Askep pada Glaukoma,

Konjungtivitis, Uveitis, dan

Orbita Selulitis
siswoyoys@yahoo.com
Keperawatan UNEJ
Glaukoma
Definition
 A group of diseases caused by damage to the
optic nerve that can gradually eliminate all
sight
(Source: PearleVision.com)
DEFINISI

Glaukoma adalah kumpulan penyakit mata ditandai oleh

kerusakan saraf optik karena tekanan intraokuler yang
terlalu tinggi. Hal ini yang menyebabkan terjadinya
peningkatan tekanan di dalam mata yang dapat menjadi
kerusakan optik secara progresif bila tak diobati
Key Facts
 Affects 65 million people worldwide
 There is no cure
 Glaucoma is one of the leading causes of

blindness
 The leading cause of blindness in African

Americans (6-8 times more common than in

Caucasians)
 Accounts for over seven million physician

visits annually
Functional Implications
 Activities of daily life
(driving, sports, etc)
may be affected by:
◦ Decreased contrast
sensitivity
◦ Light sensitivity
◦ Difficulty with glare
 Need to establish
new habits and
routines for
medication
Affected parts of the eye
 Optic Nerve

 Ciliary Body

 Angleof the
Anterior
Chamber
ETIOLOGI

 Penyakit yang ditandai dengan peninggian tekanan

intraocular , di sebabkan :
a) Peningkatan produksi cairan mata atau aqueous
humor oleh badan siliar
b) Terganggunya proses pengeluaran cairan mata atau
aqueous humor di daerah sudut bilik mata atau
celah pupil
FAKTOR RESIKO
 Usia > 40 tahun
 Jenis kelamin : perempuan lebih beresiko dari pada

laki-laki
 Kondisi medis : diabetes melitus , hipertensi
 Ras kulit hitam 4x > ras kulit putih
 Riwayat anggota keluarga yang terkena glaukoma
 Miopia
 Trauma mata
 Penggunaan steroid yang berkepanjangan
 Operasi yang berkomplikasi
Glaucoma can be:

 Congenital
 Adventitious
 Progressive
 Stable when

managed medically
KLASIFIKASI GLAUKOMA

Glaukoma
Sudut terbuka
POAG
Kronis
Primer
Sudut tertutup
PCAG
Sekunder Akut

Kongenital POAG : Primer Open Angle

Glaucoma
PCOG : Primer Closure Angle
Multiple Types of Glaucoma
 Congenital:
◦ inherited condition appearing in infants,
incomplete development of the drainage canals
during the prenatal period
 Secondary:
◦ results from another cause such as drugs, injury,
tumor, inflammation
Multiple types of Glaucoma
 Primary/Open Angle:
◦ most common form, the
correct amount of fluid can’t
drain out of the eye (clogged
pipe)

 Angle Closure
Glaucoma:
◦ rarest form, eye pressure rises
quickly when drainage canals
are blocked/covered (sink
stopper)
PERBEDAAN POAG DAN PCAG
 SUDUT TERBUKA
Frekuensi kejadian Sering, 90% dari kasus
Onset Perlahan
Penyebab Umumnya genetik, resiko >40
tahun
Tanda dan Gejala Tanpa gejala, mata lelah,
fluktuasi tajam penglihatan.
Lanjut : penyempitan lapang
pandang, buta.
Pemeriksaaan Visus baik kecuali stadium
lanjut, bilik mata depan dalam,
oftalmoskopik: tampak
penggaungan yang melebar
(CD ratio >0,5), gonioskopik:
sudut terbuka dan normal
tonometrik: tekanan >21mmHg
gangguan lapang pandang.
Gambaran Patologi Degeneratif trabekular
meshwork
SUDUT TERTUTUP
Jarang
Cepat , bertahap pada kronis
Aposisi iris tanpa proses patologis.
Misalnya: berdiam lama ditempat kurang
terang atau gelap. Obat pelebar pupil
(simpatomimetik, antikolinergik)
Akut : nyeri hebat pada mata, sakit kepala,
muntah, mata merah, berair, penglihatan
kabur.
Kronik: hampir sama dengan akut, tetapi rasa
sakit, muntah dan penglihatan kabur hilang
dengan sendirinya dan terjadi berulang kali.
Akut: visus turun hingga 1/300, konjungtiva
hiperemi, kornea keruh/udem, bilik mata
depan dangkal, pupil lebar/lonjong dengan
diameter 6-7 mm , oftalmoskopik: papil
mungkin masih normal , tonometrik : TIO
bisa capai 60 -80mmHg, gonioskopik: sudut
tertutup- COA menyempit, lapang pandang
menyempit, mungkin normal.
Oklusi trabekular meshwork
Three Parameters of
Glaucoma
 1. Origin
◦ Primary (ideopathic: disease has an unknown
cause)
◦ Secondary (associated with other ocular or
systemic conditions)
 2. State of anterior chamber angle
◦ open angle
◦ closed angle
 3. Chronicity
◦ Acute: short duration
◦ Chronic: ongoing
Diagnostic Assessment
 Tonometer:
measures pressure
 Pachymeter:
measures corneal thickness
 Visual field test:
measures peripheral vision
 Ophthalmoscopy:
direct observation of optic
nerve
 Imaging Technology:
scans optic nerve and
retinal nerve fiber
 Gonioscopy: use of mirrors
to see interior of eye
Stages
 Initially, no symptoms, pain, or loss of vision
 Loss of peripheral vision
 Visual field gradually narrows into tunnel

vision
 If allowed to progress without treatment,

leads to complete loss of sight

Treatment:
increase fluid drainage or decrease fluid production

 Medicated Eye
Drops
 Oral Prescriptions
◦ Betagan
◦ Pilocarpine
◦ Propine
◦ Timoptic
 Surgery
◦ Traditional
◦ Laser
KONJUNGTIVITIS
 KONJUNGTIVITIS

DEFINISI :
 Inflamasi pd selaput konjungtiva.

ETIOLOGI :
◦ Bakteria.
◦ Virus.
◦ Kecederaan – bahan kimia.
◦ Alahan – ubat mata topikal, kosmetik &
debunga.
 KONJUNKTIVITIS BAKTERIA

ETIOLOGI :
1. Streptokokus pneumonia.
2. Streptokokus pyogenes.
3. Stafilokokus aureus/epidermis.
4. Haemophilus influenzae.
 MANIFESTASI KLINIS :
 Kedua mata terkena infeksi.
 Mata – gatal, berpasir & tidak sakit.
 Discharge – mukopurulen/purulen,
bulu & kelopak mata melekat,
berkerak.
 Konjungtival tarsal & bulbar – merah,
kemosis akut.
 Penglihatan normal
 Kelopak mata bengkak.
 Fotofobia jika kornea terinfeksi.
 Treatment:
1. Kebersihan diri.
2. Kes pulih dlm masa 10-14 hari.
3. Cuci discharge hingga bersih.
4. Beri Obat tetes Antibiotik 4x sehari 1
tetes.
 KONJUNGTIVITIS VIRUS
ETIOLOGI :
1. Adenovirus.
2. Herpes simpleks virus.
3. Chlamydia (virus trakoma ).
MANIFESTASI KLINIS :
 Kedua mata dapat terjadi.
 Mata – merah, seperti ada benda asing.
 Kelopak - ada folikel & edema.
 Adenovirus –penglihatan kabur,
- Blepharospasma, sakit, fotofobia &
air mata meningkat ( seperti
keratitis).
 Herpes simpleks –Ulser kornea
dendritik.
TREATMENT:
1. Adenovirus.
 Bisa sembuh secara spontan
 Gutt Prednisolone 0.1% tds untuk
kurangkan inflamasi. (Rujuk jika
serius).
2. Herpes simpleks.
 Rujuk dengan segera.
 Occ. Idoxyuridine 5x sehari di
hospital.
3. Chamydia
 Rujuk
 Gutt/Occ Tetra, antibotik sistemik
& kebersihan diri.
KONJUNGTIVITIS NEONATAL

JENIS –JENIS :
1. Ophthalmia Neonatorum.
2. Chlamydia
 OPTHALMIA NEONATORUM

ETIOLOGI :
1. Neisseria Gonorrhea.
MANIFESTASI KLINIS :
 Terjadi1-3 hari setelah lahir.
 Konjunktiva – inflamasi yang berat
(sangat merah & kemosis)
 Discharge jenis mukopurulen/
purulen pekat.
 Kelopak mata bengkak.
 Kornea berulser /tembus.
TREATMENT:
1. Occ.Tetra 1% setiap jam/ tds x 2/52.
2. Gutt Homatropine 2%stat. ( ant
synaechiae).
3. IM cefoyamixine 100mg/kg bw stat
atau Im kanamycin 25mg/bw stat.
4. Isolasi pasien.
KOMPLIKASI :
5. Keratitis sekunder / perforasi
kornea
 KONJUNKTIVITIS CHLAMYDIA
Kuman yang sering menyebabkan
konjunktivitis N.

MANIFESTASI KLINIS :
 Terjadi 5-14 hari setelahlahir.
 Mata – merah akut/ discaj
mukopurulen.
TREATMENT:

1. Gutt Tetra setiap jam.

2. Tab Erythromycin 25mg/kg bw BD
x 2/52
Uveitis
Introduction
 Uveitis : inflammation of uveal tract (iris, ciliay
body & choroid)

 It is classified anatomically to
1. Ant.uveitis (iritis)
 inflammation of iris accompanied by increased vascular permeability
which allow both protein & WBCs to extravasate into the aqueous.
 2 types : granulomatous (Sarcoidosis,Syphilis, Vogt-Koyanagi-
Harada disease Sympathetic ophthalmi Multiple sclerosis Lyme
disease Tuberculosis.) nongranulomatous.
 circulating White cells could be seen in the aqueous humor of Ant.
Chamber using a slit lamp.
 Protein which leaked from BV is picked out by its
light scattering properties appear as “flare” in the beam of slit
lamp.
Anterior Uveitis with hypopyon in a patient with IBD
2. Intermediate uveitis
 Inflammation of ciliary body (cyclitis),of
the pars plana (pars planitis) and of the
vitreous (vitritis)
3. Posterior uveitis
 Inflammation of posterior uvea May also
involve the choroid(choroiditis) or
retina(retinitis)
 Panuveitis :its when inflammatory changes

involve the anterior

chamber,vitreous,retina and/or choroid.
Epidemiology

 Incidence 15/100000 (75% ant.uveitis)

8/100000 in US
 50% of pts have ass. Systemic dis.
 Hx.
pt come to clinic complaining of:
o ocular pain (less frequent with post.U)
Abrupt onset dull aching eye pain worsen when touch the eye
through eye lid, may refered to temple or periorbital region
o Photophobia
Mostly
o Blurring of vision Redness of the eye unilater
al
HISTORY
o Respiratory symptoms (S.O.B , cough , nature of
sputum)……..TB, Sarcoidosis.
o Skin problems acompained by uveitis
erythema nodosum (arms +chin) >>>> Sarcoid &
Bechet
oral & genital ulcers >> Bechet
o Joint disease
AS……….20% ant.uveitis
juvenule chronic arthrits
Reiter syndrome………..40% ant.uveitis
 Signs
 visual acuity may reduced
 ciliary injection:mostly around limbus
 Anterior uveitis:
 Keratitic precipitates
 inflam. Cells maybe visible as clumps on
endothelial of cornea (mostly Inferior)
 On slit lamp exam.
flare & hypopyon in severe inflam.
Hypopyon highly suggestive for HLAB27 related &
less commonly with infectious iritis.
 Dilated vessels on iris
 Posterior synechia……….iris adhere to lens
 Elevated IOP(inc aqeous protein or due to

occlusion of drainage angle by PAS)

 Intermediate and posterior uveitis
 Cells in the vitreous
 Retinal or choroidal foci of inflammation
 Macular edema
 Grading of flare(flare refers to liberated protein from the
inflamed iris or ciliary body which gives the aqueous a
particulate, or smoky, appearance.)
Completely
absent 0
Barely present 1+
moderate 2+
marked 3+
Intense (fibrin) 4+

 Gading of aqueous cells

trace……………… 1-5 cells

+1 …………………. 6-15
+2 …………………. 16-25
+3 ……………………. 26-50
+4 …………………….. >50
Signs
 Signs

KP: fibrous deposits on the

posterior surface of the cornea,
usually associated with uveitis.

Both the size and

distribution of keratic
precipitates are helpful
in the differential
diagnosis.
White, yellowish greasy precipitates of
inflammatory cells
Typically distributed in a wedge-shaped region
on the inferior corneal endothelium, known as
Arlt's triangle
Signs

annular s. — adhesion of the

whole rim of the iris to the
lens.
anterior s. — adhesion of the
iris to the cornea.
peripheral anterior s. —
adhesion of the peripheral
iris to the cornea.
posterior s. — adhesion of
the iris to the capsule of the
lens or to the surface of the
vitreous body.
total s. — adhesion of the
whole surface of the iris to
the lens.
Signs
Signs
Etiology
  Individual forms of uveitis may be
distinguished on the basis of location within
the eye, onset, symmetry and continuity of
inflammation, associated complications, and
distribution of cells along the corneal
endothelium.
Etiology
 Infections
 Systemic immune-mediated disease (40%)
 Syndromes confined primarily to the eye
 Masquerade syndromes
 30% of patients don’t fit an well-defined

disease category .
Infections
 Cytomegalovirus (CMV) in adults is found almost exclusively in
the immunocompromised host, especially patients with HIV
infection who have extremely low CD4 counts

 Toxoplasmosis is a surprisingly common cause of uveitis in the

normal host. In many instances, it is presumed to be a
reactivation of a congenitally acquired infection. It is suspected
on the basis of a typical chorioretinal lesion; the diagnosis is
supported by serology. Most chorioretinal scarring from
toxoplasmosis is due to infection during gestation, but scarring
is increasingly recognized as a result of recent infection .
Patients may complain of hazy vision and floaters.retina is the
target choroiditis is secondary.

 Syphilis accounts for less than 1 percent of patients with uveitis

in most large series. It may present in a variety of forms,
including posterior uveitis, such as a chorioretinitis or retinal
vasculitis
CMV retinitis(cottage cheese
lesion)
Toxoplasmosis
Infections
 Tuberculosis is an uncommon cause of uveitis in North American
referral centers. It should be considered in the differential
diagnosis when the uveitis worsens despite glucocorticoid
therapy. Additional factors that raise suspicion for this diagnosis
are active tuberculosis elsewhere in the body, cachexia,
homelessness, a granulomatous appearance for the ocular
inflammation, or immunosuppression. In some geographic
areas such as Saudi Arabia, tuberculosis is considered a common
cause of uveitis.

 Both herpes simplex and herpes zoster can cause a keratouveitis,

an inflammation of the cornea along with uveitis that is primarily
anterior. The presence of cutaneous vesicles, characteristic
corneal changes, reduced corneal sensation, elevated intraocular
pressure, and iris atrophy may be clues to the diagnosis. Both
herpes simplex and zoster can also cause a retinitis known as
acute retinal necrosis. This is a rare but treatable cause of visual
loss.
Iris atrophy in a patient with herpes simplex virus–associated
anterior uveitis.
Immune-mediated systemic
disorders
 Spondyloarthritides (SpA), such as ankylosing spondylitis and
reactive arthritis, are the most common systemic immune
disorders associated with uveitis in North America and
Europe

 20-40 %

 Male >female

 typically unilateral, and tends to resolve within three

months of its onset. Recurrences are common, and can
occur in the contralateral eye.

 The prognosis for this form of uveitis is generally excellent
provided that acute attacks are treated early and
vigorousely
Fibrin clot and posterior synechiae in a patient
with acute, anterior uveitis and ankylosing
spondylitis.
 Treatment
 Aims:
1. relief pain & inflammation
2. prevent ocular structural damage
3. prevent visual loss & retinal or optic
damage
Medication:

 cycloplegia
Long acting cycloplegic agents (cyclopentolate ,
hematropine )used to relief pain& photophobia by
medriasis .
 Corticosteroids
1. Topical , is the mainstays of therapy used
aggressively esp. in initial phases of
therapy ,
if no response in 7-10 days we use :
2. subconjunctival injection (celestone) , used
if pt poorly complies to topical type or iritis
not respond to topical ttt alone
3. oral corticosteroid maybe necessary in
severe cases of iritis and post uveitis
 Topical aqueous suppressant
in case of elevated IOP

 Little or No benefit of using NSAIDS in iritis

 Ant.uveitis:
 dilating pupil to prevent synechia
(homatropine , cyclopentolate or atropine
drops)
 To break synechia

1. initially …….intensive cyclopentolate ,

phenylphrene or tropicamide drops
2. if resistant synechia …. Subconjuctival
mydriatics
 post.Uveitis:
visual loss occur due to destructive process
by retinitis or macular edema due to fluid
acumulation…………. So here we use antiviral,
antibiotics or systemic steroids
 some rare severe uveitis may need other
immunesuppresive agents (Azathioprine,
cyclophosporin)
 Follow up:
* reexamine pt 2-3 wks later to ensure no
residual inflammation present
 Complication

* recurrent episodes of iritis & the

subsequent therapy may lead to cataract or
glucoma
 Prognosis

* Most pt expect to have recurrent iritis.

* Visual prognosis is good in absence of
either cataract or glucoma.
 Specific conditions ass. with uveitis
Prognosis Treatment Investi Signs Hx Disease
gati-
ons
Recuurent Ocular ttt HLAB2 Typical signs of Ant.uveitis AS
attacks Anti- 7 Ant.uveitis Stifness at
But good for inflammator Sacroili rest
vision physiotherapy -ac Backache
X-ray
40% with Male , Rieter’s
Acute ant uveitis HLAB27 disease
Urethritis ,
arthritis,
conjunctivitis
Ocular ttt White eye Chronic Juvenile
Systemic ttt ANA 70% shows asymptomati chronic
of arthritis bilateral c ant. Uveitis arthritis
Profound
visual defect
Not respond Mild ant. uveitis Blurred vision Fuch’s
to steroid Heterochromic iris & floaters Heterochromi
Respond to Catract 70% (not present c uveitis
cataract Glucoma,KPs, with typical
surgery No post. Synechia iritis Hx.)
Treatment investigation Signs Hx Dis.
s
Systemic +ve Creamy foci Mostly Toxoplasmosis
steroid toxoplasmosis of Congenital(50-
& Antibody test Inflammatory 75%)
clindamycin is suggestive Cells at the Hazy vision ,
margin floaters , red &
At the margin painful eye
of
chorioretinal
scar
Orbital Cellulitis
Orbital cellulitis
 Infection of the soft tissues behind the orbital
septum ( deeper to lids)
 Ocular emergency , could be life threatening
 Most frequent pathogens are; Strept.

Pneumoniae , staph aureus, strept. Pyogenes

& H influenzae - (under 5 yrs children)
Causes
 Spread from the sinuses; mostly ethmoidal in
children & young adults
 Extension from preseptal cellulitis
 Local spread; dacrocystitis, dental infection,

facial infection, infection of the eyeball

( panophthalmitis etc)
 Haemotogenous spread
 Post- traumatic; accidental/ surgical
Clinical presentation
 Symptoms; rapid onset painful swelling of the
lids & protrusion of the eye, fever, malaise &
visual loss ; history of risk factors
 Signs; moderate to severe swelling of the lids,

reduced visual acuity, proptosis,red eye with

chemosis of the conjunctiva, abnormal &
painful EOM & pupillary response
Complications
Ocular; corneal damage( exposure),raised IOP,
vascular occlusions, optic nerve damage,
endophthalmitis
Intracranial; meningitis, brain abscess,
cavernous sinus thrombosis
Orbital abscess
Management
 Symptomatic; antipyretic, NSAIDS
 Specific ; hospitalization & antibiotic therapy

◦ Ceftazidime 1 g tds , I/M

◦ Mteronidazole 500mg tds, PO
◦ Vancomycin in case of allergy to the above
mentioned
 Surgical intervention in case of local abscess
or unresponsive cases
 Consultation with ENT specialist,

neurosurgeon & paediatrician if required

 A SIH
IMA K
TER

79