MEDICAL FACULTY Makassar, October 1st 2018

MUSLIM UNIVERSITY OF INDONESIA

SPECIAL SENSE
PBL REPORT
RED EYE

Arranged by :
M. FARIZAN ATJO 11020160032
ANUGRAH FEBRIANTI AZIS 11020160033
ZULFIKAR ANAND PRATAMA 11020160034
DEWI RAHMAN 11020160035
DEFINA BUDI 11020160036
RATIH PUSMAWATI 11020160103
RATU SRI BESTARI 11020160104
RIFKA MISBAH SYARIFAH 11020160120
ANDI YUSNA KHAERUNNISA 11020160164
NUR ASHIANTY HADIJAH 11020160165
FAJRIAH SARASWATI NAWIR 11020160166
Tutor : dr. Wawan Susilo
MEDICAL FACULTY
MUSLIM UNIVERSITY OF INDONESIA
2018
 FOREWORD

Thank God we pray to Allah SWT thanks to His grace and guidance so that
report result of this tutorial can be finished well. And do not forget we send greetings
and shalawat to the Prophet Muhammad who has brought us from a foolish realm into
a realm full of cleverness. We would also like to thank those who helped make this
report and the tutors who have guided us during the tutorial process. Hopefully this
report on the results of this tutorial can be useful for any party who has read this
report and especially for the compilation team itself. Hopefully after reading this
report can broaden the reader's knowledge of special sense.

Makassar, September 28th, 2018

Group 16

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I. SCENARIO
Ms. S, 24 years old suffers from red eye in her right eye since 3 days ago.
Accompanied by complaints there is a clear lump. History of similar complaints and
self-healing. VODS: 6/6, conjunctival hyperemia, nodules (+).

II. DIFFICULT WORDS

• Hyperemia : Hyperemia is the increase of blood flow to different tissues in the

body. It can have medical implications but is also a regulatory response

• Nodule : A nodule is a growth of abnormal tissue. Nodules can develop just below
the skin. They can also develop in deeper skin tissues or internal organs.

III. KEYWORD
 Ms. S, 24 years old
 Red eye in her right eye since 3 days ago
 Complains there is a clear lump
 History of similar complaints and self-healing
 VODS: 6/6, conjunctival hyperemia, nodules (+)

IV. QUESTIONS
1. What is the etiology and pathomecanism of clear lumps?
2. What is the etiology and pathomechanism of the Red eye?
3. What is the anatomy, physiology, histology based on the case above ?
4. Why can it heal itself?
5. What diseases can make Red eyes ?
6. What are the steps to diagnose the case above ?
7. What are the differential diagnosis based on the case above ?

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 8. How to prevent the disease ?
9. What is the perspective of Islam that fits the scenario?
V. ANSWERS

1. What is the etiology and pathomecanism of clear lumps?

Clear lumps can arise from blockade and infection from the Zeiss or Moll
gland or can arise from infection in the Meibom gland located inside the tarsus.
Obstruction of these glands reacts to the tarsus and surrounding tissue. Clear lumps
can begin with the formation of pus in the lumen of the gland by infection with
Staphylococcus aureus. Usually affects the Zeis and Moll glands. Furthermore, there
is lumen reduction and static glandular secretion. This static will trigger a secondary
infection by Staphylococcus aureus. Pus formation in the lumen of the gland.
Histologically, an abscess will appear, with PMN and necrotic debris found.

2. What is the etiology and pathomechanism of the Red eye?

Widening occurs in the blood vessels in the conjunctiva, causing red eyes.
Blood vessels in the conjunctiva include:
 Posterior conjunctival artery which bleeds the bulb conjunctiva
 Anterior ciliary artery or episklera which gives branches
 Episklera artery enters the eyeball and with the posterior ciliary artery longus
joins to form the major circulatory artery or ciliary plexus, which will bleed the
iris and the ciliarybody.
 Pericorneal artery, which bleeds the cornea.
The Episklera artery, which is located above the sclera, is part of the anterior
ciliary artery which provides bleeding into the eyeball.
In addition to the widening of blood vessels, red eyes can also be caused by a rupture
of one of the two blood vessels above the blood and buried under the conjunctival
tissue. This condition is called subconjunctival hemorrhage.

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 Anatomically the conjunctiva is a transparent and thin mucous membrane that
encloses the posterior surface of the eyelid (palpebral conjunctiva) and anterior
surface of the sclera (conjunctival bulb). The palpebral conjunctiva coats the posterior
surface of the eyelid and attaches tightly to the tarsus.

(Pict 1. Anatomy of the conjungtiva)

Conjunctival anatomy 8 On the superior and inferior edges of the tarsus, the
conjunctiva folds posteriorly (in the superior and inferior form) and encapsulates the
episclastic tissue into the conjunctiva of the bulb. The bulb conjunctiva attaches
loosely to the orbital septum in the formix and folds many times. The presence of
these folds allows the eyeball to move and enlarge the surface of the secretory
conjunctiva.

Microorganisms (viruses, bacteria, fungi), allergens, irritants cause infected

eyelids so that the eyelids cannot close and open perfectly. Because the eyes become
dry and irritation causes the dilation of blood vessels due to inflammation
characterized by conjunctiva and red sclera.

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 The eyes look red due to the conjunctival vein dilation that occurs in acute eye
trade, hyperemia occurs due to increased blood vessel intake or reduced expenditure
such as in blood vessel blocking, dilation of blood vessels or bleeding between
conjunctiva and sclera which causes the eyes to look red.

3. THE ANATOMY, PHYSIOLOGY, AND HISTOLOGY OF THE EYE

The eye is one of the most complex organs of the human body. In the human
eye, three layers can be distinguished (Fig. 2). The outer region consists of the cornea
and the sclera. The cornea refracts and transmits the light to the lens and the retina
and protects the eye against infection and structural damage to the deeper parts. The
sclera forms a connective tissue coat that protects the eye from internal and external
forces and maintains its shape. The cornea and the sclera are connected at the limbus.
The visible part of the sclera is covered by a transparent mucous membrane, the
conjunctiva. The middle layer of the eye is composed of the iris, the ciliary body and
the choroid. The iris controls the size of the pupil, and thus the amount of light
reaching the retina; the ciliary body controls the power and shape of the lens and is
the site of aqueous production; and the choroid is a vascular layer that provides
oxygen and nutrients to the outer retinal layers. The inner layer of the eye is the
retina, a complex, layered structure of neurons that capture and process light. The
three transparent structures surrounded by the ocular layers are called the aqueous,
the vitreous and the lens.

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 (Pict 2. Anatomy of the eye)

THE CORNEA
The cornea is the most anterior part of the eye, in front of the iris and pupil. It
is the most densely innervated tissue of the body, and most corneal nerves are sensory
nerves, derived from the ophthalmic branch of the trigeminal nerve. The cornea of an
adult human eye has an average horizontal diameter of about 11.5 mm and a vertical
diameter of 10.5 mm, and a curvature that remains rather constant throughout life.8
The optic zone (pre-pupillary cornea), which provides most of the cornea’s refractive
function, has a diameter of 4 mm and is located in the centre of the cornea, anterior to
the pupil, in photopic conditions. The cornea is avascular and the branches of the
anterior ciliary arteries stop at the limbus where they form arcades that supply the
peripheral cornea. Therefore, the peripheral and central cornea are very distinct in
terms of physiology and pathology. Five layers can be distinguished in the human
cornea: the epithelium, Bowman’s membrane, the lamellar stroma, Desçemet’s
membrane and the endothelium. The surface of the corneal epithelium is covered by
the tear film, which protects the corneal surface from chemical, toxic or foreign body
damage and from microbial invasion and smoothes out micro-irregularities of the

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surface of the epithelium. It consists of an outer lipid layer and an inner water-
mucous layer. The mucous layer interacts with the epithelial cells, allowing the tear
film to spread with each eyelid blink. The corneal epithelium is composed of two to
three layers of superficial cells, two to three layers of wing cells and one layer of
basal cells. The surface of the superficial epithelial cells is irregular due to the
presence of microplicae (ridge-like folds of the plasmalemma) that interact with the
overlying tear film. The cells of the corneal epithelium are renewed every 7–10 days
from a pluripotent stem cell population, which resides in the palisades of Vogt at the
corneoscleral limbus. The stem cells differentiate into transient amplifying cells when
they migrate to the central cornea. Recent research has also identified oligopotent
stem cells in the corneal epithelium of mice and pigs, suggesting that the limbus is
not the only niche for corneal stem cells. The corneal epithelium is extremely
impermeable and stable due to the presence of cell junctions. It is also anchored very
strongly to the basal lamina. The latter is secreted by the basal cells and mainly
consists of type IV collagen and laminin. Because innervations are essential for the
physiology of the epithelium, practically all epithelial cells are in contact with nerve
cells. The corneal lamellar stroma (500-mm-thick) provides structural integrity to the
cornea. Stromal keratocytes secrete collagen and proteoglycans, which are ultimately
fundamental for the transparency of the cornea and hydration. The stroma is separated
from the epithelium by the Bowman’s layer, an acellular zone of 10–15 mm beneath
the basal lamina. The bulk of the stromal extracellular matrix consists of collagen
fibrils arranged in 200–250 parallel lamellae that run from limbus to limbus. The
network of collagen fibrils is responsible for the mechanical strength of the cornea
and its regular organization is essential for corneal transparency. In the pre-pupillar
cornea, the fibrils are packed more compact than in the peripheral cornea, probably
contributing to the mechanical strength and dioptric stability in the cornea. The
stromal collagen fibrils are surrounded by proteoglycans consisting of keratan sufate
or chondroitin sulfate/dermatan sulfate side chains. These proteoglycans have an
important structural function and help regulate hydration. Keratocytes are the

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predominant cell type in the stroma and play a role in maintaining its organization.
These stellar-shaped cells contact to each other by long cytoplasmatic extensions
(morphologic and functional syncytium) and also interact with the corneal epithelium.
The corneal endothelium consists of a single layer of five- to seven-sided
cuboidal cells with little or no self-renewing potential. The endothelial cell density at
birth in a normal cornea is 3500–7000 cells/mm2 . They secrete the Descemet’s
membrane that separates the endothelium from the stroma. This elastic membrane
thickens with age and is composed of an anterior layer with a banded appearance and
a posterior layer with an amorphous texture. The endothelium possesses intracellular
and membrane-bound ion transport systems that establish an osmotic gradient from a
relatively hypo-osmotic stroma to a hypertonic aqueous. The osmotic gradient
produces a net fluid flux from the stroma to the aqueous that produces a constant
percentage of water in the stroma (78% H2O), which is essential for the clarity and
transparency of the cornea.10 This process is called deturgescence. Corneal oedema
may develop if deturgescence is disturbed for some reason. Incident light on the
cornea can be transmitted, absorbed or scattered. In a normal transparent cornea,
visible light is not absorbed and scattering is negligible. Only irregularities with
dimensions similar to the wavelength of visible light (400– 700 nm) will affect the
retinal image. An increase of corneal scattering can arise in case of corneal oedema,
the relaxation of collagen fibrils, haze (extracellular matrix production by
keratocytes) or irregularities due to surgery.

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 (Pict 3. The Histology of the Cornea)

THE AQUEOUS HUMOR

Positioned between the cornea and the lens, the aqueous humour is formed by
the ciliary epithelium of the ciliary body that is located in the posterior chamber. The
aqueous humour is constantly replenished, as it flows through the pupil and fills the
anterior chamber. From there, a large portion of aqueous humour leaves the eye
through the trabecular meshwork into Schlemm’s canal and the episcleral venous
system. The remainder drains via the uveoscleral route by simple percolation through
the interstitial tissue spaces of the ciliary muscle, continuing to pass into the
suprachoroid and leaving through the sclera. The constant flow of aqueous humour
into the eye regulates its ocular pressure so that the eye’s optical properties can be
maintained. This circulating flow also delivers oxygen and nutrients to the anterior
region of the eye and removes metabolic waste products from its anterior chamber, as
the avascular region near the lens and cornea cannot rely on capillaries to serve this
function. The aqueous humour also assumes a role in the local immune response by
dispensing ascorbate, an antioxidant concentrated by the ciliary epithelium,
throughout the eye.

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 (Pict 4. Anatomy of the eye)

THE PUPIL AND IRIS

Once light has passed the aqueous humour, it moves onto the next group of
structures; the iris and pupil. These two structures regulate the amount of light
passing through the system. The iris consists of a pigmented sheet of cells that lies
directly in front of the lens and has the ability to restrict and dilate with the aid of
sphincter and dilator muscles, respectively. This contraction and dilation regulates the
pupil – the aperture of the eye. In cases of abundant light, the iris decreases the
pupillary aperture with the aid of the sphincter muscles and tries to avoid the
admittance of too much light, which would eventually result in the processing of a
muddled blur. The opposite is true when light is lacking, and the pupil becomes

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greatly dilated in an attemptto gather as many photons of light as possible for
imaging.

THE LENS

Once the optimal amount of light has entered the eye through the pupil, it
encounters the lens. The lens, com- posed of a lens epithelium layer covering a mass
of lens fibres, is primarily made up of proteins called crystallins, which further refine
the light from the cornea. Like the cornea, the molecules of the lens are densely
packed and uniformly spaced – characteristics required for its transparency. The lens
has an inherently greater index of refraction than the cornea due to its sur- rounding
environment – namely the aqueous and vitreous humours which also have relatively
high indexes of refraction. Thus, the index of the lens must be even higher if it is to
focus the image further and contribute to the optical system. Though the lens has an
inherent refractive index, it also has the ability to change its degree of refraction with
the aid of ciliary muscles and ciliary zonular fibres in the process of accommodation.
When the eye views an object at a distance beyond 6 m (20 feet), the lens is forced to
assume a flattened shape because the ciliary muscles and the zonular fibres holding it
in place will pull it outward. When the eye focuses on an object within 6 m, the lens
is forced into a bulging shape by the contraction of the ciliary muscles accompanied
with a reduced tension in the zonular fibres. This results in an increase in the lens’
optic power which brings the focal point closer, effectively creating a clear image of
an object that is within 6 m of the viewe.

THE CILIAR BODY

The circumferential tissue surrounding the lens is the ciliary body, which is
composed of ciliary muscle, ciliary zonule and the ciliary epithelium. The ciliary

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zonule consists of a series of thin, peripheral ligaments that suspend and hold the lens
in place (also known as suspensory ligaments). A double-layered ciliary epithelium
coats the ciliary body and has several important ocular functions, including the
secretion of aqueous humour, as well as the synthesis and attachment of the
suspensory zonule fibres. The inner layer of the ciliary epithelium is not pigmented
and is continuous with neural retinal tissue. The ciliary epithelium’s outer layer is
highly pigmented and is continuous with the retinal pigmented epithelium (RPE).
There are reports that have shown the presence of quiescent stem cells in the
pigmented ciliary epithelium of adult mammals. These cells have been induced to
proliferate and express markers of multiple retinal cell typesin vitro and in vivo.

THE SCLERA

The sclera is one of the most palpable parts of the human eye – the white in
contrast with the coloured iris. In non- human mammals, the visible part of the sclera
matches the colour of the iris, so the white part does not normally show. The sclera is
composed of collagen and elastic fibres, which provide a tough, opaque protective
posterior coating for the eye. The sclera and cornea are actually composed of the
same fibrous tissue, only differing in their degrees of hydration. If the tissue is more
dehydrated, it will be more transparent like the cornea, whose dehydration is main-
tained by the corneal endothelium; if the fibrous tissue is more hydrated, it will be
opaque like the sclera. The region where the sclera comes into contact with the cornea
is called the corneal limbus. Stem cells required for the repair of damage to the
corneal epithelium have been found in the basal membrane of the corneal limbus
Because the sclera is largely an avascular structure, it must, therefore, derive its
nutrients from the episclera and the choroid.

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THE CHOROID

The choroid, also known as the choroidea or choroid coat, is the vascular layer
of the eye containing connective tissue that surrounds the globe. In humans, it is
thickest at the extreme posterior eye (0.2 mm), and thinnest in the anterior surface
(0.1 mm). Located between the retina and sclera, the choroid is separated from retinal
nervous tissue by two structures: Bruch’s membrane and the RPE. Bruch’s
membrane, the basement membrane anterior to the chor- oidal vasculature, serves to
mediate the passage of nutrients into the retina, and filter out retinal debris seeking an
outlet through the choroid vessels. The choroid provides the greatest blood flow to
the retina (65–85% of total blood supply), allowing it to adequately supply oxygen
and nutrients to the photoreceptors in the outer layers of the retina.

THE CENTRAL RETINA ARTERY

The central retinal artery accounts for the remaining 20–30% of blood supply
to the mammalian retina which is not covered by the choroid vessels, providing
nourishment for the inner retinal layers. Emerging from the optic nerve, the central
retinal artery then branches into three layers of capillary networks in the retina, the
radial peripapillary capillaries (RPCs), the inner capillaries and the outer capillaries.
The RPCs are the most superficial layer of capillaries which occupy the inner part of
the nerve fibre layer. The inner capillaries lie in the GCL layer beneath the RPCs, and
the outer capillary network spans from the IPL to the OPL. These three sets of
capillaries flow in and out of each other throughout the retina and finally converge
again as they exit the eye through the central retinal vein at the optic disc. The
hyaloid canal runs from the optic disc to the surface on the back of the lens. It
contains a prolongated branch of the central retinal artery running along its length to
facilitate the transport of nutrients to the lens during fetal development. This canal
becomes avascular and filled with lymph in the adult eye.

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THE OPTIC NERVE AND OPTIC DISC

The optic nerve serves as the pathway connecting the retina to the brain’s
visual processing centre. The area where the optic nerve is crossing through the
posterior fundus of the eye is called the optic disc, also termed the optic nerve head.
Approximately 1.5 mm in diameter, the optic disc is where the nerve fibres leave the
eye en route to the brain; it is also where the central retinal vein exits the eye and the
central retinal artery enters. Because the optic disc contains no photoreceptors, it
creates a blind spot on the retina

THE RETINA
The retina is the tissue that lines the inner surface of the eye, surrounding the
vitreous cavity. During embryogenesis, the vertebral retina develops from the optic
cup. The latter is formed by invagination of the optic vesicle, which is an outgrowth
of the embryonic forebrain. The inner wall of the optic cup (surrounding the vitreous
cavity) ultimately becomes the neural retina; the outer wall (surrounded by the
choroid and sclera) becomes the retinal pigment epithelium (RPE). The retina is
protected and held in the appropriate position by the surrounding sclera and cornea.
The neural retina consists of six major classes of neurons: photoreceptors, bipolar
cells, horizontal cells, amacrine cells and ganglion cells, which capture and process
light signals, and the Müllerianglia, which act as the organizational backbone of the
neural retina. The cells of the neural retina are arranged in several parallel layers. The
nuclei of the photoreceptor cells lie in the outer nuclear layer, their outer segments lie
proximal fromthe nuclei, close to the RPE. The nuclei of the Müllerian glia, the
bipolar cells, the amacrine and the horizontal cells are located in the inner nuclear
layer of the retina. The inner nuclear layer has plexiform layers at both sides. In the
outer plexiform layer, the photoreceptors connect with bipolar and horizontal cells,
whereas in the inner plexiform layer, bipolar and amacrine cells synapse with
ganglion cells. The nuclei of the ganglion cells lie in the ganglion layer, their axons in

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the nerve fibre layer. Processes of the Müllerian glia extend throughout the retina.
The apical processes form the outer limiting membrane by making junctional
complexes with one another and with photoreceptors. The apposed end-feet of the
vitreal processes form the inner limiting membrane. Lateral processes of the
Müllerian glia contact with blood vessels and neurons and form synapses with
dendrites within the plexiform layers and axons in the nerve fiber layer. The eyes of
most vertebrates contain two types of photoreceptors: rods and cones. In humans,
rods are approximately 20 times more abundant than cones. The photoreceptors are
responsible for phototransduction, the conversion of light into an electrical signal. For
this purpose, the membranes of the outer segment discs of the photoreceptors contain
pigments. Cones, which are responsible for colour vision, have pigments with
absorption peaks in the blue, green or yellow parts of the spectrum. Pigments of the
rods have an absorption peak in the blue-green part of the spectrum. Rods are active
with low light levels, and are not involved in colour vision. The density of rods and
cones varies between different regions of the retina. In humans, about 50% of the
cones are located in the central 30% of the visual field, roughly corresponding with
the macula. The macula lutea refers to an area in the retina between the temporal
vascular arcades containing xanthophylls pigment (Figs 2,5). Histologically, the
macula has several layers of ganglion cells, whereas in the surrounding peripheral
retina the ganglion cell layer is only one-cell thick. The excavation near the centre of
the macula is called the fovea. This area of the retina is responsible for sharp central
vision and contains the largest concentration of cones in the eye. Visual acuity is
highest in the foveola, the thin, avascular bottom of the fovea, which contains only
densely packed cone cells. Due to the high density of cone cells in the foveola, the
cone synaptic terminals and the ganglion cells to which they connect are pushed away
from its centre, resulting in elongations between the nuclei and synaptic terminals of
the cone cells, called Henle’s fibres. At the level of the internal nuclear layer, the
foveola is surrounded by a circular system of capillaries, the vascular arcades. No
photoreceptor cells are present at the optic disc or optic nerve head where the axons

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from the ganglion cells exit the eye to form the optic nerve. The RPE is a monolayer
of cuboidal epithelial cells intercalated between the photoreceptors and the
choriocapillaris, a layer of capillaries adjacent to the innermost layer of the choroid.
The RPE incorporates about 3.5 million epithelial cells arranged in a hexagonal
pattern, with a density that is relatively uniform throughout the retina. At the apical
side, the cells of the RPE form long microvilli that reach up between the outer
segments of rod photoreceptors. Numerous pigment (melanin and lipofuscin)
granules are present in the apical cytoplasm of RPE cells. Important functions of the
RPE include the maintenance of photoreceptor function (phagocytosis of
photoreceptor wastes, regeneration and synthesis of pigments), retinal adhesion,
storage and metabolism of vitamin A, the production of growth factors necessary for
nearby tissues and wound healing after injury or surgery. In addition, the RPE plays
an important role in the blood–retinal barrier (BRB) function, which will be discussed
later. The retina receives its blood supply from two circulatory systems: the retinal
and the choroidal blood vessels. The retinal circulation supplies the inner retina,
except for the avascular foveal zone. The outer avascular retinal layers receive their
nutrients by diffusion from the choroid vessels. The choriocapillaris is fenestrated,
which allows leakage of molecules to the RPE. Specialized transport systems in the
RPE control the transportation of fluid and nutrients to the photoreceptors. Retinal
function depends on several factors, including the region of the retina being
illuminated, the wavelength and intensity of the light stimulus and the state of light
adaptation.

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 (Pict 5. The Sructure of the Retina)

VISUAL PATHWAYS
Light that enters the eye via its anterior components travels through the
different layers of transparent neurons of the retina where it is captured by the
photoreceptors at the back of the retina. As visual images are inverted as they pass
through the lens, the right half of the image is projected on the nasal retina of the
right eye (and the temporal retina of the left eye), whereas the left half of the image is
projected on the temporal retina of the right eye (and the nasal
retina of the left eye).
The neurons of the neural retina translate the visual information into nerve
impulses, which travel through the optic nerve to the brain. The photoreceptors, the
bipolar cells and the ganglion cells form a direct pathway to the brain (Fig. 4). The
horizontal and amacrine cells form lateral pathways that modify and control the
signal that passes through the direct pathway. The axons of the ganglion cells first
travel towards the nerve fibre layer at the vitreal surface and then towards the optic
disc, where they make a sharp turn to the optic nerve. The optic nerve extends from

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the eye to the optic chiasm. The next synapses lie deep in the brain, in the lateral
geniculate nuclei (LGN). Both LGN receive information from both eyes, but only
from one half of the visual field. This is due to a hemidecussation of both optic
nerves in the optic chiasm, before they reach the LGN. Neurons from the LGN send
their axons to the ipsilateral primary visual cortex. The left primary visual cortex
receives information from the right visual field, and vice versa. A lesion in one or
both optic nerves will result in visual loss in one or both eyes, respectively. This will
be apparent in the optic disc, which may become swollen or develop pallor (optic
atrophy). Increased intracranial pressure results in the swelling of both optic discs
(papilloedema) that may cause optic atrophy when untreated. The hallmarks of
chiasmal lesions are defects that affect the temporal visual field in each eye. A lesion
behind the optic chiasm is characterized by homonymous visual field defects
occurring in both eyes (e.g. the temporal field in one eye and the nasal field in the
other eye).

4. Why can heal itself from a history of previous illness?

From the history of previous diseases, red eyes with clear lumps can heal
themselves. This can be due to the conjunctival defense mechanism, especially by the
presence of tear film on the surface of the conjunctiva which serves to dissolve dirt and toxic
material and then drain it through the lacrimal duct into the inferior rice meatus

5. What diseases can make Red eyes ?

Red eyes generally occur due to dilation of blood vessels in the eye. Red eyes
indicate problems with the eyes, can be mild or serious problems that require further
treatment.

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 The most common cause of red eye is due to dilation of blood vessels on the
surface of the eye. This is usually caused by: hot / dry, sun exposure, dust, allergic
reactions, influenza, bacterial or viral infections.
Eye infections that cause red eyes:
1. Inflammation of the eyelash follicles (blepharitis)
2. Inflammation of the lining of the eye (conjunctivitis)
3. Inflammation of the uvea (uveitis)

Other conditions that can cause red eyes include:

1. Trauma or injury to the eye
2. Increased eye pressure that causes pain (acute glaucoma)
3. Corneal erosion due to irritation or use of contact lenses

Red-eye division
1. Red Eye Normal Visus
Regarding the vascular structure (conjunctiva or sclera) which does not
block the refractive media.
a Conjunctivitis
b. Pterygium
c. Subconjunctival hemorrhage
d. Episcleritis
e. Scleritis

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2. Visus Red Eyes Down
Regarding the vasculature structure which involves the medium of refraction
(cornea, uvea, or whole eye).
a Keratitis
b. Corneal ulceration
c. Anterior Uveitis
d. Acute glaucoma
e. Endopthalmitis

6. What are the steps to diagnose the case above ?

History
 The main complaint is red eye
 Complementary complaints include clear lumps, hyperemic conjunctiva and
nodules (+)
 Is there a decrease in visual acuity: 6/6 (normal)
 Is there pain when seeing bright light
 Is there a picture of hello when you see
 Exudate is present in the eye
 Is there a history of previous disease

Examination
 Inspection
See if there are conjunctival injections, ciliary injections, and
episklera injections. Get red eyes, clear lumps, hyperemic congestion and
nodules (+).
 Field inspection
The confrontation test of the patient is examined by sitting face to
face with the examiner at a distance of 33 cm. The right eye of the patient
with the examiner's left eye is facing each other. The patient's left eye and the

21
 examiner's right eye are asked to close. An object with the same distance is
shifted slowly from the periphery of the field of view to the center. If the
patient has seen it he is asked to tell. In this situation, if the patient sees at the
same time as the examiner, the patient's field of view is normal. The
requirement for this examination is that the examiner's field of view is normal.
 Pupil examination
Note the size of the pupil when it is seen anisocoria stand away
from the patient and darken the room and look through the ophthalmoscope.
Look for red reflexes from the oculus fundus and compare the pupil size
directly to glaucoma. In acute glaucoma, there is an oval pupil, asymmetry in
the translucent eye and abnormal oscillation in the Adietonic pupil
syndrome.The pupil reflexes are:
1. Direct pupillary reflex
Direct pupillary reflexes, diminished irradiated pupils. The eyes are
irradiated to 3 seconds and pupillary constriction is seen. If there is no
constriction of this irradiation while the adjacent pupils constrict this
occurs in iris parese due to trauma.
2. Indirect pupillary reflexes
Indirect pupillary reflexes, diminished irradiated pupils. this effect
occurs due to deception.
3. Coclear reflex
Cochlear reflex, with tone fork stimulation will occur mydriasis after
miosis.
4. Light reflexes
Light reflexes, with light stimulation of both pupils shrinking
5. Orbicular reflexes
Orbicular reflexes, with stimulation of closing the petals with strong
monocular miosis.

22
 6. The trigeminal reflex
The trigeminal reflex, stimulating the cornea will occur in the midriasis
followed by miosis
 Examination of eye pressure is done with a device called a tonometer.
Pressure checks performed with a tonometer on an eyeball are called
tonometry. Examination of the pressure of the eyeball, can also be palpated,
looks very low or very hard or high. Known Some tonometer tools such as,
schiot tonometer tools and goldman application tonometers.
 Sharp visual examination of this test to determine whether visual acuity is
lacking due to refractive abnormalities or organic abnormalities of the visual
media. The patient sat facing a Chinese card with a distance of 6 meters.
Patients are told to see the letters that are still visible clearly. then the eye is
placed on a small hole with a pinhole or hole of 0.755 mm) if there is a sharp
improvement in vision by looking through a small hole, there is a refractive
abnormality. (If there is a retreat in visual acuity, there is a disturbance in the
visual media. It may be due to corneal turbidity, cataracts, turbidity in the
glass body, and lutea macular abnormalities.

7. What are the differential diagnosis based on the case above ?

• CONJUNCTIVITIS
Definition
Conjunctivitis is inflammation of the conjunctiva and this disease is the
most common eye disease in the world. Because of its location, conjunctiva exposed
to many microorganisms and other environmental factors annoying. This disease
varies from mild hyperemia with watery eyes to severe conjunctivitis with many

23
purulent secretions thick. The number of agents that are pathogenic and can cause
infection in more and more eyes, caused by increased use of oat-medicines topical
and systemic immunosuppressive agents, as well as increasing numbers of patients
with HIV infection and patients who undergo organ transplants and undergo
immunosuppressive therapy.

Distribution of conjunctivitis

1. Bacterial conjunctivitis

A. Definition

Bacterial conjunctivitis is inflammation of the conjunctiva caused by

bacteria. In this conjunctivitis patients usually present with eye complaints red,
secretions in the eyes and eye irritation.

B. Etiology and Risk Factors

Bacterial conjunctivitis can be divided into four forms, namely hyperacute,

acute, subacute and chronic. Hyperacute bacterial conjunctivitis usually caused by
N gonnorhoeae, Neisseria kochii and N meningitidis. Form the acute is usually
caused by Streptococcus pneumonia and Haemophilus aegyptyus. The most
frequent cause of the form Subacute bacterial conjunctivitis is H influenza and
Escherichia coli, whereas chronic forms occur most often in secondary
conjunctivitis or in patients with nasolacrimal duct obstruction. Bacterial
conjunctivitis usually starts in one eye later concerning the eye that is next to the
hand and can spread to people other. This disease usually occurs in people who
contact too often with sufferers, sinusitis and immunodeficiency states.

24
C. Pathophysiology

Tissue on the surface of the eye is colonized by normal flora such as

streptococci, staphylococci and Corynebacterium types. Changes to the body's
defense mechanism or the number of normal flora colonies this can cause clinical
infection. Changes to normal flora can occurs due to external contamination,
spread from surrounding organs or through the bloodstream. The use of long-term
topical antibiotics is one causes of changes in normal flora in eye tissue, and
resistance to antibiotics.

D. Clinical Symptoms
Symptoms that arise in bacterial conjunctivitis are usually found segmental
or overall conjunctival injection. Besides that, the secretary is on Bacterial
conjunctivitis is usually more purulent than type conjunctivitis another, and in
mild cases often edema of the eyelids. Visual acuity usually does not experience
interference bacterial conjunctivitis but may be slightly blurred due to secretions
and debris in the tear layer, while the pupillary reaction is still normal. Symptoms
the most typical are the eyelids that stick together in the morning when you wake
up.
E. Diagnosis
At the time of history, you need to ask about age, because it is possible only
the disease is related to the body's defense mechanism in patients older. In patients
who are sexually active, it needs to be considered sexually transmitted diseases
and a history of illness in a sexual partner. Need also asked the duration of the
disease, the same disease history previously, a history of systemic diseases, drugs,
use of drugs chemotherapy, a work history that might have something to do with
illness, history of allergies and allergies to drugs, and history use of contact lenses.

25
 F. Complications
Chronic marginal blefaritis often accompanies battery conjunctivitis, except
in very young patients who are not targeted for blepharitis. Grate it on conjunctiva
most often and can damage the lacrimal gland accessory and remove the lacrimal
gland duct. This can drastically reduce the components of acoustics in the
precorneal tear film and also mucosal components due to loss of some goblet cells.
Scarring it can also change the shape of the superior palpebrae and cause tricycasis
and entropion so that the lashes can rub the cornea and cause ulceration, infection
and scarring of the cornea.
G. Management
Specific treatment of bacterial conjunctivitis depends on the agent's findings
microbiology. Therapy can be started with a topical antimicrobial spectrum large.
Every purulent conjunctivitis suspected is caused by Gram-negative diplococcus
should be started immediately topical and systemic therapy. In purulent and
mucopurulent conjunctivitis, the sac conjunctivalis must be rinsed with saline
solution to remove conjunctival secretions.

2. Viral conjunctivitis
A. Definition
Viral conjunctivitis is a common disease that can be caused by various types
of viruses, and range from severe diseases that can cause disability to mild
infections that can heal itself and can last longer than bacterial conjunctivitis.
B. Etiology and Risk Factors
Viral conjunctivitis can be caused by various types of viruses, but
Adenovirus is the virus that causes the most disease, the most dangerous herpes
simplex virus. Besides this disease too can be caused by the Varicella zoster virus,
picornavirus (enterovirus 70,Coxsackie A24), poxvirus, and human
immunodeficiency virus. This disease often occurs in people who often contact

26
 sufferers and can spread through respiratory droplets, contact with objects that
spread viruses (fomites) and are in swimming pools contaminated.
C. Pathophysiology
The mechanism of this viral conjunctivitis varies in each the type of
conjunctivitis or microorganism that causes it. Microorganisms that can cause this
disease are explained in etiology.
D. Clinical Symptoms
Clinical symptoms of viral conjunctivitis vary according to etiology. In
epidemic keratoconjunctivitis caused by adenovirus is usually found with fever
and eyes such as tearing, watery eyes heavy and sometimes found
pseudomembran. Also found infiltrates corneal subepithelium or keratitis after
conjunctivitis and persist for more than 2 months. In this conjunctivitis usually
patients also complain of symptoms in the upper and upper respiratory tract Other
symptoms of common infections such as headaches and fever. In herpetic
conjunctivitis caused by the herpes simplex virus (HSV) which is usually related
to small children there is unilateral injection, irritation, mucoid discharge, pain,
mild photophobia and often with herpes keratitis. Acute hemorrhagic
conjunctivitis which is usually caused by enterovirus and coxsackie viruses have
clinical symptoms of pain, photophobia, sensation foreign body, tear
hypersecretion, redness, palpebral edema and bleeding subconjunctival and
sometimes chimosis can occur.
E. Diagnosis
The diagnosis of viral conjunctivitis varies depending on the etiology,
therefore the diagnosis is focused on the symptoms that differentiate types
according to the cause. Information about, duration and systemic and ocular
symptoms, severity and frequency of symptoms, factors risk and environmental
conditions to establish a diagnosis viral conjunctivitis. An important history also
for asked about onset, and also whether just one eye or two eyes infected. Viral
conjunctivitis is difficult to distinguish from bacterial conjunctivitis based on its

27
 clinical symptoms and for that it must be examined continued, but follow-up
examinations are rarely done because they are spent time and cost.
F. Complications
Viral conjunctivitis can develop into chronic, like blefaroconjunctivitis.
Other complications can be the emergence pseudomembran, and a smooth or flat
grated linear scar, and corneal involvement and vesicles arise on the skin.
G. Management
Viral conjunctivitis that occurs in children over 1 year or in people adults
generally recover themselves and may not need therapy, but topical or systemic
antivirus must be given to prevent the cornea. Conjunctivitis patients are also
given instructions hygiene to minimize the spread of infection.

3. Allergic conjunctivitis
A. Definition

Allergic conjunctivitis is a form of allergies in the eye that is often and often
caused by an inflammatory reaction in the conjunctiva mediated by University of
Northern Sumatra immune system. The most frequent hypersensitivity reaction
involved in allergies in the conjunctiva is type 1 hypersensitivity reaction.

B. Etiology and Risk Factors

Allergic conjunctivitis is divided into five subcategories, namely

conjunctivitis seasonal allergies and common allergic plant conjunctivitis grouped
into one group, vernal keratoconjunctivitis, atopic keratoconjunctivitis and giant
papillary conjunctivitis (Vaughan, 2010). Etiology and risk factors for allergic
conjunctivitis vary accordingly with its subcategory. For example seasonal and plant
allergic conjunctivitis usually caused by allergic pollen, grass, animal hair, and is
accompanied by allergic rhinitis and arises at certain times. Vernal conjunctivitis is
often accompanied by a history of asthma, eczema and rhinitis seasonal allergies.

28
Atopic conjunctivitis occurs in patients with a history atopic dermatitis, whereas
papillary conjunctivitis shelves in contact users or artificial eyes from plastic.

C. Clinical Symptoms

Clinical symptoms of allergic conjunctivitis vary according to the

subcategory. In seasonal allergic conjunctivitis and plant allergies main complaints
are itching, redness, tears, mild injection of conjunctiva, and often found severe
chemosis. Patients with keratoconjunctivitis vernal often complains of very itchy
eyes with eye feces fibrous, the conjunctiva appears milky white and many fine
papillae on inferior tarsal conjunctiva. Burning sensations, mucoid discharge, red
discharge, and photophobia is the most common complaint of atopic
keratoconjunctivitis. Jupa erythematous and visible conjunctival edges are found
milky white. In severe cases decreased visual acuity, whereas University of
Northern Sumatra in giant papillary conjunctivitis it has similar signs and symptoms
vernal conjunctivitis.

D. Diagnosis

Allergic history is needed in both the patient and the patient's family and
observation of clinical symptoms to diagnose allergic conjunctivitis. The most
important symptom for diagnosing this disease is itching in the eyes, which may
be accompanied by watery eyes, redness and photophobia.

E. Complications

The most common complication of this disease is an ulcer in the cornea and
secondary infections.

29
 F. Management

This disease can be treated with antihistamine-vasoconstrictor droplets topical

and cold compresses to treat itching and topical steroids short term to relieve other
symptoms.

• EPISCLERITIS
Definition
Is a local inflammation process that is limited to episclera tissue. The course
of the disease is acute, mild, self-limiting, but often experiences recurrence.
Epidemiology
It is difficult to determine because the disease is self-limiting and sometimes
asymptomatic so the patient does not force himself. Episcleritis tends to be about
young people, typically the third or fourth decade usually occurs at the age of 20-50
years; concerning women three times more often than men; are two thirds of the
cases; but it can also occur in children, and there is no predilection for certain sexes.
Pathophysiology
Associating with fibrola expresses HLA, although it is not well understood. In
episcleritis, underlying systemic disease is only found in a small proportion of
patients. Some systemic diseases associated with episcleritis are rheumatoid arthritis,
systemic lupus erythematosus (SLE), vasclulitis, gout, atopy, and microorganism and
parasite infections in the body.
Clinical Manifestations
Patients with episcleritis generally complain of red eye without irritation
(slight irritation) in the exposed area of the eye, and complaints of discomfort /
foreign body sensation to mild pain. The attack only lasts briefly with acute onset,
and will stop by itself (in hitiungan days to weeks). This self-limited nature that
makes episcleritis rarely requires medication.

30
 Episcleritis appears in two classic forms. The first form of attack or simple
episcleritis usually lasts for 5-10 days with perfect resolution in 2-3 weeks. This form
has a tendency to relapse with a recurrence rate reaching 60%. The first recurrence
usually occurs within 2 months after the first attack. The recurrence will continue to
occur until 3-6 years later with a decrease in recurrence frequency after 3-4 years.
Inflammation in simple episcleritis is usually moderate and not associated with
systemic disease. In the second form or nodular episcleritis, the episode of attack is
longer with more pain, with an irregular attack interval.
Examination
The usual examination is done by an Ophthalmology examination.
Patients with features like the following usually have systemic involvement.

(Pict 6. Clinical manifestation of Episkleritis)

31
A. On ophthalmological examination, there is dilation and congestion of superficial
episclavies.
B. At an ophthalmologic examination, there was good visual acuity, visible
inflammation that was localized to the episclera in the form of edema and
inflammation, with pink injection and dilation of superficial episclera vessels.
Episclera inflammation does not involve the tissues and blood vessels of the
sclera and subtarsal conjunctiva, but the conjunctiva above the inflamed episclera can
be affected.
The pink episclera injection distinguishes episcleritis from scleritis which has a bluish
red injection. If the peisklera blood vessel is compressed and moved with a cotton
swab, it will appear that the blood vessels can be moved and with 10%
ophrenylephrine drops, the injection of episcleritis will decrease. Eyelid edema and
khemosis can occur in cases of beating due to extravasation of vascular fluid in the
inflamed area. The forms of episcleritis include conjunctivitis, subconjunctival
hematoma, irritated pletirgium, and scleritis.

Epscleritis rarely causes complications, but if it occurs adjacent to the cornea,

infiltrate can form in the peripheral cornea and even corneal edema. This can make
the peripheral surface or even corneal edema. This can make the corneal peripheral
thinner and new vascularization (neoaskularisation) can occur.

Treatment

Self-healing without treatment, this disorder is also a benign management

given if it is not accompanied by systemic disease give artificial conditioning tears
every 4-6 hours until the redness subsides. But some of these patients can be
disrupted by pain caused. In patients with systemic abnormalities can be given oral or
topical NSAIDs. Most patients need more education that the condition of the eye
disorder does not threaten vision and can be treated with topical lubrication alone.
The use of topical corticosteroids is limited to mild and self-limiting conditions. in

32
severe cases that do not respond to lubricant therapy and NSAIDs, short-term
corticosteroids can be given. It is very important not to give excessive therapy to
episcleritis because it will cause complications, or it can be treated according to the
causes.

Complications

A. Side effects of excessive corticosteroid administration:

B. Cataract

C. Ocular hypertension

D. Herpetic keratitis

E. Steroid-induced glaucoma.

• SCLERITIS

Definition

Scleritis is defined as a chronic granulomatous disorder characterized by

destruction of collagen, a cell and vascular abnormalities that indicate vasculitis.

Epidemiology

Scleritis is a rare disease. In the United States the incidence is estimated at 6

cases per 10,000 population. Of the patients found, 94% were anterior scleritis,
whereas 6% were posterior scleritis. In Indonesia there is no research on this disease.
This disease can occur unilaterally or bilaterally, with onset slowly or suddenly, and
can occur once or recur. The increase in the incidence of scleritis does not depend on
geography or race. Women are more affected than men with a ratio of 1.6: 1. The

33
incidence of scleritis mainly occurs between 11-87 years, with an average age of 52
years.

Etiology

In many cases, pure scelritis disorders are mediated by the immunological

process of type IV reactions (slow type hypersensitivity) and type III (immune
complexes) and accompanied by systemic disease. In some cases, a direct microbial
invasion may occur, and in some cases the immunological process appears to be
triggered by local processes, such as cataract surgery.

Pathophysiology

Enzyme degradation of collagen fibers and invasion of inflammatory cells

including T cells and macrophages in the sclera plays an important role in the
occurrence of scleritis. Inflammation of the sclera can develop into ischemia and
necrosis which will cause thinning of the sclera and perforation of the eyeball.
Inflammation affecting the sclera is closely related to systemic immune disease and
vascular collagen disease. Disregulation in autoimmune disease is generally a
predisposing factor of scleritis. Inflammatory processes can be caused by immune
complexes associated with vascular damage (type III hypersensitivity reaction and
granulomatous chronic response (type IV hypersensitivity reaction). These
interactions are part of the active immune system which can cause sclera damage due
to immune complex deposition in the episclastic vessels and sclera which causes per
capillary capillary and venous perforation and intermediate cell immune response.

34
Classification

Scleritis is classified as:

1) Episcleritis

I. Simple Usually benign, often bilateral, inflammatory reactions occur at a young

age that have the potential to experience recurrence. Clinical symptoms that
appear in the form of discomfort in the eye, accompanied by various degrees of
inflammation and photophobia. There is diffuse and segmental blood vessel
dilation. Women are more affected than men and often about the age of the 40s.

II. Nodular Both the shape and incidence are almost the same as simple scleritis.
About 30% of causes of nodular scleritis are associated with systemic disease,
5% are associated with vascular collagen disease such as rheumatoid arthritis, 7%
are associated with ophthalmic herpes zoster and 3% are associated with gout.

2) Anterior scleritis

95% of causes of scleritis are anterior scleritis. The incidence of anterior

scleritis is 40% and nodular anterior scleritis occurs around 45% annually. Necrotic
scleritis occurs in about 14% which is usually dangerous. The specific form of
scleritis is usually not associated with a specific cause of disease, although the
clinical cause and prognosis are thought to originate in an inflammation. Various
variants of anterior scleritis are mostly benign where the nodular type is more painful.
Necrotic types are more dangerous and difficult to treat.

3) Posterior scleritis

As many as 43% of cases of posterior scleritis are diagnosed together with

anterior scleritis. Posterior scleritis is usually characterized by pain and decreased
ability to see. Objective examination revealed fundal changes, exudate mass
adhesions in part of the retina, choroid ring adhesions, retinal mass, optic nerve

35
edema and macular edema. Further inflammation of posterior scleritis can lead to
shallow anterior oculi spaces, proptosis, limited extra ocular movement and lower
eyelid retraction.

Diagnosis

Scleritis can be established based on history, physical examination and

supported by various investigations.

History

At the time of history it is necessary to ask the patient's main complaint, the
course of the disease, past medical history including history of infection, trauma or
history of surgery as well as examination of all systems in the body. Symptoms can
include pain, watery eyes, photophobia, spasm, and decreased visual acuity. The
primary sign is red eyes. Pain is the most frequent symptom and is an indicator of
active inflammation. Pain arises from direct stimulation and stretching of the nerve
endings due to inflammation. Characteristics of pain in scleritis are severe pain, sharp
pain spread to the forehead, eyebrows, jaw and sinuses, the patient wakes up
throughout the night, relapse due to touch. Pain can be lost temporarily with the use
of analgesic drugs. Watery eyes or photophobia in scleritis without mucopurulent
discharge. The decrease in ordinary visual acuity is caused by an extension of scleritis
to adjacent structures which can develop into abnormal keratitis, uveitis, glaucoma,
cataracts and fundus.

Past medical history and history of the eye explaining the presence of
systemic disease, trauma, medications or surgical procedures can cause scleritis such
as:

a. Vascular disease or connective tissue disease

b. Infectious disease

36
c. Miscellanous disease (atopy, gout, chemical trauma, rosacea)

d. Blunt trauma or sharp trauma to the eye

e. Medications such as pamidronate, alendronate, risedronate, zoledronic acid and

ibandronate.

f. Post surgery on the eye

g. Past medical history such as gastric ulceration, diabetes, liver disease, kidney
disease, hypertension which affects subsequent treatment.

h. Acquired treatment and ongoing treatment and response to treatment.

Sclera Physical Examination

I. Daylight Sklera

Can be seen diffuse bluish or purplish red. After a severe attack of sclera
inflammation, the sclera and translucent thinning areas can also appear and also
appear dark uvea. Black, gray and brown areas surrounded by active inflammation
indicating a necrotic process. If tissue necrosis continues, the area of the sclera can
become avascular which results in a white sequence in the middle surrounded by a
blackish brown circle. The peeling process can be replaced gradually with granulation
tissue leaving an empty uvea or a thin layer of conjunctiva.

II. Slit Lamp Check

In scleritis, a massive dam occurs in the tissues in the episclera with several
dams in the episclera superficial tissue. On the anterior edge and posterior slit lamp
light shifts forward because of the episclera and sclera edema. In scleritis with the use

37
of phenylephrine only pale superficial episclera tissue is seen without significant
effects on the episclera tissue.

III. Red-free Light Check

This examination can help establish an area that has maximum vascular
congestion, an area with a new vascular appearance and also a total avascular area. In
addition, general examination of the eye includes extra ocular muscles, cornea, uvea,
lens, intraocular pressure and fundus.

Laboratory Inspection

Based on past medical history, systemic examination and physical examination can
be determined to be suitable tests to ascertain or rule out diseases associated with
scleritis.

The laboratory tests include:

- Complete blood count and blood sedimentation rate

- Serum complement levels (C3)

- Serum immune complex

- Serum rheumatoid factor

- Anti-12 antibodies

- Average Erythrocyte Sediment

- Serological tests

- HBs Ag

38
39
Radiology Check

Various types of radiological examinations that are needed in determining the cause
of scleritis are as follows:

- Thorax photos

- Paranasal sinus X-ray

- Lumbosacral photos

- Photos of long bone joints

- Ultrasonography (Scan A and B)

- CT Scan

- MRI

Management

Scleritis therapy is adjusted to the cause. The initial treatment of scleritis is a

systemic non-steroidal anti-inflammatory drug. The drug of choice is indomethacin
100 mg per day or ibuprofen 300 mg per day. In most cases, pain quickly subsides
followed by a reduction in inflammation. If there is no response within 1-2 weeks or
immediately after the appearance of vascular blockages should be started high-dose
systemic steroid therapy. These steroids are usually given orally, prednisone 80 mg
per day which is rapidly drained within 2 weeks until the maintenance dose is around
10 mg per day. Sometimes, severe illness requires pulsed intravenous therapy with 1
g of methyl prednisolone every week.

40
 Other immunosuppressive drugs can also be used. Cyclophosphamide is very
useful when there are many immune complexes in the blood. But topical steroids
alone are not useful but can be an additional therapy for systemic therapy. If infection
can be identified, specific therapy must be given. The role of systemic steroid therapy
will then be determined by the nature of the disease process, namely whether the
disease is a hypersensitive response or the effect of direct microbial invasion.

Surgical procedures are rarely performed except to correct scleral or corneal

perforation. This action is most likely needed in the event of severe damage due to
direct microbial invasion, or in Wegener's granulomatosis or polyarteritis nodosa
accompanied by complicated corneal perforation. Scleral thinning in scleritis that is
solely due to inflammation rarely results in perforation except if there is also a
galucoma or direct trauma, especially in an attempt to take a biopsy. Sclera bruising
was once used as a prophylactic action in the treatment of scleritis, but such staining
is not infrequently melted except when accompanied by chemotherapy.

Scleromalacia perforans is not affected by therapy unless therapy is given at

the earliest stages of the disease. Because at this stage symptoms rarely arise, most
cases are not treated until complications arise.

Complications

The complications of sleritis are keratitis, uveitis, galucoma, subretinal

granuloma, ablation of exudative retina, proptosis, cataracts and hypermetropia.
Keratitis manifests as peripheral flow formation, peripheral vascularization, or deep
vascularization with or without corneal influence. Uveitis is a bad sign because it
often does not respond to therapy. This disorder is often accompanied by a decrease
in vision due to macular edema. Open and closed angle galucoma can occur.
Glaucoma can also occur due to steroids.

41
 Scleritis is usually accompanied by inflammation in the surrounding area such
as uveitis or sclerotic keratitis. In scleritis due to scleral necrosis or scleromalasia
there can be a perforation in the sclera. Complications in the cornea can be in the
form of sclerotic keratitis, where corneal turbidity occurs due to the inflammation of
the nearest sclera. The form of sclerotic keratitis is a triangle that is located near
inflamed scleritis. This occurs due to stromal collagen fiber disorders. In this state
neovascularization never occurs into the corneal stroma. The corneal healing process
is in the form of becoming a clear cornea which starts from the central part. Often the
central part of the cornea is not seen in sclerotic keratitis.

Prognosis

The prognosis for scleritis depends on the cause of the disease. Scleritis in
spondiloartropathy or in SLE is usually relatively benign and self-limiting which is a
type of diffuse scleritis or uncomplicated nodular scleritis in the eye Scleritis in
Wagener's disease is a severe disease that can cause permanent blindness which is a
type of necrotic scleritis with eye complications.

Scleritis in rheumatoid arthritis or polycondritis is a type of diffuse, nodular or

necrotic scleritis with or without complications in the eye. Scleritis in systemic
disease is always more benign than scleritis with infectious or autoimmune diseases.
In cases of idiopathic scleritis it can be mild, short duration, and more responsive to
steroid eye drops.

42
SIGN & KONJUNGTIVITIS EPISKLERITIS SKLERITIS PTERYGIUM
SYMPTOMS

WOMAN 24
YEARS
OLD + + + -

CLEAR
LUMP
- + + +

VODS 6/6
(NORMAL)
+ + +/- +/-

RED EYE

- + + +

SELF
LIMITING
+ + - -

43
 8. How to prevent the disease ?
The agent spreads through direct contact via contaminated fingers, medical
instruments, swimming pool water, or personal items; in one study, 46% of infected
people had positive cultures grown from swabs of their hands. Because of the high
rates of transmission, hand washing, strict instrument disinfection, and isolation of
the infected patients from the rest of the clinic has been advocated. Incubation and
communicability are estimated to be 5 to 12 days and 10 to 14 days, respectively.

9. What is the perspective of Islam that fits the scenario?

One of the noble teachings in Islam is to submit a proposition even he is
commanded by Allah 'azza wa jalla to those who believe from his servants, and this
shows the nobility of what is commanded, Allah Subhanahu wa Ta'ala said,

"Say to men who believe," Let them submit

his gaze, and guard his cock. That is more sacred to them,
Allah is All-Knowing what they are doing ".
(QS: An Nuur [24]: 30).

In this verse Allah Subhanahu wa Ta'ala prioritizes the mention of subjecting

the view from the aw, then this shows concern as a means to cleanse the heart of
diseases that can penetrate into it.

• Eye function: seeing and perfecting the sense of hearing

• Purpose: ask in the dark, see the verses of God

44
 • Taklifi's Law:

A. Mandatory: see al quran manuscripts, useful books, distinguish between the lawful
and the unlawful.

B. Haram: see women with lust.

C. Sunnah: look at the faces and palms of prospective wives who are intensive with
their proposals, read useful books, see scholars and parents to respect.

D. Makruh: see something that has no benefit.

E. Mubah: suddenly accidentally looking at the opposite sex, husband-looking at the

partner's body, seeing same-sex (aurat)

F. Therapy: self-awareness that God is always seeing, praying and asking for God's
help, ablution, renewing repentance.

45
 REFERENCE

1. Colin E Willoughby MD, PhD. Anatomy and physiology of the human eye.
Clinical and Experimental Ophthalmology; 38: 2–11. Journal compilation. Royal
Australian and New Zealand College of Ophthalmologists)
2. Sherwood Lauralee, 2012, human physiology from cell to system 6th edition, EGC
medical book publisher : Jakarta.
3. Sidarta, Ilyas. Eye Disease. Third edition. Jakarta: FK UI. 2006.
4. Budhiastara, Putu. 2017. Eye Health. Denpasar: Udayana University Press. Page 2-
3.
5. Ilyas, Sidarta.2014. You're Eye Disease. Issue 5. Jakarta: FK UI Publishing
Agency. 31, 41, 43, 46.
6. Conjunctivitis bacterial treatment in karang village. Ramadhanisa A. Faculty of
Medicine, Universitas Lampung. 2014.
7. Robert H Graham, MD. Red eye. Emedicine. 2017.
8. Eva PR. Sklera. Dalam:Vaughan DG, Asbury T, Riordan-Eva P, Suyono J, Editor.
Oftalmologi Umum Edisi 14. Jakarta: EGC, 2000.169-73
9. Foulks GN, Langston DP. Cornea and External Disease. In: Manual of Ocular
Diagnosis and Therapy. Second Edition. United States of America: Library of
Congress Catalog. 1988; 111-6
10. Amir A. Azari, MD., 2013. Conjunctivitis: A Systematic Review of Diagnosis
and Treatmen. National Institutes of Health.
11. Thyleforts B, Negrel AD, Pararajasegaram R, Dadzie KY. Global Data on
Blindness. Bull World Health Organization, 2005;73:115-121

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