PENYAKIT

SKLERA
RIRIN NISLAWATI
STANDAR KOMPETENSI DOKTER
INDONESIA
ANATOMI BOLA MATA
ANATOMI SKLERA
ANATOMI
Mata memiliki 3 lapisan pelindung / tunika :
1. Luar : Kornea dan sklera  Lapisan fibrous jaringan ikat
terluar
2. Tengah : Traktus Uvea  lapisan vaskuler tengah
3. Dalam : Retina  lapisan neural
Fungsi jaringan ikat terluar yang padat :
1. Menjaga struktur-struktur yang terdapat di dalamnya
2. Menjaga bentuk bola mata
3. Mengurangi tekanan yang dari luar dan dari dalam bola
mata
4. Menjadi tempat pelekatan insersi oto-otot ekstraokuler
Sklera merupakan bagian mata yang berwarna putih padat
dan ditutupi oleh konjungtiva yang transparan
Daerah transisi dari korne ke sklera dan konjungtiva adalah
limbus
Sklera menutupi 4/5 dari permukaan bola mata.
Foramen pada sklera yaitu:
• anterior  kornea
• posterior  nervus optik
Tendon-tendon m. rektus masuk hingga ke kolagen sklera
superfisial
Paling tipis : di belakang insersi muskulus rektus  0,3 mm
Paling tebal : di polus posterior sekitar nervus optik  1.0
mm
Di ekuator : 0,4-0,5 mm
Anterior dari insersi muskulus rektus : 0,6 mm
 ruptur sklera karena trauma tumpul pada bola mata :
• Sirkumferensial , paralel limbus kornea di daerah opposite
dari tekanan
• Insersi muskulus rektus
• Ekuatur bola mata
• Quadran superonasal dekat limbus  paling sering
Vaskularisasi : cenderung avaskuler krn tdk ada capillary
beds, nutrisi  A. episklera, koroid dan cabang arteri siliaris
posterior longus.
Inervasi : Sensoris  posterior sclera cabang n. siliaris
brevis; selebihnya cabang n. silaris longus
EPISKLERA
Episklera merupakan jaringan ikat yang longar,
bervaskularisasi yang bersatu dengan bagian superfisial
sklera.
Pembuluh darah episklera yang besar dapat dilihat melalui
konjungtiva.
Pembuluh darah episklera yang udem, memberikan warna
ungu muda atau merah muda yang menunjukkan adanya
inflamasi kornea ataupun penyakit di iris atau korpus siliaris
 Injeksio siliaris / perikornea
PENYAKIT PADA
SKLERA
Episkleritis
• Noduler
• Difus (Simple)
Skleritis
• Anterior
• Difus
• Nodular
• Necrotizing
• With inflammation
• Without inflammation (scleromalacia perforans)
• Posterior
EPISKLERITIS
PATOGENESIS :
• Episcleritis is a self-limited, generally benign inflammation of the episcleral
tissues . An underlying systemic cause is found in only a minority of patients

CLINICAL PRESENTATION
• a sudden-onset
• transient (usually days to weeks)
• self-limited disease  adults aged 20-50 years,
• >>  women

THE CHIEF COMPLAINT

• ocular redness without irritation  resolves spontaneously.
• Slight tenderness may be present
• >>  the exposed interpalpebral zone of the eye, the area of a pinguecula.
• 1/3  bilateral
EPISKLERITIS

HOW TO DIAGNOSED ?
• inflammation episclera bedakan dgn skleritis !
• Episcleral inflammation is superficial.  Tidak ada nyeri dalam
• Color  bright red or salmon pink in natural light
• application of 2.5% topical phenylephrine  menghilang !

CLASSIFICATION :
• Simple (diffuse injection) or nodular
• simple episcleritis  the inflammation is localized to a sector of
the globe in 70% of cases and to the entire episclera in 30% of
cases.
• A localized mobile nodule develops in nodular episcleritis
EPISKLERITIS
MANAGEMENT
• Sering rekurens ? cari  autoimmune connective tissue
disease : Sjogren syndrome or rheumatoid arthritis;  gout,
herpes zoster, syphilis, tuberculosis, Lyme disease, or
rosacea
• Episcleritis generally clears without treatment
• Boleh  topical or oral NSAIDs  bothered by the pain,
tidak mempan ?  corticosteroid
• Yakinkan :  not sight threatening and can be treated with
lubricant
SKLERITIS
PATHOGENESIS

Severe ocular inflammatory condition than episcleritis.

Caused by an immune-mediated (typically immune-complex)
vasculitis that frequently leads to destruction of the sclera.
>>  associated systemic immunologic disease; 
connective tissue or autoimmune disease.
Scleritis causes significant pain and may lead to
structural alterations ofthe globe, with attendant visual
morbidity.
Jarang  children, >>  dekade 4 atau 5, >>  women
½ kasus  bilateral
SKLERITIS
CLINICAL PRESENTATION
onset : gradual, extending over several days.
severe boring or piercing ocular pain, worsen at night  occasionally
awaken them from sleep.
The pain referred to other regions of the head or face on the involved side
Bola mata : tender to the touch
The inflamed sclera has a violaceous hue best seen in natural sunlight.
scleral vessels  crisscross pattern, adhere to the sclera, and cannot be
moved with a cotton-tipped applicator

CLASSIFIED
(anterior versus posterior scleritis) + appearance of scleral inflammation
SKLERITIS
SKLERITIS ANTERIOR
DIFUS
KARAKTERISTIK :
zone of scleral edema and redness
SKLERITIS ANTERIOR
NODULAR
deep red-purple color, immobile, and separated from the
overlying episcleral tissue, which is elevated by the nodule
NECROTIZING
SCLERITIS
Necrotizing scleritis  most destructive form of scleritis.
60%  develop ocular and systemic complications
40%  loss of vision
minority  may die prematurely as a result of complications
of vasculitis
NECROTIZING SCLERITIS
WITH INFLAMMATION
Severe pain
Most commonly, a localized patch of inflammation is noted
initially, with the edges of the lesion more inflamed than the
center.
advanced disease (25% of cases)  an avascular edematous
patch of sclera is seen (Fig 7-23)
Untreated  may spread posteriorly to the equator and
circumferentially  entire anterior globe is involved
Severe loss  if treatment is not intensive and prompt
blue-gray appearance (due to thinning, which allows the
underlying choroid to show)
NECROTIZING SCLERITIS
WITH INFLAMMATION
NECROTIZING SCLERITIS
WITHOUT
INFLAMMATION
Berhubungan dengan inflamasi, namun penampakannya tidak
seperti kondisi skleritis anterior yang terdapat tanda-tanda
inflamasi

Scleromalacia perforans
Pasien2  long-standing rheumatoid arthritis
Signs ofi nflammation are minimal + generally painless
Makin lama -> sclera thins  underlying dark uveal tissue
becomes
visible
A bulging staphyloma develops  IOP elevated -> jarang
spontaneous perforation TAPI minimal trauma may rupture
SCLEROMALACIA
PERFORANS
POSTERIOR
SCLERITIS
Bisa berdiri sendiri atau bersamaan dengan skleritis anterior
Gejala :
• Pain may be referred to other parts ofthe head
• Tenderness
• Proptosis
• vision loss
• occasionally, restricted motility
• Choroidal folds
• exudative retinal detachment
• Papilledema
• angle-closure glaucoma secondary
• Retraction ofthe lower eyelid may occur in upgaze The pain
Diagnosis :
Thickened posterior sclera  echography, CT or MRI
Often  no related systemic disease can be found in patients with
posterior scleritis
SKLERITIS
POSTERIOR
COMPLICATIONS OF
SCLERITIS
peripheral keratitis (37% ofcases),
scleral thinning (33%)
uveitis (30%),
glaucoma (18%)
cataract (7%)
 MANAGEMENT
CORTICOSTEROIDS
Topical (prednisolone acetate 1% or difluprednate ophthalmic
emulsion 0.05%) – mild case ant. skleritis
systemic  general the treatment
NSAIDs may be effective. 600 mg of ibuprofen 3 times a day.

Severe necrotizing disease potent anti-inflammatory therapy. TNF

Inhibitor

No Responds?  systemic immunosuppressive therapy with an

antimetabolite (eg, methotrexate), an immunomodulator (eg,
cyclosporine), or a cytotoxic agent (eg,
cyclophosphamide) is recommended
the ophthalmologist and rheumatologist
TERIMA KASIH
REFERENSI
Remington, L.E, Clinical Anatomy and Physiology Of The
Visual System, 3 ed., Elseiver, 2012
American Academy Ophthalmology, Fundamental and
Principles of Ophthalmology, 2014
SCLERAL OPACITY
The opacity of the sclera depends on a number of factors, including the
number of GAGs, the amount of water, and the size and distribution of
the collagen firils. The sclera contains one-fourth the number of GAGs
that are present in the cornea, and as a probable consequence, the
sclera is relatively dehydrated (68%) compared with the cornea.151 The
greater variation in firil size and the irregular spacing between scleral
components induce light scattering, which renders the sclera
opaque.33,145

SCLERAL COLOR
The anterior sclera is visible through the conjunctiva and, if healthy, is
white but may appear colored as a result of age or disease. In the
newborn, the sclera has a bluish tint because it is almost transparent
and the underlying vascular uvea shows through. The sclera also may
appear blue in connective tissue diseases that cause scleral thinning.
The sclera might appear yellow in the presence of fatty deposits, which
can occur with age. Likewise, the sclera may appear yellow in liver
disease because of the buildup of metabolic wastes.