,

Rochester New York) Bausch and Lomb withdrew the solution from the world market

on May 15, 2006.

Chang DC, Grant GBO Donnell

K

e a1 Fusarium Keratitis Investigation Team Multistate

outbreak of Fusarium keratitis associated with use of a contact lens solution. lAMA. 2006

296(8),953-963.

CLINICAL PRESENTATION Patients with fungal keratitis tend to have fewer inflammatory

signs and symptoms during the initial period than those with bacterial keratitis and may

have ittle or no conjunctival injection upon in i ia l presentation. Filamentous fungal

litis frequently manifests

as

a gray-white, dry-appearing infiltrate that has irregular feath-

ery or filamentous margins (Fg 5 18) Superfca lesions may appear gray-white, elevate

Figure

5

8

Fu

n

ga

l

ke

ratiis caused by Fusarium so ani

with

characte

r

stic d

ry

whi

te

stromal

ini trate with feahe y edges.


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KERATITIS

Investigation

1. Gram and Giemsa2. CulturesSabouraud dextrose agar

3. Histology


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KERATITIS

Treatment1. Removal of the epithelium2. Topical treatment

Antifungal : natamycine 5%, econazole 1%,Amphotericin B 0.15%, miconazole 1%3. Subconjunctival antifungal

Fluconazole4. Systemic

Itraconazole, Voriconazole5. Mydriatic6. Keratoplasty in unresponssive cases


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ENDOPHTHALMITIS

Endophthalmitis is a clinical diagnosis made when

intraocular inflammation involving both the posteriorand anterior chamber is attributable to bacterial orfungal infection


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ENDOPHTHALMITIS

Jenis endophthalmitis

1. post operative endophthalmitis2. endogenous bacterial endophthalmitis3. endogenous fungal endophthalmitis


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ENDOPHTHALMITIS

Diagnosis

Clinical features

1. History (trauma, intra-ocular operative, corneal ulcer)2. Presenting symptoms (severe pain, photophobia, blurred vision)3. Signs

- ciliary injection- infiltrate of the cornea (history of corneal ulcer)- hypopyon- signs of previous intra-ocular operative- Vitreous Cells !!!!!!! (USG)


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ENDOPHTHALMITIS

Treatment

1. Antibiotics/antifungal- topical- systemic- intravitreal

2. Mydriatics- prevent the formation of posterior synechiae- reduce pain from ciliary spasm

3. Vitrektomi4. Evisceration


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EPISCLERITIS

Epicleritis

Inflammation of the episcleral tissue

- Nodular- Diffuse

>> female

Nodular less acute and more prolonged

course


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EPISCLERITIS

Symptoms

-

Sudden red eye- Uncomfortable

- Hotness

- Pain!unussual

Signs

-

Episcleral injection-

Diffuse/ nodular

-

Often interpalpebral

-

Ant scleral surface is

flat

Diagnosis


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EPISCLERITIS

First attact

-

Topical steroid

- Artificial tears

Recurrent

- Mild : no treatment

- Extremely frequent n disabling : NSAID can be used for 2-3months

Treatment


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SCLERITIS

- Uncommon

- Oedema n cellular infiltration of the entire thickness of the sclera

-

Threaten vision

- >> female

- Categorized into 4 class

1. Anterior non-necrotizing scleritis

2. Anterior necrotizing scleritis (with / without inflammation)

3. Scleromalacia perforance

4. Posterior scleritis

Prevalence

Watson Foster

I . A nt er ior s cl er it is 9 8% 9 4%a) Diffuse 40% 45%b) Nodular 44% 23%c) Necrotizing 14 % 26 %

i) Withi nf la mm at io n (10 % ) (23 % )

ii) Withoutinflammation= scleromalaciaperforans (4 %) (3 %)

I I. Po st er ior s cl er it is 2 % 6 %

Prevalence

Watson Foster

I . A nt er ior s cl er it is 9 8% 9 4%a) Diffuse 40% 45%b) Nodular 44% 23%c) Necrotizing 14 % 26 %

i) Withi nf la mm at io n (10 % ) (23 % )

ii) Withoutinflammation= scleromalaciaperforans (4 %) (3 %)

I I. Po st er ior s cl er it is 2 % 6 %


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SCLERITIS

Anterior non-necrotizing scleritis Anterior necrotizing scleritis

Scleromalacia perforance Posterior scleritis[

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SCLERITIS

Symptoms- Photophobia

- Uncomfortable

- Hotness

- Pain

Signs-

Scleral injection

-

Diffuse/ nodular

-

Scleral thinning

-

Yellow scleral necrotic

plaque

Diagnosis


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SCLERITIS

-

Work up: Systemic autoimmune disease (Rheumatoid arthritis, SLE)- Topical steroid ( non-necrotizing)- Systemic NSAID ( non-necrotizing)

- Periocular steroid injection ( non-necrotizing or necrotizing)

-

Systemic steroid (necrotizing!if NSAID not appropriate)

- Cytotoxic agent ( ex: cyclophosphamide, azathioprine)

- Immune modulators!less useful but may be considered as a short termtreatment before cytotoxic agent

Treatment


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EPISCLERITIS VS SCLERITIS

Episcleritis Scleritis

Main symptom Redness Severe,radiatingpain

Redness Br ig ht red Bluish red

Maximum Superficial Deep

Vasc ul ar Episcl er al Episcl er al

Congest ion Vessels Vessels

Tenderness Rare +

Scleral thinning Rare +

Vision affected Rare +

Intraocularinvolvement Rare +


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UVEITIS

UVEA


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UVEITIS

- Inflammation of the uvea

- InfectiousTraumaticNeoplasticAutoimmune


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UVEITIS


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UVEITISSigns of Uveitis

Conjunctiva: Perilimbal/ diffuse injection, nodules

Corneal endothelium : Keratic precipitates, fibrin

AC : Inflammatory cells, flare

Iris: nodules, post synechiae,

atrophy, heterochromia

Vitreous: inflammatory cell, traction bands

Choroid: inflammator infiltrate, neovascularisasiInfl cells, edema, cystoid macular edema,

RPE loss/hypertrophy, epiretinal membrane

Edema, neovascularization


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UVEITIS

Anterior

Uveitis

Intermediate

Uveitis

Posterior

UveitisPanuveitis

Classification of uveitis


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UVEITIS

Anterior uveitis- Low grade inflammatory reaction moderate /severe inflammation

- Mostly sterile inflammatory reaction, and unknown cause

- Example :

- Behcet syndrome- Glaucomatocyclitic crisis

- Lens associated uveitis

- IOL associated post-operative inflammation

- Herpetic disease

- Drug induce uveitis

- Juvenile rheumatoid arthritis

- Fuchs Heterochromic Iridocyclitis

- Idiopathic iridocyclitis


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UVEITIS

Intermediate uveitis- Inflammation concentrate in the anterior vitreous and the vitreos base

overlying the ciliary body peripheral retinal pars plana complex

- Inflammatory cells may aggregate in the vitreous (snowballs) or

accumulate on the inferior pars plana(snowbanking)

- Example :

- Pars planitis (most common)

- Sarcoidosis

- Multiple Sclerosis

- Lyme diseases

- Syphilis

- Tuberculosis


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UVEITIS

Posterior uveitis- Inflammation may affect the choroid alone (choroiditis) or both choroid and

retina (retinochoroiditis)

- Visual symptoms may be caused by: involvement of the macula, and

reduction of the peripheral vision, or

inflammatory cells on the vitreous (floaters)

- Mostly caused by infectious agent (viral, protozoal,

fungal, bacteria)

- Example :

- Rubela

- Toxoplasmosis ocular

- Citomegalovirus

- Systemic lupus erythematosus


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UVEITIS

Laboratory and medical evaluation :

- Important in making the Diagnosis

-

Most recommended test:complete blood count, erythrocyte sedimentation, ACE,chest radiograph, tuberculosis test

- Evaluation of certain type of uveitis, ancillary testing can be

extremely helpful:

- Fundus Fluorescein angiography (FFA)

- Ultrasonograaphy- Vitreous biopsy


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UVEITIS

Fundus Fluorescein ngiography

U

S


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UVEITIS

Medical management of uveitis

1. Mydriatic and cyclopegic :

- breaking and preventing posterior synechiae

- relieving photophobia caused by ciliary spasm

2 Corticosteroid :

- mainstay of uveitis therapy

- treatment of active inflamation in the eye

- prevention or treatment of complications such as cystoid

macular edema

- reduction of inflammatory infiltration of the retina, choroid,

or optic nerve


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UVEITIS

Medical management of uveitis

3. NSAID

4. Immunomodulating and immunosuppressive agent

5. Treatment of underlying cauused ( infectious uveitis)

6. Surgery


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UVEITIS

Topical administrationSubtenon injection

Intravitreal injection


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HYPHEMA

! Hemorrhage into the anterior chamber.

!

The source of bleeding is the iris or ciliary body! Common complication of blunt trauma.


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HYPHEMA

SIGNSRed blood cells sediment inferiorly with a resultant

fluid level

The height of which should be measured anddocumented


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HYPHEMA

OBSERVATION- Required in most cases

- Immediate risk : secondary hemorrhage( anytime up to week after the first injury)


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HYPHEMA

TREATMENT

- Hospitalize, evaluate the IOP and blood

- Anti-fibrinolytic agent!prevent sec hemorrhage

- Steroid

- Antiglaucoma medication if needed

- Atropine (controversy)


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