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dr.

Petty Purwanita, SpM

Inflammatory or infectious nodules that develop


in the eyelid

Most frequently inspissation or


infection of sebaceous glands

Those occuring in the anterior eyelid in the


gland of zeiss or lash follicles external
hordeolum

Those occuring in the posterior eyelid from


meibomian gland inspissation
internal
hordeolum

secondary

Hordeolum

Usually caused by Staphylococcus aureus


Clinical presentation:

- Painful, tender, red nodular masses near the


eyelid margin
- They may rupture purulent drainage
- Generally self limited, improving
spontaneously in 1-2 weeks
Management:
- Warm compress with massage over the
lesion
- Topical & systemic AB not really
necessary
- Incision and drainage in persistent lesion

Localized lipogranulomatous inflammation


involving either meibomian or zeiss glands
Develop slowly and are typically painless
Management:
- Warm compress
- Attempted expression of the inflamed
meibomian gland
- Incision drainage persistent lesion

KALAZION

Causes:

- Can happen in severe cases of viral or bacterial


conjunctivitis
- Trauma
- Haemotological disorders (bleeding disorders,
leukaemias)
- Spontaneous with increased vennous
pressure : coughing, sneezing, vomitting
- Severe hypertension
Treatment:
- Self limiting condition that requires no
treatment in the absence of infection or
significant trauma
- Warm compress

A conjunctival foreign body should be suspected

if a patient presents with a sensation of


something in the eye.
Patients with a conjunctival foreign body often
state that their eye feels as if an irritating object
like grit, junk, sand, or glassis in it but that
they cannot localize exactly where the
sensation is.
The foreign body sensation is often worse upon
blinking when the foreign body is located on the
conjunctival (inner) surface of the upper lid.

Before any manipulation of the eyelid or eye, measure

the visual acuity in both the affected eye and the


fellow eye. A conjunctival foreign body should not
cause a significant decrease in visual acuity.

Less common cause in adult conjunctivitis


The source of infection is either direct contact

with an infected individuals secretion or the


spread of infection from the organism colonizing
the patients own nasal and sinus mucosa
Clinical presentantion:

- Rapid onset
- Conjunctival inflammation & purulent discharge

Bacterial Conjunctivitis

Clinical classification of bacterial conjunctivitis

Management:

- Topical antibiotic definitive


treatment should be based on culture
results
- Artificial tears
- Systemic antibiotic gonococcal
conjunctivitis

Clinical presentation :
- Bleeding spot
- Hyperlacrimation
- Secretion minimal
- Follicle in upper tarsal conjunctiva
Management :
- Hygiene
- Artificial tears
- Antibiotic secondary infection

Viral Conjunctivitis

Age 5 25 yo
Types: palpebral type and limbal type
Symptoms :
- Itchy
- Usually recurrrent in summer
Signs
:
- Bilateral inflammation
- Papil, giant papil, cobblestone in upper
tarsal conjunctiva
- Trantas dots in limbal cornea

Palpebral Type Vernal Keratoconjunctivitis

Limbal Type Vernal Keratoconjunctivitis

Management:

- Avoid outdoor activities, especially in


summer
- Cold compress
- Steroid topical in acute phase
- Topical antihistamine
- Topical mast cell stabilizer
- Injection steroid in tarsal conjunctiva
severe case

Acute, benign, usually idiopathic, recurrent

and frequently bilateral condition.


Usually self-limiting, attacks typically lasts a
few days
Adult > children
Classifications :
Simple episcleritis
Nodular episcleritis

cases, predominantly affects females


Great tendency to recur
Presentation :
Redness, mild discomfort

Signs :
Redness maybe sectoral or diffuse
The attack often reaches its peak within 12

hours and then gradually fades the next few


days
Often flits from one eye to the other or may be
bilateral

Simple sectorial
episcleritis

Simple diffuse
episcleritis

Tends to affect young females, less acute

onset, more prolonged course


Presentations :
Red eye, typically first noted on waking
2-3 days later, area of redness become larger

Signs :
One or more tender nodules within the

episcleral tissue
Bright red to pink in colour
Nodule may be tender to touch and usually
mobile

Localized nodule which can


be moved over sclera

Deep scleral part of


slit-beam
not displaced

Self-limiting benign disease, frequently

doesnt need any treatment


If severe or prolong enough : topical steroid 12 weeks
Benefit over topical NSAID and topical

lubricants
Systemic th/ :
Oral NSAID
Less morbidity

Characterized by oedema and cellular

infiltration of the entire thickness of the sclera


Much less common than episcleritis
Classifications :
Anterior :
Non-necrotizing : diffuse, nodular
Necrotizing with inflammation : vaso-occlusive,
granulomatous, surgically induced
Scleromalacia perforans
Posterior scleritis

Most common form of scleritis


May occur at any age, typically middle-aged

and older adults


Women > men
May be isolated ocular inflammatory condition
or may be associated with underlying
infection (8%) or systemic autoimmune
disease (40-50%)

Most common form


Presentation : ocular redness, pain

and aching
Signs :
Vascular congestion and
dilatation associated with
edema
Redness may be generalized or
localized to one quadrant
The swollen sclera loses its
normal appearance and takes
on a dusky hue
Globe usually tender to touch

Presentations :
Insidious onset of pain followed by increasing

redness, tenderness of the globe and appearance of


scleral nodule
Signs :
Nodules may be single or multiple, in interpalpebra

region 3-4mm away from limbus, blue-red color


The adjacent episclera is often swollen and may

resemble nodular episcleritis except that the


scleral nodule is fixed and cannot be moved over
the underlying tissue, and is tender to palpation

Nodular Anterior Scleritis

On cursory examination resembles


Scleral nodule cannot be
Nodular scleritis
moved over underlying
tissue

Initial treatment:
Systemic non-steroidal anti-inflammatory drugs

(NSAIDs).

Indomethacin 75mg twice daily after meal


COX-2 inhibitors have been reported to be equally

successful and minimise the side effects. However, no


clinical trials have been conducted.

Over 90 percent of patients with diffuse or

nodular scleritis treated with a NSAID will achieve


control of the inflammation, while the addition of
steroids or immunosuppressants will control the
inflammation in most of the remaining cases
Topical steroid

Most severe and destructive form of

scleral inflammation.
The onset of pain and localised
redness may at first be gradual,
however within three to four days,
extremely severe and persistent pain
has usually developed, radiating to the
patients temple, brow or jaw. It
characteristically worsens at night

Vaso-Occlusive :
Associated with rheumatoid arthritis
Isolated patches of scleral oedema with

non-perfused episclera and conjunctiva


coalesce necrosis
Granulomatous :
Associated with Wegener Granulomatosis
Injection adjacent to limbus, extends
posteriorly, sclera-episclera-cornea
become irregularly edematous
Surgically induced :
Any type of surgery : strabismus, sclera
buckling pterygium

Vaso-occlusive necrotizing scleritis

Granulomatous necrotizing scleritis

Surgically induced necrotizing scleritis

Known as scleromalacia perforans


Rare form of anterior scleritis
Usually affects women with long-standing

rheumatoid arthritis
Pain is absent, vision unaffected
Presence of asymptomatic yellow/grey
patches near the limbus without vascular
congestion. These patches are necrotic areas
of sclera caused by obliterative arteritis
involving the deep scleral plexus

The necrotic areas continue to enlarge

and represent areas of infarcted sclera


surrounded by thinned scleral tissue,
eventually leaving a thin layer of fibrous
tissue over exposed choroid and
formation of staphylomas appear
blue/black in colour
Unless the intraocular pressure rises
significantly, the risk of perforation is rare
and no treatment is required or effective

Anterior necrotizing scleritis


without inflammation
(scleromalacia perforans)

Progressive scleral thinning with exposure of underlying


uvea

Systemic autoimmune disease presents in

40-50%
Rheumatoid Arthritis
Wegeners Granulomatosis
Systemic Lupus Erythematosus
Inflammatory bowel disease
Relapsing polychondritis

Immunosuppresant: Cyclophosphamide (100

mg per day orally and tapered monthly) should


be the first choice WG, polyarteritis nodosa
Failure Infliximab
Other alternative : daclizumab, rituximab

awaits further study


Periocular steroid injections should be applied
Pulse intravenous cyclophosphamide may be

required in case of emergencies and may be


followed by maintenance therapy

Inflammation of the sclera posterior to the

ora serrata, involving the choroid, retina and


optic nerve.
Uncommon and under-recognised condition.
Increasing use of B-mode ultrasonography
has revealed that posterior scleritis occurs
much more frequently than previously
thought and can lead to rapid and
permanent visual loss.
It may present with a range of clinical
findings, depending on the location, extent
and severity of the inflammation

Posterior scleritis
SIGNS

Proptosis and
ophthalmoplegia

Ring choroidal detachment

retinal
Disc swelling Exudative
detachment

Choroidal folds

Subretinal exudation

Ultrasonography is the key investigation

thickening of the posterior sclera and a clear


zone immediately posterior to the globe,
which is fluid in Tenons space causing
separation and the characteristic T sign
appearance
USG differentiate
between diffuse and
nodular posterior
scleritis.

Histopathological studies have reported that

necrotising posterior scleritis does rarely


occur. However, ultrasonography is currently
unable to differentiate it from diffuse scleritis.
As the early signs of necrotising inflammation
such as ischaemia and thinning cannot be
visualised, it is most frequently being
discovered incidentally by vitreo-retinal
surgeons

First line treatment : Corticosteroid such

prednisolone

Administered in high doses either orally or

intravenously to achieve disease remission


Oral corticosteroids started at high doses between 6080mg/day in adults then tapered to an acceptable
maintenance dose.
Intravenous corticosteroids are used when rapid
remission is required for patients with necrotising
scleritis with potential globe perforation.
Immunosuppressive agents are indicated for

patients with severe scleritis, in situations where


corticosteroids are inadequate to control disease or
when the dose is too high to be tolerated for long
term treatment

The cornea is composed of five layers.


The outermost layer is the epithelium. When the

epithelium does not stay attached correctly to


the corneal tissue below, including the layer
called the Bowman's layer or the basement
membrane, this can cause a condition called
corneal erosion.
Symptoms include:
- Mild to severe pain
- Feeling of something in the eye;
- Light sensitivity;
- Blurred vision;
- Watery eyes (particularly on awakening);
- Dryness.

Corneal erosion can occur spontaneously and

happen to anyone.
Certain factors increase your risk for corneal
erosion:
- Having a history ofeye injury
- Having a corneal disease, such as corneal
dystrophy
- Having had an eye ulcer, such as from a
herpes simplex infection
- Wearingcontact lensesincluding lenses that
are improperly fitted or not properly cared for.

Initial treatment:

- Bandage contact lens


- Topical antibiotic
- Artificial tears

Staphylococcu Filamenteo
s
us
Streptoccocus Fusarium
Pseudomonas Aspergillu
s
Yeast
Candida

Herpes
simplex
Herpes
zoster

Acanthamo
eba
Microsporid
ium

History and Symptoms


Decreased visual acuity
Pain
Superficial ulcer >> deep corneal ulcer
A sudden relief in pain in a case of progressing
corneal ulcer ~ perforation of the ulcer
Redness and photophobia
Discharge
Watery viral ulcer, small bacterial ulcer, reflex
tearing
Mucopurulent Gonococcus, Pseudomonas
(greenish - yellowish discharge)

Onset of the Disease


The pattern depends on
The nature of predisposing factor
Virulence of the organism
Status of the ocular and systemic immunity of the patient

Bacterial keratitis sudden onset and rapid

progression (esp. Staph. aureus, P. aeruginosa,


Pnemucoccus sp)
Certain bacteria ex. Moraxella, coagulase negative
Staphylococcus, Nocardia species, atypical
Mycobacteria gradual onset and indolent course
Fungi and parasites (Acanthamoeba) chronic
course

Bacterial Keratitis

Rapid onset of pain is accompanied by conjunctival

injection, photophobia, and decreased vision


The rate of progression ~ virulence of the infecting
organism
Sharp epithelial demarcation with underlying
dense, suppurative stromal inflammation that has
indistinct edges and is surrounded by stromal
edema
An endothelial inflammatory plague, marked
anterior chamber reaction, and hypopyon
frequently occur

P aeruginosa stromal necrosis with a

shaggy surface and adherent mucopurulent


exudate

Initial

Topical antibiotic ED high tissue levels --

preferred choice of treatment


Topical antibiotic ointment at bedtime
adjunctive treatment
Sub-conjunctival antibiotics imminent
scleral spread or perforation or patient
compliance?
Systemic therapy scleral/intraocular
involvement or systemic infection

Pain <<
Discharge <<
Eyelid edema or conjunctival injection <<
Density of the stromal infiltrate << (in the

absence of progressive stromal loss)


Stromal edema & endothelial inflammatory
plaque <<
Consolidation and sharper demarcation of the
perimeter of the stromal infiltrate
Reduced anterior chamber cell, fibrin, or
hypopyon
Initial re-epithelialisation
Cessation of progressive corneal thinning

Fungal Keratitis

Symptoms
Foreign body sensations
Gradually increasing pain
Diminution of vision

Signs
Non-specific
Conjunctival injection
Epithelial defect
Grayish white or yellowish white

Specific
Feathery margins (70%)
Elevated edges
gray/brown pigmentation
Rough texture
Satelite lessions (10%)
Fixed hypopyon (45-66%)
Endothelial plaque
Posterior corneal abcess (rare)
Ring infiltrates

Candida keratitis

Filamentous keratitis, with


satelite lession & hypopion

Satelite lession

Infiltrat ring

Onset : insidious
During initial period Fewer inflammatory

sign and symptoms than bacterial keratitis


Extension fungal infection into the AC
rapid progressive AC inflammation very
difficult to eradicate

Natamycin 5% suspension : initial DOC for fungal

keratitis
Given hourly during day time
Given 2 hourly during night time
Continued for 2 weeks after the resolution of infection
If worsening : use topical amphotericin B 0,15% with or

without fluconazole 2%

Broad spectrum AB (fluoroquinolone) : to

prevent secondary bacterial infection


Cyclopegics (homatropine) 3x/day : to relieve
the component of iridocyclitis
Antiglaucoma medication : if IOP is high

Asses liver function test every 2 wks after


starting ketoconazole
Sistemic therapy : 6-8 weeks

Responds slowly
Improvement :
Diminution of pain
Decrease in size of infiltrate
Disappearance of stellite lesions
Rounding out of the feathery margins of ulcer

and hyperplastic masses or fibrous sheets

Viral Keratitis

Predominantly unilateral
Bilateral only 3%
Manifestation of HSV Keratitis
Infectious epithelial keratitis
Neurotrophic epithelial keratitis
Herpetic stromal keratitis
Endothelitis

Punctate
keratitis

Dendritic keratitis

Geographic Ulcers

Antiviral agent and Corticosteroid

Antiviral
Agent

Route

Strengt

Frequency

Vidarebine

Topical

3% EO

5x/day

Trifluridine

Topical

1% Sol

2 hly while
awake

Topical, Oral

3% EO
200mg, 400mg
tab

5x/day

1000 mg tab

3x/day

Acyclovir

Valacyclovir

Topical, Oral

Protozoal

Severe ocular pain, photophobia, and progressive

course
Localized to the corneal epithelium in early cases
May manifest as a diffuse punctate epitheliopathy or
dendritic epithelial lesion ~ misdiagnosed as herpetic
keratitis
Stromal infection ~ central cornea in early cases
have a gray-white superficial, nonsuppurative
infiltrate
As the disease progresses a partial or complete ring
infiltrate in the paracentral cornea
Enlarged corneal nerves radial perineuritis
Limbitis or focal, nodular, or diffuse scleritis

Early diagnosis!
Early epithelial stage respond well to

epithelial debridement followed by a relatively


short (3-4 months) course of antiamebic
therapy
Stromal infiltrates appear eradication of
organisms is more difficult -- treatment
needed for 6- 12 months

Topical administration include


Diamidines: propamidine, hexamidine
Biguanides: polyhexamethylene
biguanide (polyhexanide), chlorhexidine
Aminoglycosides: neomycin,
paromomycin
Imidazolesl/triazoles: voriconazole,
miconazole. clotrimazole. ketoconazole.
itraconazole