MATA MERAH VISUS NORMAL

&
MATA MERAH VISUS TURUN

Figure 2-13 Inflammation of the corn eal stroma. A, Suppurative keratitis. B, Nonsuppurative,
non necrotizing (disciform ) stromal keratitis.

Table 2-3 Common Causes of Corneal Inflammation

Findin g Examples

Pun ctate epithe li al erosio ns Lia Meuthia Zaini

Dry-eye syndrom e
Toxic ity

FK Unsyiah / RSUDZA
Punctate epith eli al kerat itis
Stromal kerati ti s, suppurative
Stroma l keratit is, nonsuppurative
Perip hera l keratitis
Atopic keratoconjunctivitis
Ad enovi rus keratoconjunctiv itis
Herpes sim pl ex vi rus epi t helial ke ratitis
Thygeso n su perficial punctate kerat itis
Bacteria l keratiti s
Fungal ke ratiti s
Herpes simp lex virus st romal keratitis
Varicella -zoster virus stromal keratitis
Syphilit ic in terstitia l keratitis
Blepharitis-associated marginal i nfiltrates
Periphe ral ulcerative keratitis caused by co nn ective tissue
diseases
Moo ren ulcer
 MATA MERAH
VISUS TURUN
MATA MERAH
VISUS NORMAL
Keratitis
Glaukoma Akut
Konjungtivitis
Endophthalmitis
Pinguecula
Episcleritis
Pterygium
Scleritis
Uveitis
Hyphema
CONJUNCTIVITIS
Features of conjungtival inflammation

SYMPTOMS
Lacrimation
Gritty irritation
Stinging
Burning
Itching
Pain
Photophobia
Foreign body sensation
 CONJUNCTIVITIS
Features of conjungtival inflammation

SIGNS Conjunctival reaction

- conjunctival injection
- haemorrhagic conjunctivitis
Discharge - chemosis
- watery - membranes
- mucoid - infiltration
- scarring
- mucopurlent - follicular reaction
- purulent - Papillary reaction
 CONJUNCTIVITIS
Bacterial Allergic Viral Chlamidya

Pain Minimal No pain Minimal Minimal

Itching Occasional Common Common Occasional

Discharge Mucopurulent Watery/Mucoid Watery Mucopurulent

Saph, Strep, Adenoviral

Causes Allergen C. Trachomatis
Gonnococcus Herpes Simplex
- Immunofluorescence
Investigation Gram PCR -PCR
- Inclussion bodies
 CONJUNCTIVITIS
Bacterial Allergic Viral Chlamidya

- 60% resolve Topical

without treatment - Mast cell stabilizers
symptomatically - Erythromicyn EO
(sodium
- cold compress - Tetracyclin EO
- Broad spectrum cromoglycate
- artificial tears
Treatment antibiotic lodoxamide
- spontaneous Systemic
- drops - Steroid
resolution within 3 - Doxixycline 2x100mg
- ointment - Antihistamines
weeks - Azythromicyne 1 gr
- systemic - Artificial tears
single dose
 PTERYGIUM
- Triangular fibrovascular subepithelial ingrowth of
degenerative bulbar conjuctival tissue over the limbus
onto the cornea
- Hot climates
- Chronic dryness
- Ultraviolet exposure
 PTERYGIUM
Type I Type II
Type III

Extends less than - Involve up to

4 mm of the
- Invade more than
2 mm onto the 4 mm of the cornea
cornea
Cornea - Involve Visual Axis
- Induce astigmatism
 PTERYGIUM
Differential Diagnosis

Pseudopterygium
- adhesion of a fold of conjuctiva to a pefipheral corneal
ulcer/ thinning
- only in the apex of cornea
 PTERYGIUM
Treatment
Medical
- symptomatic patients (tear subtitutes, topical steroid
ultraviolet sunglasses)

Surgery
- type 2 n 3
- technique
bare sclera
amnion graft
conjuctival limbal graft and or MMC
pterygioplasty
PTERYGIUM
392 Ext ernal Disease and Cornea

IJ

B c

o E

Figure 14' Surgical wound closu res following pterygium excision . A, Ba re scl era, although
sutures can be placed to tack down conjunctival wound edges. B, Simple closure with fine,
absorbable sutures. C, Sliding flap t hat is closed with interrupted and/or runn ing suture. D, Ro-
tational flap from the superior bulbar conjunctiva. E, Conjunctival autograft that is secured
with interrupted and/or running 'suture. (Reproduced with permission from Gans LA. Surgical treatment of
pterygium. Focal POintS: Clinical Modules for Ophthalmologists. San Francisco. American Academy of Ophrhalmology;
1996, module 12. lI1usrration by Christine Gralapp.)
 PINGUECULA
- Extremely common, innocuous, usually bilateral,
assymptomatic
- Signs
Yellow white deposit on the bulbar conjunctiva adjacent
to the nasal or temporal limbus
- Treatment
Usually not necessary
! inflamed cases ! weak steroid
 KERATITIS
Bacterial Keratitis

- Very uncommon in a normal eye (only develop when ocular

surface 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
 KERATITIS

Risk Factor :
1. Contact lens wear
2. Trauma
3. Ocular surface disease
4. Systemic immunosuppression
5. Diabetes
6. Vitamin A deficiency
 KERATITIS
Diagnosis

Clinical features
1. 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 and
small hypopyon
- severe infiltration
- progressive ulceration corneal perforation endophthalmitis
 KERATITIS

peripheral infiltration enlargement of infiltrate

hypopyon advance keratitis

 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
 KERATITIS
Treatment

General principles
1. Decision
Treatment should be initiated even gram stain is negative and before the
result of culture are available
2. 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
KERATITIS
 KERATITIS
Causes of failure
1. Incorrect diagnosis
2. Inappropriate choice of antibiotics
3. Drug toxicity
4. Gram negative ulcers

Ciprofloxacin corneal precipitates

 KERATITIS

Visual rehabilitation
1. Lamelar keratoplasty
2. Rigid contact lenses
3. Cataract surgery
 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)
 CHAPTER 5: Infectious Diseases/Ext erna l Eye: Microbial and Parasitic Infections. 165

are gardeners who use weed trimmers or other similar motorized lawn care equipment

KERATITIS
without wearing protective eye wear. Trauma related to contact lens wear is another com
mon risk factor for the development of fungal keratitis. Topical corticosteroids are a major
risk factor as \vell, as they appear to activate and increase the virulence of fungal
isms by reducing the cornea's resistance to infection. Candida species cause ocular
tions in immunocompromised hosts and in corneas with chronic ulceration from other
causes. The increasing use of topical corticosteroids during the past 4 decades has been
implicated as a major cause for the rising incidence of fungal keratitis during this period.
Furthermore, systemic corticosteroid usage may suppress the host's immune response,
thereby predisposing to fungal keratitis. Other common risk factors include corneal sur-
gery (eg, PK, radial keratotomy) and chronic keratitis (eg, herpes simplex [HSV], herpes
loster, or vernal/allergic conjunctivitis).
In early 2006, an outbreak of contact lens- associated fungal keratitis was observed,
fi rst in Singapore and the Pacific Rim and then in the United States. The epidemic oc-
curred in association with the use ofRenu with MoistureLoc solution (Bausch and Lomb,
Rochester, New York). Bausch and Lomb withdrew the solution from the world market
on May 15, 2006.

Clinical features Chang DC, Grant GB, O'Donnell K, et a1; Fusarium Keratitis Investigation Team. Multistate
outbreak of Fusarium keratitis associated with use of a contact lens solution. lAMA. 2006;

1. Presenting symptoms
296 (8),953 - 963.

CLI NICA L PRESENTATION Patients with fungal keratitis tend to have fewer inflammatory

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

signs and symptoms during the initial period than those with bacterial keratitis and may
have little or no conjunctival injection upon in itial presentation. Filamentous fungal
litis frequently manifests as a gray-white, dry-appearing infiltrate that has irregular feath-

- history of trauma or chronic ocular surface diseases

ery or filamentous margins (Fig 5- 18). Superficial lesions may appear gray-white, elevate

2. Signs
a. Filamentous keratitis
- grey yellow stromal infiltrate with indistinct margins
- satellite lesions
- hypopyon
- feathery edge Figure 5-1 8 Fungal ke ratit is caused by Fusarium so/ani with charact eri stic dry white stromal
infiltrate with feathery edges.

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

1. Gram and Giemsa

2. Cultures
Sabouraud dextrose agar
3. Histology
 KERATITIS
Treatment
1. Removal of the epithelium
2. Topical treatment
Antifungal : natamycine 5%, econazole 1%,
Amphotericin B 0.15%, miconazole 1%
3. Subconjunctival antifungal
Fluconazole
4. Systemic
Itraconazole, Voriconazole
5. Mydriatic
6. Keratoplasty in unresponssive cases
 ENDOPHTHALMITIS
Endophthalmitis is a clinical diagnosis made when
intraocular inflammation involving both the posterior
and anterior chamber is attributable to bacterial or
fungal infection
 ENDOPHTHALMITIS

Jenis endophthalmitis
1. post operative endophthalmitis
2. endogenous bacterial endophthalmitis
3. endogenous fungal endophthalmitis
 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)
 ENDOPHTHALMITIS
Treatment

1. Antibiotics/antifungal
- topical
- systemic
- intravitreal
2. Mydriatics
- prevent the formation of posterior synechiae
- reduce pain from ciliary spasm
3. Vitrektomi
4. Evisceration
 EPISCLERITIS
Epicleritis
Inflammation of the episcleral tissue
- Nodular
- Diffuse
>> female
Nodular less acute and more prolonged
course
 EPISCLERITIS
Diagnosis
Symptoms Signs
- Sudden red eye - Episcleral injection
- Diffuse/ nodular
- Uncomfortable
- Often interpalpebral
- Hotness
- Ant scleral surface is
- Pain ! unussual flat
 EPISCLERITIS
Treatment

First attact
- Topical steroid
- Artificial tears
Recurrent
- Mild : no treatment
- Extremely frequent n disabling : NSAID can be used for 2-3
months
 SCLERITIS
- Uncommon
52 Chapter 5 Scleritis
- Oedema n cellular infiltration of the entire thickness of the sclera
- Threaten vision Table 5.1. Classification of scleritis Table 5.2. Scleritis vs. episcleritis

- >> female Prevalence Episcleritis Scleritis

- Categorized into 4 class Watson Foster Main symptom Redness Severe,

radiating
1. Anterior non-necrotizing scleritis I. Anterior scleritis 98% 94% pain
a) Diffuse
2. Anterior necrotizing scleritis (with / without inflammation) 40%
b) Nodular 44%
45%
23%
Redness Bright red Bluish red
Maximum Superficial Deep
3. Scleromalacia perforance c) Necrotizing
i) With
14% 26%
Vascular Episcleral Episcleral
4. Posterior scleritis inflammation (10%) (23%) Congestion Vessels Vessels
ii) Without
Tenderness Rare +
inflammation
= scleromalacia Scleral thinning Rare +
perforans (4%) (3%) Vision affected Rare +
II. Posterior scleritis 2% 6% Intraocular
involvement Rare +

ease entities does not infer aetiology, but pro-

5.1
Introduction
Scleritis represents a spectrum of relatively rare
inflammatory disorders of the sclera. Because of
the potentially devastating ocular complica-
tions and possible association with serious sys-
temic disease, the diagnosis of scleritis should
not be missed. Overall, scleritis most often pres-
ents within the 4th6th decades with a mild pre-
disposition towards women over men (1.6:1)
[34, 42, 45]. This entity is rarely seen in children.
No specific genetic, racial, or geographic risk
factors have been elucidated for scleritis,
beyond those seen with associated systemic
conditions. One-third to one-half of patients
(2545 %) with scleritis present with or progress
to bilateral disease; however, disease can be uni-
lateral, simultaneously bilateral, or alternate
between each eye [34, 42, 45].
5.1.1
Classification
In 1976, Watson and Hayreh proposed a clinical
classification of scleritis (Table 5.1) based upon
the anatomic location of the inflammation and
the observed alterations in the associated vas-
cular structures [45]. This categorization of dis-
vides valuable information regarding severity of
inflammation, prognosis, management options,
and association with systemic diseases and with
ocular complications. Few patients (<10 %)
progress to a different form of scleritis from
their initial presentation [42].
Scleritis is defined as anterior or posterior
based upon the location of inflammation, rela-
tive to the equator of the globe. The majority of
scleritis is anterior and can be categorized as
non-necrotizing or necrotizing. Diffuse (40
45 %) and nodular (2344 %) scleritis are non-
necrotizing and represent the most common
forms of anterior scleritis (Table 5.2). The
necrotizing types of anterior scleritis are less
common (1426 %), but represent a more severe
disease entity [34, 45]. Necrotizing scleritis is
classified as either with inflammation or with-
out inflammation, with the latter being synony-
mous with scleromalacia perforans.
Posterior scleritis represents a more hetero-
geneous spectrum of inflammation that is less
amenable to classification. The prevalence of
212 % for posterior scleritis may be underrep-
resentative, due to its low incidence and under-
recognition on clinical examination [3, 34, 45].
Singh and Foster previously subdivided poste-
rior scleritis as either chronic or acute [40]. Ul-
trasonographic classification categorizes poste-
rior scleritis as diffuse or nodular, based upon

58 Chapter 5 Scleritis
5.2.2
Physical Examination: Ocular Signs
Anterior scleritis is a clinical diagnosis that
requires careful examination to localize the
anatomic location and depth of structures in-
volved in the inflammatory process. In compar-
ison to tungsten, fluorescent, and cobalt blue
light, examination of the eye under natural light
greatly accentuates visualization of deep discol-
oration, extent of scleral edema, and areas of in-
creased transparency [45].With the slit lamp ex-
amination, particular attention should be
directed towards distinguishing the level of
maximum vascular congestion, the most exten-
sive areas of scleral edema, and the presence of
episcleral infiltration.
A hallmark finding that distinguishes scleri-
tis from episcleritis is the presence of scleral
edema. Edematous sclera can bow forward, dis-
placing the deep episcleral vascular plexus and
exacerbating deep vascular congestion. To as-
sess the degree of scleral involvement, blanch-
ing the superficial conjunctival and episcleral
vasculature with topical 2.5 % phenylephrine
can improve visualization of the underlying tis-
sue. Further examination using a red-free filter
is instrumental in evaluating the vascular archi-
tecture, areas of avascularity, and cellular infil-
tration of the episclera. The anatomic location
of the inflammation and typical alterations in
the vessels form the basis of the classification of
anterior scleritis [45].
Diffuse anterior scleritis is the most benign
form of scleritis (Fig. 5.3). The area of involve-
ment can be segmental (60 %) or global (40 %),
with mild to severe inflammation and redness.
Distortion of the superficial and deep vascular
structures with subsequent loss of the normal
radial vascular pattern and replacement with
large, tortuous anastomotic channels can be
seen [45].
Nodular anterior scleritis can present with a
single or multiple scleral nodules (Fig. 5.4). Typ-
ically, the nodule is a darker hue of red, separate
from the overlying episclera, immobile, and ten-
der to palpation. These features distinguish this
form of scleritis from nodular episcleritis. The
lack of necrosis within the nodule and the con-
SCLERITIS
Anterior non-necrotizing scleritis
Fig. 5.3. Diffuse anterior scleritis
Scleromalacia perforance
tainment of inflammation within the borders of
the nodules differentiate this form from necro-
tizing anterior scleritis with inflammation. All
of the vascular layers overlying the nodule are
displaced forward [45].
Necrotizing scleritis with inflammation is
the most destructive form of anterior scleritis,
attributed to the extensive release of proteolytic
enzymes (Fig. 5.5). Commonly, the initial pres-
entation is a localized area of scleral edema with
overlying inflammation, greatest at the leading
edge.
Fig. 5.4.A less common
Nodular presentation
anterior scleritis is a focal area
of avascular episclera, adjacent to or overlying
an area of scleral edema. Thinning of the sclera
with increased visualization of the underlying
uveal tissue may result in a bluish-grey hue to
the sclera. Scleral transparency is attributed to
alterations in the collagen and ground sub-
stance, allowing increased visualization of the
darker uveal tissue. However, transparency does
not always indicate thinning of the sclera. A
hallmark feature of necrotizing scleritis is find-
ings of scleral ischaemia.Without treatment, the
inflammation can progress in both directions
circumscribing the globe, until the entire anteri-
or segment is involved. Vascular changes in-
clude postcapillary venous congestion, vascular
Fig. 5.5. Necrotizing scleritis
thrombosis, and the development of deep, anas-
tomotic vessels [45].
Minimal to no signs of inflammation are
minishes.
seen withNecrotic sclera
necrotizing can slough
scleritis or become
without inflam-
sequestered. With severeperforans.
mation or scleromalacia scleral thinning,
As the over-
creased visualization
lying episcleral tissue of thepatches
thins, dark underlying
of the scle-
uvea mayappear
ra may occur.yellowish
Due to decreased
or greyish.sclera
Thevascu-
sclera
larity attributed
may appear to arteriolar
porcelain-like, as thevaso-occlusion,
vascularity di-
large, abnormal vessels may cross and surround
the areas of affected sclera [45].
The findings of posterior scleritis on exami-
nation are variable, based upon on the severity,
extent, and location of the inflammation. Dif-
fuse scleritis with generalized scleral thickening
without nodules or nodular scleritis can devel-
op in the posterior segment [22]. The most com-
mon signs of posterior scleritis are posterior
extension of anterior scleritis (34 %), a serous or
exudative retinal detachment (21 %), optic disc
edema (18 %), a circumscribed subretinal mass
(13 %), choroidal folds, retinal striae, elevated
intraocular pressure, and a bullous or annular
choroidal detachment [22]. Extension of scleral
5.2 Clinical Presentation 59
inflammation to the adjacent choroid can lead
to an overlying serous detachment of the neu-
rosensory retina [22, 34, 43, 45], which repre-
sents the most common sign of posterior scleri-
tis (21 %) [22]. Exudative macular detachments
occurred predominantly in young women, with
a mean age of 26, and often without any other
signs [3]. In posterior scleritis, a circumscribed
fundus mass or subretinal granuloma with as-
sociated choroidal folds and retinal striae
should be differentiated from a choroidal neo-
plasm. Choroidal folds and retinal striae can
Fig. 5.4. Nodular anterior scleritis occur as independent signs of mild diffuse in-
flammation [3, 40]. Bullous choroidal detach-
Anterior necrotizing scleritis ments and, more commonly, annular cilioreti-
nal effusions can occur as an extension of
scleral inflammation [3]. Some patients (9
17 %) with posterior scleritis will have no pre-
senting signs [3, 22].
If inflammation extends beyond the globe,
proptosis, lid retraction, and restriction of ex-
traocular muscle motility may be seen [3, 45].
Orbital myositis may be associated with poste-
rior scleritis in up to 30 % of cases, as an exten-
sion of the scleral inflammation [6]. Consider-
able overlap can be seen between the diagnoses
of idiopathic inflammatory pseudotumour of
Fig. 5.5. Necrotizing scleritis the orbit and posterior scleritis, representing
5.2 Clinical Presentation 59
Posterior scleritis different manifestations within a disease spec-
trum. However, in idiopathic inflammatory
inflammation to the adjacent
minishes.choroid
Necroticcan leadcan slough or become
sclera pseudotumour, involvement of the adjacent ex-
to an overlying seroussequestered.
detachmentWith of the neu- scleral thinning, in-
severe traocular orbital structures is the predominant
rosensory retina [22, creased
34, 43, 45], which repre-
visualization of the dark underlying feature [3].
sents the most common sign of posterior
uvea may occur. Duescleri-
to decreased sclera vascu-
tis (21 %) [22]. Exudative macular
larity detachments
attributed to arteriolar vaso-occlusion,
occurred predominantly in abnormal
large, young women, vesselswith
may cross and surround 5.2.3
a mean age of 26, andthe often
areaswithout any sclera
of affected other [45]. Associated Ocular Manifestations
signs [3]. In posterior scleritis, a circumscribed
The findings of posterior scleritis on exami-
nationgranuloma
fundus mass or subretinal are variable, based
with as- upon on the severity, In the series by Watson and Hayreh, the rate of
extent,and
sociated choroidal folds and retinal
locationstriae
of the inflammation. Dif- complications in patients with scleritis was
fusefrom
scleritis with generalized 57 %, excluding scleral thinning [45]. Decreased
should be differentiated a choroidal neo- scleral thickening
visual acuity, keratitis, cataract, uveitis, and
plasm. Choroidal folds and retinal striae can scleritis can devel-
without nodules or nodular
glaucoma are ocular associations indicating the
occur as independentop in the
signs of posterior segment
mild diffuse in- [22]. The most com-
mon signs of posterior spread of scleral inflammation to adjacent tis-
flammation [3, 40]. Bullous choroidal detach-scleritis are posterior
extension of anterior scleritis (34 %), a serous or sues [34, 42, 45]. Complications are more fre-
ments and, more commonly, annular cilioreti-
exudative retinal detachment (21 %), optic disc quent in severe necrotizing scleritis and poste-
nal effusions can occur as an extension of
rior scleritis [34, 42, 45]. Due to potential ocular
scleral inflammation edema (18 %),patients
[3]. Some a circumscribed
(9 subretinal mass
(13 %), choroidal complications related to scleritis, early diagno-
17 %) with posterior scleritis will have folds,
no pre- retinal striae, elevated
sis and treatment of scleritis and its associated
senting signs [3, 22]. intraocular pressure, and a bullous or annular
choroidal detachment
If inflammation extends beyond the globe, [22]. Extension of scleral ocular manifestations are critical.
proptosis, lid retraction, and restriction of ex-
traocular muscle motility may be seen [3, 45].
Orbital myositis may be associated with poste-
rior scleritis in up to 30 % of cases, as an exten-
sion of the scleral inflammation [6]. Consider-
able overlap can be seen between the diagnoses
of idiopathic inflammatory pseudotumour of
the orbit and posterior scleritis, representing
different manifestations within a disease spec-
trum. However, in idiopathic inflammatory
pseudotumour, involvement of the adjacent ex-
in-
traocular orbital structures is the predominant
feature [3].
5.2.3
Associated Ocular Manifestations
In the series by Watson and Hayreh, the rate of
complications in patients with scleritis was
57 %, excluding scleral thinning [45]. Decreased
visual acuity, keratitis, cataract, uveitis, and
glaucoma are ocular associations indicating the
spread of scleral inflammation to adjacent tis-
sues [34, 42, 45]. Complications are more fre-
quent in severe necrotizing scleritis and poste-
rior scleritis [34, 42, 45]. Due to potential ocular
complications related to scleritis, early diagno-
sis and treatment of scleritis and its associated
ocular manifestations are critical.
 SCLERITIS
Diagnosis
Symptoms Signs
- Photophobia - Scleral injection
- Uncomfortable - Diffuse/ nodular
- Hotness - Scleral thinning
- Pain - Yellow scleral necrotic
plaque
 SCLERITIS
Treatment

- 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 term
treatment before cytotoxic agent
 EPISCLERITIS VS SCLERITIS
52 Chapter 5 Scleritis

Table 5.1. Classification of scleritis Table 5.2. Scleritis vs. episcleritis

Prevalence Episcleritis Scleritis

Watson Foster Main symptom Redness Severe,

radiating
I. Anterior scleritis 98% 94% pain
a) Diffuse 40% 45% Redness Bright red Bluish red
b) Nodular 44% 23%
c) Necrotizing 14% 26% Maximum Superficial Deep
i) With Vascular Episcleral Episcleral
inflammation (10%) (23%) Congestion Vessels Vessels
ii) Without
Tenderness Rare +
inflammation
= scleromalacia Scleral thinning Rare +
perforans (4%) (3%) Vision affected Rare +
II. Posterior scleritis 2% 6% Intraocular
involvement Rare +

ease entities does not infer aetiology, but pro-

5.1
Introduction
Scleritis represents a spectrum of relatively rare
inflammatory disorders of the sclera. Because of
the potentially devastating ocular complica-
tions and possible association with serious sys-
temic disease, the diagnosis of scleritis should
not be missed. Overall, scleritis most often pres-
ents within the 4th6th decades with a mild pre-
disposition towards women over men (1.6:1)
[34, 42, 45]. This entity is rarely seen in children.
No specific genetic, racial, or geographic risk
factors have been elucidated for scleritis,
beyond those seen with associated systemic
conditions. One-third to one-half of patients
(2545 %) with scleritis present with or progress
to bilateral disease; however, disease can be uni-
lateral, simultaneously bilateral, or alternate
between each eye [34, 42, 45].
5.1.1
Classification
In 1976, Watson and Hayreh proposed a clinical
classification of scleritis (Table 5.1) based upon
vides valuable information regarding severity of
inflammation, prognosis, management options,
and association with systemic diseases and with
ocular complications. Few patients (<10 %)
progress to a different form of scleritis from
their initial presentation [42].
Scleritis is defined as anterior or posterior
based upon the location of inflammation, rela-
tive to the equator of the globe. The majority of
scleritis is anterior and can be categorized as
non-necrotizing or necrotizing. Diffuse (40
45 %) and nodular (2344 %) scleritis are non-
necrotizing and represent the most common
forms of anterior scleritis (Table 5.2). The
necrotizing types of anterior scleritis are less
common (1426 %), but represent a more severe
disease entity [34, 45]. Necrotizing scleritis is
classified as either with inflammation or with-
out inflammation, with the latter being synony-
mous with scleromalacia perforans.
Posterior scleritis represents a more hetero-
geneous spectrum of inflammation that is less
amenable to classification. The prevalence of
212 % for posterior scleritis may be underrep-
resentative, due to its low incidence and under-
recognition on clinical examination [3, 34, 45].
Singh and Foster previously subdivided poste-
UVEITIS

UVEA
 UVEITIS

- Inflammation of the uvea

- Infectious
Traumatic
Neoplastic
Autoimmune
 UVEITIS
Symptoms of Uveitis

- blurred vision
- floaters
- pain
- photophobia
- redness
- epiphora
 UVEITIS
Signs of Uveitis
Conjunctiva: Perilimbal/ diffuse injection, nodules

Corneal endothelium : Keratic precipitates, fibrin

Edema, neovascularization
AC : Inflammatory cells, flare

Iris: nodules, post synechiae,

atrophy, heterochromia

Choroid: inflammator infiltrate, neovascularisasi

Infl cells, edema, cystoid macular edema,
RPE loss/hypertrophy, epiretinal membrane
Vitreous: inflammatory cell, traction bands
 UVEITIS
Classification of uveitis
Anterior Intermediate
Uveitis Uveitis

Posterior
Panuveitis
Uveitis
 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
 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
 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
 UVEITIS
Panuveitis

- Affected the entire inner eye

- Mostly associated with systemic diseases
- Generally bilateral although one eye may be
infected first
- Example :
- Syphilis,
- Tubercuosis
- Sarcoidosis
- Sympathetic Ophthalmia
- Voght Koyanagi Harada Disease
 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
 UVEITIS

Fundus Fluorescein Angiography

U
S
G
 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
 UVEITIS
Medical management of uveitis

3. NSAID

4. Immunomodulating and immunosuppressive agent

5. Treatment of underlying cauused ( infectious uveitis)

6. Surgery
 UVEITIS
Corticosteroid administration

Topical administration
Subtenon injection

Intravitreal injection
 HYPHEMA

! Hemorrhage into the anterior chamber.

! The source of bleeding is the iris or ciliary body
! Common complication of blunt trauma.
 HYPHEMA
SIGNS
Red blood cells sediment inferiorly with a resultant
fluid level
The height of which should be measured and
documented
 HYPHEMA
OBSERVATION
- Required in most cases
- Immediate risk : secondary hemorrhage
( anytime up to week after the first injury)
 HYPHEMA
TREATMENT
- Hospitalize, evaluate the IOP and blood
- Anti-fibrinolytic agent ! prevent sec hemorrhage
- Steroid
- Antiglaucoma medication if needed
- Atropine (controversy)
!ank Y"