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PEMICU 2

INTAN SARI 405140013


LI
1. Menjelaskan kelainan kelopak mata
PALPEBRA
HORDEOLUM
Infection of the glands of the
eyelid
◦ meibomian glands  large
swelling occurs (hordeolum
internum)
◦ Zeis's or Moll's glands 
smaller & superficial swelling  Treatment
(external hordeolum) ◦ warm compresses three or four times a day for
 Etiology 10–15 minutes
◦ Staphylococcus aureus ◦ not begin to resolve within 48 hours  incision
 but culture seldom required and drainage of the purulent material
 Principal symptoms  vertical incision should be made on the conjunctival
surface to avoid cutting across the meibomian
◦ Pain, redness, and swelling glands
 incision should not be squeezed to express residual
pus
 Externally pointed hordeolum  horizontal incision
(minimize scar formation)
CHALAZION
An idiopathic sterile chronic  Symptoms
granulomatous inflammation of ◦ painless localized swelling that
a meibomian gland develops over a period of weeks
◦ may begin with mild
inflammation and tenderness
resembling hordeolum
 differentiated from hordeolum by the
absence of acute inflammatory signs
◦ slightly reddened or elevated
◦ Large  press on the eyeball
and cause astigmatism  Th/
excision
CHALAZION
 Histologic exam  Treatment
◦ proliferation of the endothelium ◦ Surgical excision with vertical
of the acinus and a incision  careful curettement of
granulomatous inflammatory the gelatinous material and
response that includes glandular epithelium
Langerhans-type gland cells ◦ Intralesional steroid injections
 Biopsy is indicated for recurrent alone may be useful for small
chalazion  meibomian gland lesions
carcinoma may mimic chalazion
 combination with surgery in difficult
cases
LO 2
 Menjelaskan kelainan mata merah dengan visus normal
CONJUNCTIVA
PTERYGIUM
DEFINITION
 A pterygium (plural pterygia)
is a triangular fibrovascular
subepithelial ingrowth of
degenerative bulbar
conjunctival tissue over the
limbus onto the cornea

Kanski. Clinical Opthalmology. 8th ed


PTERYGIUM TREATMENT
 Medical treatment
 sunglasses
SYMPTOM  Surgery. Simple excision (‘bare sclera’
 enlargement are more likely to require technique)
early excision for subsequent ◦ Simple conjunctival flap.
aggressive growth. Aggressive growth ◦ Conjunctival autografting
or an atypical appearance should ◦ Adjunctive treatment with mitomycin C or
prompt excision biopsy. betairradiation
 Most small lesions are asymptomatic. ◦ Peripheral lamellar keratoplasty
 Irritation and grittiness are caused by a
dellen – localized drying – effect at the
advancing edge due to interference
with the precorneal tear film (more
likely if the head of the pterygium is
especially elevated).
 Lesions may interfere with vision by
obscuring the visual axis or inducing
astigmatism.

Kanski. Clinical Opthalmology. 8th ed


SUBCONJUNCTIVAL HAEMORRHAGE
ETIOLOGY :
 Surgery  In younger people contact lens
 conjunctivitis wear is a common association
 trauma (from minor unnoticed to  In older individuals systemic
severe skull base) vascular disease is prevalent,
 often idiopathic especially hypertension, and blood
pressure should be checked.
 and apparently spontaneous
particularly in older patients.  A local ocular cause should be
ruled out by slit lamp examination.
 The vision is usually unaffected unless Bleeding diatheses are a very rare
a substantially elevated association
haemorrhage leads to a large
localized corneal wetting deficit  vitamin C deficiency and abusive
(dellen), which is often uncomfortable. trauma should always be
considered in infants.

Kanski. Clinical Opthalmology. 8th ed


SUBCONJUNCTIVAL HAEMORRAGHE
PRESENTATION
 The bleed is usually asymptomatic
until noticed by the patient or others
 a momentary sharp pain or a
snapping or popping sensation is
sometimes felt
 Coughing, sneezing and vomiting
are common precipitants.

Kanski. Clinical Opthalmology. 8th ed


CONJUNCTIVITIS
CONJUNCTIVITIS
SYMPTOMS OF CONJUNCTIVITIS
 foreign body sensation
 scratching or burning sensation
◦  associated with the swelling and papillary hypertrophy that
normally accompany conjunctival hyperemia
 sensation of fullness around the eyes
 Itching
 photophobia
 If there is pain, the cornea is probably also affected
CONJUNCTIVITIS
 Exudation
◦ feature of all types of acute conjunctivitis
◦ Bacterial  flaky and amorphous; allergic  stringy
◦ "Mattering" of the eyelids occurs upon awakening
◦ exudate is copious and the lids are firmly stuck together  bacterial / chlamydial
 Pseudoptosis
◦ drooping of the upper lid secondary to infiltration of Müller's muscle  trachoma
and epidemic keratoconjunctivitis
 Papillary hypertrophy
◦ conjunctiva is bound down to the underlying tarsus or limbus by fine fibrils
◦ tuft of vessels that forms the substance of the papilla reaches the basement
membrane of the epithelium, it branches over the papilla like the spokes in the
frame of an umbrella
◦ accumulates between the fibrils  heaping the conjunctiva into mounds
CONJUNCTIVITIS
 Chemosis
◦ suggests acute allergic conjunctivitis, acute gonococcal conjunctivitis,
especially in adenoviral conjunctivitis
 Follicles
◦ most cases of viral conjunctivitis, all cases of chlamydial conjunctivitis except
neonatal inclusion conjunctivitis, some cases of parasitic conjunctivitis & toxic
conjunctivitis induced by topical medications
◦ when they are located on upper tarsus  chlamydial, viral, or toxic
conjunctivitis
 Granulomas
◦ Sarcoid, syphilis, cat-scratch disease, and, rarely, coccidioidomycosis
◦ Parinaud's oculoglandular syndrome  conjunctival granulomas and a
prominent preauricular lymph node
CONJUNCTIVITIS
 Pseudomembranes & membranes
◦ Pseudomembrane  coagulum on the surface of the epithelium, and when it is
removed, the epithelium remains intact
◦ Membrane  coagulum involving the entire epithelium, if it is removed, a raw,
bleeding surface remains
◦ accompany
 epidemic keratoconjunctivitis,
 primary herpes simplex virus conjunctivitis,
 streptococcal conjunctivitis,
 diphtheria,
 cicatricial pemphigoid,
 erythema multiforme major
 Ligneous conjunctivitis
◦ peculiar form of recurring membranous conjunctivitis
◦ bilateral, seen mainly in children, and predominantly in females, and it may be
associated with other systemic findings, including nasopharyngitis and vulvovaginitis
CONJUNCTIVITIS
 Phlyctenules
◦ delayed hypersensitivity reaction to microbial antigen, eg,
staphylococcal or mycobacterial antigens
◦ perivasculitis with lymphocytic cuffing of a vessel
◦ When they progress to ulceration of the conjunctiva  ulcer bed has
many polymorphonuclear leukocytes
 Preauricular lymphadenopathy
◦ large or small preauricular node, sometimes slightly tender 
primary herpes simplex conjunctivitis, epidemic keratoconjunctivitis,
inclusion conjunctivitis, and trachoma
◦ Small but nontender preauricular lymph nodes 
pharyngoconjunctival fever and acute hemorrhagic conjunctivitis
BACTERIAL CONJUNCTIVITIS
2 forms :  General symptoms
◦ acute (including hyperacute and ◦ bilateral irritation and injection
subacute) ◦ purulent exudate with sticky lids on
 benign and self-limited, lasting no
waking
more than 14 days
 hyperacute (purulent) conjunctivitis ◦ lid edema
caused by Neisseria gonorrhoeae or
Neisseria meningitidis
◦ Chronic
 secondary to eyelid disease or
nasolacrimal duct obstruction
BACTERIAL CONJUNCTIVITIS
 Hyperacute (purulent) bacterial  Acute mucopurulent (catarrhal)
conjunctivitis conjunctivitis
◦ e/  N gonorrhoeae, Neisseria kochii, and N ◦ acute onset of conjunctival hyperemia and a
meningitidis moderate amount of mucopurulent
◦ Sign & symptoms discharge
 profuse purulent exudate ◦ e/ 
◦ immediate laboratory investigation and  Streptococcus pneumoniae in temperate climates
and Haemophilus aegyptius in warm climates
immediate treatment  May be accompanied by subconjunctival
 If delayed  severe corneal damage or loss of the hemorrhages
eye, or the conjunctiva could become the portal of  staphylococci and other streptococci
entry for either N gonorrhoeae or N meningitidis 
septicemia / meningitis
 Chronic bacterial conjunctivitis
 Subacute conjunctivitis ◦ patients with nasolacrimal duct obstruction
◦ e/  H influenzae and occasionally by and chronic dacryocystitis; usually unilateral
Escherichia coli and proteus species ◦ associated with chronic bacterial blepharitis
 Thin, watery, or flocculent exudate or meibomian gland dysfunction
BACTERIAL CONJUNCTIVITIS
 Laboratory findings  Complications & sequelae
◦ organisms can be identified by the ◦ Chronic marginal blepharitis often
microscopic examination of conjunctival accompanies staphylococcal
scrapings stained with Gram's stain or conjunctivitis
Giemsa's stain ◦ Conjunctival scarring may follow
  numerous polymorphonuclear both pseudomembranous and
neutrophils membranous conjunctivitis
◦ Conjunctival scrapings for microscopic ◦ Marginal corneal ulceration may
examination and culture are follow infection with N gonorrhoeae,
recommended (especially if purulent, N kochii, N meningitidis, H aegyptius,
membranous, or pseudomembranous) S aureus, and M catarrhalis
◦ Antibiotic sensitivity studies ◦ toxic products of N gonorrhoeae
 But empirical antibiotics should be started diffuse through the cornea into the
anterior chamber  toxic iritis
BACTERIAL CONJUNCTIVITIS
 Treatment  Course & prognosis
◦ start topical therapy with a broad- ◦ almost always self-limited
spectrum antibacterial agent (eg,  Untreated, it may last 10–14 days; if
polymyxin-trimethoprim) properly treated, 1–3 days
◦ Neisseria  systemic and topical  exceptions are
therapy started immediately  staphylococcal conjunctivitis (which may
progress to blepharoconjunctivitis and
◦ no corneal involvement  single enter a chronic phase)
intramuscular dose of ceftriaxone, 1 g  gonococcal conjunctivitis (which, when
untreated, can lead to corneal
◦ corneal involvement  5-day course perforation and endophthalmitis)
of parenteral ceftriaxone, 1–2 g daily ◦ Chronic bacterial conjunctivitis may
◦ purulent and mucopurulent conjunctivitis not be self-limited and may become
 conjunctival sac should be irrigated a troublesome therapeutic problem
with saline solution + remove the
conjunctival secretions
◦ Personal hygiene
Acute viral follicular conjunctivitis
 Pharyngoconjunctival fever ◦ Epidemiology
◦ e/  adenovirus type 3, 4, 7  more common in children than in
adults and can be transmitted in
◦ Symptoms poorly chlorinated swimming pools
 fever of 38.3–40 °C, sore throat,
and a follicular conjunctivitis in one or
both eyes
 follicles are often very prominent on
both the conjunctiva & pharyngeal
mucosa
 Injection and tearing
 transient superficial epithelial
keratitis
 Preauricular lymphadenopathy
(nontender)
ACUTE VIRAL CONJUNCTIVITIS
◦ Examination
 As the disease progresses, it can also be diagnosed serologically by a
rising titer of neutralizing antibody to the virus
 Conjunctival scrapings 
 predominantly mononuclear cells, and no bacteria grow in cultures

◦ Treatment
 no specific treatment, but the conjunctivitis is self-limited, usually lasting
about 10 days
KERATOCONJUNCTIVITIS
 Epidemic keratokonjunctivitis  A tender preauricular node
 Pseudomembranes
◦ e/  adenovirus types 8, 19, 29,
and 37  conjunctivitis lasts for 3–4 weeks at
most
◦ Symptoms
 Bilateral
 onset is often in one eye only, however,
and as a rule the first eye is more
severely affected
 conjunctival injection, moderate pain,
and tearing
 followed in 5–14 days by
photophobia, epithelial keratitis, and
round subepithelial opacities
 Edema of the eyelids, chemosis, and
conjunctival hyperemia  follicles and
subconjunctival hemorrhages in 48
hours
KERATOCONJUNCTIVITIS
◦ In children
 may be such systemic symptoms of viral infection as fever, sore throat, otitis
media, and diarrhea

◦ Examination
 Virus can be isolated in cell culture and identified by neutralization tests
 Scrapings from the conjunctiva 
 primarily mononuclear inflammatory reaction
 when pseudomembranes occur, neutrophils may also be prominent

◦ Treatment
 no specific therapy at present, but cold compresses will relieve some symptoms
 Antibacterial agents should be given if bacterial superinfection occurs
 danger of contaminated solution bottles should be avoided
HERPES SIMPLEX CONJUNCTIVITIS
 Herpes simplex conjunctivitis  Herpetic vesicles may sometimes
appear on the eyelids and lid margins
◦ Type 1  major; type 2   small tender preauricular node
newborn
◦ Symptoms
 unilateral injection,
 irritation,
 mucoid discharge,
 pain,
 mild photophobia
 associated with herpes simplex keratitis
 single or multiple branching
epithelial (dendritic) ulcers
 follicular or, less often,
pseudomembranous
HERPES SIMPLEX CONJUNCTIVITIS
◦ Examination ◦ Treatment
 No bacteria are found in scrapings or  conjunctivitis occurs in a child over 1
recovered in cultures year of age or in an adult  self
 conjunctivitis is follicular  mononuclear limited
inflammatory reaction  Topical or systemic antivirals should be
 Pseudomembranous conjunctivitis  given, however, to prevent corneal
involvement
polymorphonuclear inlf. reaction
 Corneal ulcers  debridement with a
 Intranuclear inclusions (because of the dry cotton swab, applying antiviral
margination of the chromatin) can be seen drops, and patching the eye for 24
in conjunctival and corneal cells if Bouin hours
fixation
 Topical antivirals alone should be
 can be readily isolated by gently rubbing a applied for 7–10 days (eg, trifluridine
dry Dacron or calcium alginate swab over every 2 hours while awake)
the conjunctiva  transferring the infected
cells to a susceptible tissue culture  Herpetic keratitis may also be treated
with 3% acyclovir ointment five times
daily for 10 days / oral acyclovir, 400
mg five times daily for 7 days
ACUTE HEMORRHAGIC CONJUNCTIVITIS
 Acute hemorrhagic conjunctivitis  subconjunctival hemorrhages
 Punctate at onset; upper to lower
◦ e/  enterovirus type 70 and
 Chemosis
occasionally by coxsackievirus A24
 preauricular lymphadenopathy,
 short incubation period (8–48 hours) conjunctival follicles, and epithelial
and course (5–7 days) keratitis
◦ Sign & symptoms  Fever , malaise, and generalized
 pain, myalgia
 photophobia,  Anterior uveitis
 foreign-body sensation,
 copious tearing,
 redness,
 lid edema,
◦ transmitted by close person-to-
person contact and by such
fomites as common linens,
contaminated optical instruments,
and water

◦ Treatment
 no known treatment
Konjungtivitis dry eyes
 ~keratokonjungtivitis sika  suatu keadaan keringnya permukaan
kornea & konjungtiva yg diakibatkan berkurangnya fungsi air mata
 Kelainan ini terjadi pada penyakit yg mengakibatkan
◦ Def komponen lemak air mata
 Blefaritis menahun, distikiasis, pembedahan kelopak mata
◦ Def kelenjar air mata
 Sindrom syogren & riley day, alakrimia kongenital, aplasi kongenital saraf trigeminus,
sarkoidosis, limfoma kelenjar air mata, diuretik, atropin, usia
◦ Def komponen musin
 Benign ocular pempigoid
◦ Akibat penguapan berlebihan
 Keratitis neuroparalitik, hidup di gurun pasir, keratitis lagoftalmus
◦ Karena parut kornea / hilangnya mikrovili kornea
 Tanda & gejala  Pengobatan
◦ Gatal, seperti berpasir, silau, penglihatan ◦ air mata buatan yg diberikan selamanya
kabur
◦ Sekresi mukus >>  Komplikasi
◦ Sukar menggerakan kelopak mata, mata ◦ Ulkus kornea
tampak kering, terdapat erosi kornea
◦ Konjungtiva bulbi edema, hiperemik ◦ Infeksi sekunder oleh bakteri
menebal & kusam ◦ Parut kornea
◦ Kadang terdapat benang mukus ◦ Neovaskularisasi kornea
kekuningan pd forniks konjungtiva bawah

 Pemeriksaan
◦ Uji Scheimer  resapan < 5 menit 
abnormal
SCLERA
EPISCLERITIS
DEFINITION
CLINICAL PRESENTATION
Episcleritis is an inflammatory
 mild-to-moderate discomfort
condition affecting the episcleral
tissue that lies between the  an area of painless injection.
conjunctiva and the sclera.  Photophobia and watery
discharge may be noted.
EPISCLERITIS
DIAGNOSIS PHARMACOTHERAPY
 Phenilefrin test
Topical ophthalmic :
 0.5% prednisolone
 0.1% dexamethasone
 loteprednol etabonate 0.5%
 0.1% betamethasone
NSAID systemic :
 flurbiprofen (100 mg tid)
 indomethacin (100 mg daily initially
and decreased to 75 mg daily)
 naproxen (220 mg up to 6 times per
day).
ANTIBIOTIC
ETIOLOGY
INFECTION SCLERITIS  Herpes zoster is the most common infective
cause. Necrotizing scleritis is extremely
resistant to treatment and may result in a
 Infectious scleritis is rare but may present thinned or punched-out area
diagnostic difficulty as the initial clinical features
are similar to those of immune-mediated disease.  Tuberculous scleritis is rare and difficult
to diagnose. The sclera may be infected
 In some cases infection may follow surgical or by direct spread from a local conjunctival
accidental trauma, endophthalmitis, or may occur or choroidal lesion, or more commonly by
as an extension of corneal infection. haematogenous spread. Involvement may
be nodular or necrotizing.
 Leprosy. Recurrent necrotizing scleritis can
occur, even after apparent systemic cure.
Nodular disease may be seen in
lepromatous leprosy.
 Syphilis. Diffuse anterior scleritis may
occur in secondary yphilis, and
occasionally scleral nodules may be a
feature of tertiary syphilis.
 Lyme disease. Scleritis is common but
typically occurs long after initial infection.

Kanski. Clinical Opthalmology. 8th ed


INFECTION SCLERITIS
TREATMENT
 Once the infective agent has
been identified, specific
antimicrobial therapy should
be initiated.
 Topical and systemic steroids
may also be used to reduce
the inflammatory reaction.
 If appropriate, surgical
debridement can be used to
debulk a focus of infection

Kanski. Clinical Opthalmology. 8th ed


PALPEBRA
ANTERIOR BLEPHARITIS
Anterior blepharitis affects the area
surrounding the bases of the eyelashes
and may be staphylococcal or
seborrhoeic.
It is sometimes regarded as related more
to chronic infective elements and hence
more amenable to treatment and
remission than the posterior form.

Kanski. Clinical Opthalmology. 8th ed


ANTERIOR BLEPHARITIS
Common chronic bilateral  Chief symptoms
inflammation of the lid margins ◦ irritation, burning, and itching of the
◦ 2 types  lid margins
 Staphylococcal (ulcerative)  ◦ “red-rimmed”
e/ Staphylococcus aureus ◦ scales or "granulations" can be seen
 Seborrheic (non-ulcerative)  clinging to the lashes of both the
upper and lower lids
e/ Pityrosporum ovale
 Staphylococcal  dry, the lids are red,
 Mixed tiny ulcerated areas are found along
the lid margins, and the lashes tend to
fall out
 Seborrheic  greasy, ulceration does
not occur, and the lid margins are less
red

Paul Riordan-Eva, John PW. Vaughan & Asbury general ophtalmology. 17th ed.
ANTERIOR BLEPHARITIS
 Other etiologic disease  Treatment
◦ hordeola, chalazia, epithelial ◦ Seborrheic type 
keratitis of the lower third of the  scalp, eyebrows, and lid margins must be
cornea, and marginal corneal kept clean (means of soap and water
infiltrates shampoo)
 scales must be removed from the lid
margins daily with a damp cotton
applicator and baby shampoo
◦ Staphylococcal type 
 antistaphylococcal antibiotic or
sulfonamide eye ointment applied on a
cotton applicator once daily to the lid
margins
POSTERIOR BLEPHARITIS
Inflammation of the eyelids secondary to dysfunction of the
meibomian glands; bilateral, chronic condition
◦ Seborrheic dermatitis is commonly associated with meibomian
gland dysfunction
◦ Colonization or frank infection with strains of staphylococci
 Bacterial lipases  inflammation of the meibomian glands and
conjunctiva and disruption of the tear film.

 Anterior and posterior blepharitis may coexist


POSTERIOR BLEPHARITIS
Posterior blepharitis is caused by  CLINICAL MANIFESTATION :
meibomian gland dysfunction and ◦ papillary conjunctivitis, inferior
alterations in meibomian gland ◦ corneal punctate epithelial erosions, corneal
secretions. scarring and vascularization including Salzmann
 ETIOLOGY: nodular degeneration
◦ S. Aureus ◦ marginal keratitis
◦ Demodex Folliculorum ◦ occasionally bacterial keratitis (especially in
contact lens wearers)
 PATHOGENESIS :
◦ Bacterial lipases may result in the
formation of free fatty acids. This
increases the melting point of the meibom.
◦ preventing its expression from the glands,
contributing to ocular surface irritation
and possibly enabling growth of S.Aureus
◦ Demodex infestation may lead to
cylindrical dandruff-like scaling
(collarettes) around the base of
eyelashes.

Kanski. Clinical Opthalmology. 8th ed


CHRONIC BLEPHARITIS
TREATMENT PHARMACOTHERAPY
 A warm compress  Antibiotics
 Lid cleaning is subsequently  Topical sodium fusidic acid,
performed to mechanically erythromycin, bacitracin, azithromycin
 remove crusts and other debris or chloramphenicol is used
 scrubbing the lid margins with a cotton  Oral antibiotic regimens include
bud or clean facecloth dipped in a doxycycline (50–100 mg twice daily
warm dilute solution of baby shampoo for 1 week and then daily for 6–24
or sodium bicarbonate. weeks), other tetracyclines, or
azithromycin (500 mg daily for 3 days
 Commercially produced soap/alcohol
for three cycles at 1-week intervals
impregnated pads
 Children, pregnant and breastfeeding
woman: Erythromycin 250 mg once or
twice daily is an alternative.

Kanski. Clinical Opthalmology. 8th ed


DRY EYE
DEFINITION :
Dry eye occurs when there is inadequate
tear volume or function, resulting in an
unstable tear film and ocular surface
disease. It is an extremely common
condition, particularly in postmenopausal
women and the elderly.
 Keratoconjunctivitis sicca (KCS) refers to
any eye with some degree of dryness.
 Xerophthalmia describes a dry eye
associated with vitamin A deficiency.
 Xerosis refers to the extreme ocular
dryness and keratinization that occurs in
eyes with severe conjunctival cicatrization.
 Sjögren syndrome is an autoimmune
inflammatory disease of which dry eyes
is a feature.

Kanski. Clinical Opthalmology. 8th ed


DRY EYE

PATHOGENESIS
The four core inter-related
mechanisms thought to be
responsible for the manifestations
of dry eye :
 Tear instability
 Tear hyperosmolarity
 Inflammation
 Ocular surface damage.

Kanski. Clinical Opthalmology. 8th ed


KERATOCONJUNCTIVITIS SICCA
The ocular surface is an integrated
anatomical unit consisting of 7 key
interactive and interdependent components:
 Tear film
 Lacrimal
 accessory lacrimal apparatus
 Nasolacrimal drainage system
 Eyelids bulbar
 tarsal conjunctiva
 cranial nerve V, and cranial nerve VII.

ETIOLOGY: ocular surface disease (OSD),


ocular allergy, meibomian gland dysfunction
(MGD).
KERATOCONJUNCTIVITIS SICCA
 Examination
◦ Schirmer test are abnormal
◦ Rose bengal or lissamine green staining
of the cornea and conjunctiva in the
palpebral aperture
 Diagnosis
◦ lymphocytic and plasma cell infiltration
of the accessory salivary glands in a
labial biopsy obtained by means of a
simple surgical procedure
 Treatment
◦ Replace tear film  artificial tears,
side shields, moisture chambers, and
Buller shields
◦ preservative-free, low-dose
corticosteroid preparations and topical
cyclosporine or doxyxycline
SJORGEN SYNDROME
Sjögren syndrome (SS) is an autoimmune
disorder characterized by lymphocytic
inflammation and destruction of lacrimal and
salivary glands and other exocrine organs.

The classic clinical triad :


 dry eyes
 dry mouth
 parotid gland enlargement

Kanski. Clinical Opthalmology. 8th ed


SJORGEN SYNDROME – SIGN & SYMPTOM

Kanski. Clinical Opthalmology. 8th ed


DRY EYE - INVESTIGATION

 Stability of the tear film as related to its


break-up time (BUT)
 Tear production (Schirmer, fluorescein
clearance and tear osmolarity).
 Ocular surface disease (corneal stains and
impression cytology).

Kanski. Clinical Opthalmology. 8th ed


DRY EYE - THERAPY
Level 1 Level 3
Education and environmental/dietary modifications  Serum eye drops. Autologous or umbilical cord
 Establishment of realistic expectations and emphasis serum.
on the importance of compliance.  Contact lenses.
 Lifestyle review including the importance of blinking  Permanent punctal occlusion.
whilst reading, watching television or using a
computer screen (which should be orientated below
eye level to minimize palpebral aperture size) Level 4
 management of contact lens wear.  Systemic anti-inflammatory agents.
Level 2  Surgery
 Anti-inflammatory agents such as topical steroids,
◦ Eyelid surgery, such as tarsorrhaphy.
oral omega fatty acids and other agents such as ◦ Salivary gland autotransplantation.
topical ciclosporin. ◦ Mucous membrane or amniotic membrane
 Tetracyclines (for meibomianitis, rosacea). ◦ transplantation for corneal complications.
 Punctal plugs.
 Secretagogues, e.g. pilocarpine, cevilemine,
rebamipide.
 Moisture chamber spectacles and spectacle side
shields.
Kanski. Clinical Opthalmology. 8th ed
APPARATUS LACRIMALIS
DACRYOCYSTITIS
DEFINITION
Infection of the lacrimal sac is
usually secondary to obstruction of
the nasolacrimal duct. It may be
acute or chronic and is most
commonly staphylococcal or
streptococcal.

Kanski. Clinical Opthalmology. 8th ed


ACUTE DACRYOCYSTITIS
PRESENTATION TREATMENT
 subacute onset of pain in the  Warm compresses
medial canthal area  oral antibiotics such as
 Epiphora flucloxacillin or co-amoxiclav
 tense red swelling develops at  irrigation and probing should
the medial canthus not be performed.
 Commonly progressing to  Incision and drainage may be
abscess formation considered if pus points and
 there may be associated an abscess is about to drain
preseptal cellulitis. spontaneously.

Kanski. Clinical Opthalmology. 8th ed


PINGUECULA
A pinguecula (plural pingueculae) is an
innocuous but extremely common
asymptomatic elastotic degeneration of
the conjunctival stroma.

Treatment :
 Irritation may be treated with topical
lubrication.
 Topical steroid.
 Excision may be indicated for cosmetic
reasons or for significant irritation
 Thermal laser ablation can be effective
 Gentian violet
Kanski. Clinical Opthalmology. 8th ed
CHRONIC DACRYOCYSTITIS
PRESENTATION TREATMENT
 Chronic epiphora  Dacryocystorhinostomy
 may be associated with a
chronic or recurrent unilateral
conjunctivitis.
 A mucocoele a painless
swelling at the inner canthus
swelling is absent pressure
over the sac, commonly still
results in mucopurulent
canalicular reflux

Kanski. Clinical Opthalmology. 8th ed


HYPOPION
 Medical condition involving inflamatory
in the anterior chamber of the eye.
 It is a leukocyte exudate, seen in ther
anterior chamber, usually accompanied
by redness of the conjunctiva and the
underlying episclera.
 It is a sign of inflammation of the
anterior uvea and iris, which is a form
of anterior uveitis. The exudate settles
at the dependent aspect of the eye
due to gravity.
 It can be sterile (in bacterial corneal
ulcer) or not sterile (fungal corneal
ulcer).

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