CASE REPORT

SECONDARY GLAUCOMA ET CAUSA TRAUMATIC CATARACT

AND ANTERIOR UVEITIS

Created by:
Sri Nowo Minarti
I11110042

SMF MATA RSUD DOKTER SOEDARSO

MEDICAL FACULTY
TANJUNGPURA UNIVERSITY
PONTIANAK
2014

AGREEMENT SHEET

Shall been agreed a case report with a title

SECONDARY GLAUCOMA ET CAUSA TRAUMATIC CATARACT
AND ANTERIOR UVEITIS
This working paper was arranged to fulfill the requirement of
Opthalmology Module Clinical Assistant

Agreed by,
Pontianak,

September 2014
Consulent,

Arranged by :

dr. Liesa Zulhidya, Sp.M

Sri Nowo Minarti

NIP. 196703121993092001

NIM. I11110042

CHAPTER I
INTRODUCTION
Ocular trauma is a common cause of unilateral blindness in children and
young adults; persons in these age groups sustain the majority of severe ocular
injuries. Young adults, especially men, are the most likely victims of penetrating
ocular injuries. Domestic accidents, violent assaults, exploding batteries, sportsrelated injuries, and motor vehicle accidents are the most common circumstances
in which ocular trauma occurs. Severe ocular trauma may cause multiple injuries
to the lids, globe, and orbital soft tissues (Eva and Whitcher, 2007).
Open-globe injuries or penetrating injuries are the most devastating forms of
ocular trauma. They are caused by sharp objects that penetrate the cornea and
sclera into deeper structure (Lang, 2006). These damage can induce occurence of
some sequelae, such as secondary glaucoma, traumatic cataract, uveitis, and
corneal ulcer, which affecting the visual acuity (Eva and Whitcher, 2007).
Glaucoma refers to certain eye diseases that affect the optic nerve and cause
vision loss. Many factors are associated with an increased risk of developing
glaucoma, some of which are elevated IOP, a family history, ethnic background,
and older age. Most, but not all, of these diseases typically produce elevated
pressure inside the eye, called intraocular pressure (IOP). An elevated IOP is the
most important risk factor for the development of glaucoma. Secondary glaucoma
refers to an increased IOP that is a result of a structural problem within the eye.
Secondary glaucoma is a type of glaucoma which is caused by other ocular
diseases or factors such as inflammation, trauma, bleeding, tumors, medication,
and physical or chemical influences (Lang, 2006). This form of glaucoma is
different because treatment is aimed at treating the underlying cause as well as
lowering the increased pressure within the eye.
Uveitis is one of the major causes of blindness in the world. Uveitis is
composed of a diverse group of disease entities, which in total has been estimated
to cause approximately 10% of blindness. Uveitis is broadly classified into

anterior, intermediate, posterior and panuveitis based on the anatomical

involvement of the eye. (Agrawal et al, 2010).
Uveitis has many subtypes and many potential associations with systemic
conditions and has always been one of the most challenging diagnoses in
ophthalmology (Babu; Rathinam, 2010). Anterior uveitis is the commonest form
of intraocular inflammation with a varying incidence in the general population of
various countries around the world. The potential severe consequences of
recurrent or untreated anterior uveitis are probably underestimated. Anatomically,
anterior uveitis involves inflammation of the iris alone (iritis), anterior part of
ciliary body (anterior cyclitis) or both structures (iridocyclitis) (Agrawal et al,
2010). Anterior uveitis can caused by trauma, chronic diarrhea, Reiter disease,
herpes simplex, Behcet syndrome, Posner Schlosman syndrome, post-operative,
adenovirus, parotitis, influenza, chlamydial infection, rheumathoid arthritis and
etc. (Ilyas S, 2007)
Traumatic cataract can occur by penetrating eye injury or blunt trauma that
can be seen in days or years (Ilyas, 2007). The lens becomes white soon after the
entry of a foreign body, since interruption of the lens capsule allows aqueous and
sometimes vitreous to penetrate into the lens structure. (Vaughan and Asburys,
2007).

CHAPTER II
LITERATURE REVIEW
2.1.

Penetrating Injuries of the Eye

Penetrating injuries cover the entire spectrum of clinical syndromes.
Symptoms can range from massive penetration of the cornea and sclera with
loss of the anterior chamber to tiny, nearly invisible injuries that close
spontaneously. The latter may include a fine penetrating wound or the entry
wound of a foreign body. Depending on the severity of the injury, the
patients visual acuity may be severely compromised or not influenced at all.
One of the most common sequelae is atraumatic cataract. The rupture in the
lens capsule allows aqueous humor to penetrate, causing the lens to swell.
This results in lens opacification of varying severity. Large defects will lead
to total opacification of the lens within hours or a few days. Smaller defects
that close spontaneously often cause a circumscribed opacity. Typically,
penetration results in a rosette-shaped anterior or posterior subcapsular
opacity (Lang, 2006). Depending on the severity of the injury, the

followingdiagnostic signs will be present in an open-globe injury:

a. The anterior chamber will be shallow or absent.
b. The pupil will be displaced toward the penetration site.
c. Swelling of the lens will be present (traumatic cataract).
d. There will be bleeding in the anterior chamber and vitreous body.
e. Hypotonia of the globe will be present.
The rupture of the lens capsule and vitreous hemorrhage often render
examination difficult as they prevent direct inspection. These cases, and any

patient whose history suggests an intraocular foreign body, require one or

both of the following diagnostic imaging studies:
a. Radiographs in two planes to determine whether there is a foreign body in
the eye.
b. CT studies, which allow precise localization of the foreign body and can
also image radiolucent foreign bodies such as Plexiglas.
Treatment
First aid.Where penetrating trauma is suspected, a sterile bandage should be
applied and the patient referred to an eye clinic for treatment. Tetanus
immunization or prophylaxis and prophylactic antibiotic treatment are
indicated as a matter of course. Surgery.Surgical treatment of penetrating
injuries must include suturing the globe and reconstructing the anterior
chamber. Any extruded intraocular tissue (such as the iris) must be removed.
Intraocular foreign bodies should be removed when the wound is repaired
(i.e., by vitrectomy and extraction of the foreign body).
Late sequelae
a. Improper reconstruction of the anterior chamber may lead to adhesions
between the iris and the angle of the anterior chamber, resulting in
secondary angle closure glaucoma.
b. A retinal injury (for example at the site of the impact of the foreign body)
can lead to retinal detachment.
c. Failure to remove iron foreign bodies can lead to ocular siderosis, which
causes irreparable damage to the receptors and may manifest itself years
later.
d. Copper foreign bodiescause severe inflammatory reactions in the eye
(ocular chalcosis) within a few hours. Symptoms range from uveitis and
hypopyon to phthisis bulbi (shrinkage and hypotonia of the eyeball).
e. Organic foreign bodies(such as wood) in the eye lead to fulminant
endophthalmitis.
2.2.

Glaucoma

a. Definition

Glaucoma is a disorder in which increased intraocular pressure

damages the optic nerve. This eventually leads to blindness in the affected
eye. Primary glaucoma refers to glaucoma that is not caused by other
ocular disorders. Secondary glaucoma may occur as the result of another
ocular disorder or an undesired side effect of medication or other therapy.
Two major forms of glaucoma exist: open-angle glaucoma, in which
aqueous humor has free access to the trabecular meshwork, and angleclosure glaucoma, in which access of the aqueous humor to the trabecular
meshwork is obstructed. Both forms of glaucoma demonstrate a
progressive optic neuropathy with visual field loss and characteristic
structural changes, including thinning of the retinal nerve fiber layer and
excavation of the optic nerve head. Intraocular pressure (IOP) does not
define glaucoma, and many with glaucoma have IOP measurements that
are also found in individuals without glaucoma.
b. Epidemiology
Glaucoma is the second leading cause of blindness worldwide. The
frequency of bilateral blindness amongst persons with glaucoma varies
across populations, with substantial bilateral blindness from glaucoma
observed in developing countries with poor access to eye care, and in
populations where angle-closure glaucoma predominates. Combining
demographic projections with prevalence models for open-angle and
angle-closure glaucoma, it has been estimated that 61 million people
worldwide will have glaucoma by 2010, and 8.4 million will be bilaterally
blind from the disease . Growth and aging of the worlds population are
expected to result in significant increases in these numbers. While PACG
remains less common than POAG, the numbers of individuals expected to
be blind from both types of glaucoma is nearly equal given the higher
morbidity of PACG.
Population-based studies with low rates of pseudoexfoliation report
rates of secondary glaucoma (resulting from pseudoexfoliation, vein
occlusions, diabetes, uveitis, trauma and other causes) between 0.15% and

0.7%, with secondary glaucoma comprising 418% of all glaucoma cases.

Whether or not pseudoexfoliation glaucoma is a primary or secondary
form of glaucoma depends on definition, and researchers vary in how they
present their data. Secondary glaucomas other than pseudoexfoliation
occur infrequently. In populations where pseudoexfoliation is found, its
prevalence varies substantially, with the highest rates found in
Scandinavian

populations.

People

with

pseudoexfoliation

have

substantially higher mean intraocular pressures, and have a significantly

higher risk of glaucoma.
c. Pathophysiology
The average normal intraocular pressure of 15mm Hg in adults is
significantly higher than the average tissue pressure in almost every other
organ in the body. Such a high pressure is important for the optical
imaging and helps to ensure several things:
1) Uniformly smooth curvature of the surface of the cornea.
2) Constant distance between the cornea, lens, and retina.
3) Uniform alignment of the photoreceptors of the retina and the
pigmented epithelium on Bruchs membrane, which is normally taut
and smooth.
The aqueous humor is formed by the ciliary processes and secreted
into the posterior chamber of the eye. At a rate of about 26 l per minute
and a total anterior and posterior chamber volume of about 0.20.4ml,
about 12% of the aqueous humor is replaced each minute.
The aqueous humor passes through the pupil into the anterior
chamber. As the iris lies flat along the anterior surface of the lens, the
aqueous humor cannot overcome this pupillary resistance until sufficient
pressure has built up to lift the iris off the surface of the lens. Therefore,

the flow of the aqueous humor from the posterior chamber into the anterior
chamber is not continuous but pulsatile.
Any increase in the resistance to pupillary outflow (pupillary block)
leads to an increase in the pressure in the posterior chamber; the iris
inflates anteriorly on its root like a sail and presses against the trabecular
meshwork. This is the pathogenesis of angle closure glaucoma.Various
factors can increase the resistance to pupillary outflow.

The aqueous humor flows out of the angle of the anterior chamber
through two channels:
1) The trabecular meshwork (Fig. 10.1 [C]) receives about 85% of the
outflow, which then drains into the canal of Schlemm. From here it is
conducted by 2030 radial collecting channels into the episcleral
venous plexus (D).
2) A uveoscleral vascular system receives about 15% of the outflow,
which joins the venous blood (E).

3) The trabecular meshwork (C) is the second source of physiologic

resistance.
4) The trabecular meshwork is a body of loose sponge-like avascular
tissue between the scleral spur and Schwalbes line. Increased
resistance in present in open angle glaucoma.

d. Classification

e. Glaucoma Associated With Ocular Trauma

1) Definition
Glaucomatous damage to the optic nerve related to elevated intraocular
pressure associated with acute or prior ocular trauma.
2) Epidemiology
Glaucoma is a common complication following ocular trauma. It
can present immediately following injury or even years or decades later.
There exists a plethora of potential causes of glaucoma following ocular
trauma. It is important to be familiar with the various types of glaucoma
in this setting as well as their pathogenesis. Recent cohort studies
examining the relationship of glaucoma following ocular injury to
several baseline structural and functional ocular characteristics are now
available. The risk of developing glaucoma in 3627 patients in the
United States Eye Injury Registry with penetrating ocular injury was
2.67%. The development of glaucoma in these patients was
independently associated with advancing age, lens injury, poor baseline
acuity, and inflammation.
In a similar study, 6021 patients in the registry who experienced
ocular contusion injury were found to have a 3.4% risk of developing
glaucoma at 6 months after their injury. The development of glaucoma
was independently associated with: advancing age, visual acuity worse
than 20/200, iris injury, lens injury, or angle recession.
A smaller prospective review of 100 consecutive patients with
traumatic glaucoma in India were found to have a greater risk of
postconcussional glaucoma associated with traumatic cataracts, angle
recession of more than 180, significant iris injury, and displacement of
the lens. Penetrating injuries were more likely to result in glaucoma if
there was evidence of an adherent leucoma and/or evidence of lenticular
damage or displacement..

3) Pathophysiology
In the initial period following an ocular injury, the intraocular
pressure may be normal, high, or low. Several mechanisms exist to
explain a low pressure. These mechanisms include aqueous
hyposecretion based on ciliary contusion and inflammation, increased
egress of aqueous through a cyclodialysis cleft, or loss of integrity of
the wall of the globe. The presence of ocular hypotension or normal
intraocular pressure does not preclude the development of glaucoma at
a later date. Whether glaucoma is present initially or at a later date, it is
generally a reflection of reduced facility of outflow of aqueous humor.
One may categorize the existence of traumatic glaucoma relative to
the time of onset of the glaucoma (immediate or delayed) and the type
of trauma that caused the injury. The type of trauma may be divided
into blunt force trauma or penetrating trauma. A broader classification
would include chemicals, electromagnetic radiation, and surgery as
additional causes of trauma that might induce glaucoma. We must also
remind ourselves that glaucoma may also occur as a result of the
therapeutic modalities.

4) Immediate or Early-Onset Glaucoma After Trauma

Contusion
Intraocular pressure elevation in the setting of blunt trauma with a
notable absence of clinical evidence of tissue damage may be noted on
occasion. Gonioscopy is entirely normal with no evidence of angle
recession and there is no evidence of blood or abnormal pigment in the
angle. Flare and cells may be evident at the slit lamp. The presumed
mechanism of this type of glaucoma is reduced outflow facility as a
result of trabecular inflammation. The course of this glaucoma is

usually brief and self limited although a trial of topical antiinflammatory drops in addition to any intraocular pressure-lowering
agents may hasten improvement and shorten the clinical course.
Trabecular Disruption
Evidence of trauma-related changes to the trabecular meshwork has
been previously documented in a study utilizing gonioscopy within the
first 48 h following injury. Documented abnormalities ranged from
sharply demarcated hemorrhage into Schlemms canal and possibly the
outer trabecular sheets to full-thickness rupture of the trabecular
meshwork for part of its circumference. A trabecular flap may be
created with a point of rupture at or just below the insertion of the
trabecular sheets at Schwalbes line. This flap is typically hinged in the
region of the scleral spur. Lesions such as these at the trabecular
meshwork may or may not be associated with elevated intraocular
pressure at the time of injury. Trabecular lesions may scar with time and
become increasingly difficult to recognize over time. Although angle
recession is associated with the late development of glaucoma, the
occurrence of late glaucoma may correlate better with the amount of
trabecular disruption observed acutely.
Hyphema
The presence of hyphema following ocular trauma is an indicator
of significant intraocular injury. Cho et al. compared the clinical
characteristics of 18 patients with very poor visual outcome after
nonperforating hyphema to 166 patients with better visual outcome
after nonperforating hyphema. The presence of posterior segment
injuries, anterior segment injuries, poor initial visual acuity, glaucoma,
vitreous hemorrhage, and eyelid laceration were all associated with
long-term poor visual outcome. Hyphema may produce glaucoma via
several mechanisms including contusion/inflammation of the trabecular
meshwork, physical disruption of the meshwork, and plugging of the
meshwork with red blood cells. In addition, a large clot in the anterior

chamber may even produce pupillary block by entirely occluding the

pupillary aperture.
Pressure elevation in association with hyphema may threaten vision
as a result of optic nerve damage, compromised blood flow to the
posterior segment, or corneal blood staining. Intraocular pressure
elevation occurs in up to 27% of patients acutely; however, this
pressure elevation is often mild and self-limited.
The duration and level of intraocular pressure required to damage
the optic nerve for a given individual is difficult to determine. Read and
Goldberg studied 137 hyphema patients prospectively and determined
that optic atrophy tended to occur with intraocular pressures at or
greater than 35 mmHg with durations varying from 5 to 14 days. Optic
atrophy as a direct result of the trauma itself may be a confounding
factor in such studies.
Corneal blood staining occurs more readily in the presence of an
intraocular pressure greater than 25 mmHg that has persisted for at least
6 days. If the corneal endothelial cells are already compromised as a
result of the trauma itself or pre-existing disease, the risk of staining
with only marginal pressure elevation is even greater.
Rebleeding into the anterior chamber can be a devastating
complication that typically occurs between days 2 and 6 following the
initial injury. The reported incidence of rebleeding is somewhere
between 6% and 33% based on several studies. Markedly elevated
intraocular pressure and its attendant complications are a particular
concern with rebleeding. Aminocaproic acid decreases the rate of
rebleeding in some patients. Systemic corticosteroids have been
recommended by some to reduce the incidence of rebleeding.
However, Spoor and associates showed no benefit from oral
corticosteroids in a prospective study. Although aminocaproic acid may
reduce the incidence of rebleeding in some patients, exaggerated clot
lysis in patients with larger hyphemas may develop 1-2 days following
therapy discontinuation with associated acute pressure elevation as a
result of lysed cells and debris obstructing outflow. This and the fact

that aminocaproic acid may have systemic side effects including nausea
and vomiting as well as the relatively low incidence of rebleeds overall
may account for why some clinicians choose not to employ this drug.
Acute pressure elevation in the setting of hyphema may be treated
with conventional pharmacologic agents, with the exception of miotic
agents and prostaglandin agents. Both of these agents may excacerbate
any inflammation that is already present and so they are not generally
used as first-line agents. Cycloplegic agents and topical corticosteroids
are often employed in the treatment of any associated inflammation
following hyphema. The potential for either topical or systemic steroids
to produce intraocular pressure elevation with more chronic use must be
kept in mind.
If the intraocular pressure remains elevated at a level that threatens
the optic nerve or the cornea in spite of medical therapy, then surgical
intervention may be necessary. Many surgical procedures have been
reported in the literature including anterior chamber washout,
mechanical clot expression, delivery of the clot with a cryoprobe,
automated hyphemectomy, and ultrasonic emulsification and aspiration
of the clot. Adjunctive procedures may include peripheral iridectomy to
relieve clot-induced papillary block. Trabeculectomy has been used to
achieve pressure normalization. Cyclodiathermy to control recurrent
bleeding has also been described.
Paracentesis and anterior chamber washout is the simplest and
safest procedure for clot evacuation. This can be performed by simple
irrigation or by manual coaxial irrigation and aspiration. Removal of the
entire clot may not be necessary. This technique also spares the
conjunctiva for future filtration surgery if it becomes required.

2.3.

Traumatic Cataract
The incidence of these lens opacities is higher in men than in women due
to occupational and sports injuries (Lang, 2006). Traumatic cataract can occur
by penetrating eye injury or blunt trauma that can be seen in days or years
(Ilyas S, 2007). The lens becomes white soon after the entry of a foreign

body, since interruption of the lens capsule allows aqueous and sometimes
vitreous to penetrate into the lens structure (Eva and Whitcher, 2007).
Blunt trauma does not result in rupture of the capsule, may cause an
anterior and/or posterior subcapsular cataract or both. Initially, fluid influx
causes swelling and thickening of the lens fibers. Later the fibers become less
swollen; the anterior subcapsular region whitens and may develop a
characteristic flower-shaped pattern, or an amorphous or punctate opacity
(Yanoff, 2009). Small perforation caused by penetrating injury will close
immediately because of ephitelial proliferation so the opacity only in the
small area (Ilyas, 2007). A small capsular penetrating injury may result in a
localized lens opacity. A larger rupture results in rapid hydration and complete
opacification. Penetrating injuries can be caused by accidental or surgical
trauma such as a peripheral iridectomy or during a vitrectomy. (Yanoff, 2009)

Traumatic Cataract

Traumatic cataract and iridodialysis

Concussion cataract occurs mainly due to imbibition of aqueous and
partly due to direct mechanical effects of the injury on lens fibres. It may
assume any of the following shapes (Khurana, 2007):
a. Discrete subepithelial opacities are of most common occurrence.

b. Early rosette cataract (punctate). It is the most typical form of

concussion cataract. It appears as feathery lines of opacities along the
star-shaped suture lines; usually in the posterior cortex.
c. Late rosette cataract. It develops in the posterior cortex 1 to 2 years after
the injury. Its sutural extensions are shorter and more compact than the
early rosette cataract.
d. Traumatic zonular cataract. It may also occur in some cases, though
rarely.
e. Diffuse (total) concussion cataract. It is of frequent occurrence.
f. Early maturation of senile cataract may follow blunt truma.
2.4. Uveitis
a. Definition
The term "uveitis" denotes inflammation of the iris (iritis,
iridocyclitis), ciliary body (intermediate uveitis, cyclitis, peripheral uveitis,
or pars planitis), or choroid (choroiditis). Common usage, however,
includes inflammation of the retina (retinitis), retinal vasculature (retinal
vasculitis), and intraocular optic nerve (papillitis). Uveitis may also occur
secondary to inflammation of the cornea (keratitis), sclera (scleritis), or
both (Riordan-Eva; Whitcher, 2007)
b. Epidemiology
Uveitis usually affects people 2050 years of age and accounts for 10
20% of cases of legal blindness in developed countries. Uveitis is more
common in the developing world than in the developed countries, due in
large part to the greater prevalence of infections that can affect the eye,
such as toxoplasmosis and tuberculosis. (Riordan-Eva; Whitcher, 2007).
Large series of uveitis patients show variation in terms of the relative
prevalence of different forms of uveitis. In surveys of patients referred to
tertiary centers, anterior uveitis has been shown to account for 28-66% of

cases, intermediate uveitis for 5-15%, posterior uveitis for 19-51%, and
panuveitis for 7-18%. (Yanoff, 2009)
c. Etiology
Uveitis can caused by trauma, chronic diarrhea, Reiter disease, herpes
simplex, Behcet syndrome, Posner Schlosman syndrome, post-operative,
adenovirus, parotitis, influenza, chlamydial infection, rheumathoid arthritis
and etc. (Ilyas S, 2007). Traumatic uveitis is often seen in accidental or
operative injuries to the uveal tissue. Different mechanisms which may
produce uveitis following trauma include (Khurana, 2007):
1) Direct mechanical effects of trauma.
2) Irritative effects of blood products after intraocular haemorrhage
3) Microbial invasion.
4) Chemical effects of retained intraocular foreign bodies
5) Sympathetic ophthalmia in the other eye.
d. Classification
Depend on the anatomical location, uveitis can be classified as:
Anatomical Classification of Uveitis
Type
Anterior uveitis
Intermediate
uveitis
Posterior uveitis

Panuveitis

Primary site of
inflammation
Anterior chamber
Vitreous
Retina or choroid

Anterior chamber,
vitreous,
and
retina or choroid

Include
Iritis, Iridocyclitis, Anterior cyclitis
Pars planitis, Posterior cyclitis,
Hyalitis
Focal, multifocal, or diffuse
choroiditis,
Chorioretinitis,
Retinochoroiditis,
Retinitis,
Neuroretinitis

Anatomical Classification of Uveitis

Acute uveitis describes the course of a specific uveitis syndrome
characterized by sudden onset and limited duration. Chronic uveitis
describes persistent inflammation characterized by prompt relapse (in less
than 3 months) after discontinuation of therapy. Recurrent uveitis is
characterized by repeated episodes of uveitis separated by periods of
inactivity without treatment lasting at least 3 months. (Kanski, 2011)
e. Occular Manifestation
The clinical manifestations of uveitis vary depending on several
factors - the primary site of involvement in the eye, the course of the
inflammatory process (e.g., acute or chronic), and the presence of
secondary complications arising from the uveitis itself. (Yanoff, 2009)
The symptoms of acute anterior uveitis (e.g., human leukocyte antigen
HLA-B27-related entities, such as ankylosing spondylitis) generally
include pain, redness, photophobia, and blurred vision, which typically
develop over a period of hours or days. On the other hand, patients who
have chronic anterior uveitis, such as that seen with JIA or Fuchs
heterochromic iridocyclitis, may present merely with blurring of vision or
mild redness, with little pain or photophobia. Patients who have
intermediate or posterior uveitis typically present with floaters or impaired
vision secondary to cystoid macular edema or chorioretinal involvement.
Patients who have panuveitis may present with any or all of these
symptoms. (Yanoff, 2009)
f. Examination Method
The slit lamp is used to examine the surface of the iris under a focused
beam of light. Normally no vessels will be visible. Iris vessels are only
visible in atrophy of the iris, inflammation, or as neovascularization in
rubeosis iridis.Where vessels are present, they can be visualized by iris

angiography after intravenous injection of fluorescein sodium dye. Defects

in the pigmented layer of the iris appear red under retroillumination with a
slit lamp. Slit lamp biomicroscopy visualizes individualcells such as
melanin cells at 40-power magnification. The anterior chamber is normally
transparent. Inflammation can increase the permeability of the vessels of
the iris and compromise the barrier between blood and aqueous humor.
The pigmented epithelium of the retina permits only limited evaluation
ofthe choroid by ophthalmoscopy and fluorescein angiography or
indocyaninegreen angiography. Changes in the choroid such as tumors or
hemangiomascan be visualized by ultrasound examination. (Lang, 2006)
g. Pathology of Uveitis
Inflammation of the uvea fundamentally has the same characteristics
as any other tissue of the body, i.e, a vascular and a cellular response.
However, due to extreme vascularity and looseness of the uveal tissue, the
inflammatory responses are exaggerated and thus produce special results.
(Khurana, 2007)
Pathologically, inflammations of the uveal tract may be divided into
suppurative (purulent) and nonsuppurative (non-purulent) varieties. Wood
has further classified non-suppurative uveitis into a nongranulomatous and
granulomatous types. (Khurana, 2007)
Purulent inflammation of the uvea is usually a part of endophthalmitis
or panophthalmitis occurring as a result, of exogenous infection by
pyogenic organisms which include staphylococcus, streptococcus,
psuedomonas, pneumococcus and gonococcus. The pathological reaction
is characterised by an outpouring of purulent exudate and infiltration by
polymorphonuclear cells of uveal tissue, anterior chamber, posterior
chamber and vitreous cavity. As a result, the whole uveal tissue is
thickened and necrotic and the cavities of eye become filled with pus.
(Khurana, 2007)
The pathological alterations of the nongranulomatous reaction consists
of marked dilatation and increased permeability of vessels, breakdown of
blood aqueous barrier with an outpouring of fibrinous exudate and
infiltration by lymphocytes, plasma cells and large macrophages of the

uveal tissue, anterior chamber, posterior chamber and vitreous cavity. The
inflammation is usually diffuse. As a result of these pathological reactions
iris becomes waterlogged, oedematous, muddy with blurring of crypts and
furrows. As a consequence its mobility is reduced, pupil becomes small in
size due to sphincter irritation and engorgement of radial vessels of iris.
Exudates and lymphocytes poured into the anterior chamber result in
aqueous flare and deposition of fine KPs at the back of cornea. Due to
exudates in the posterior chamber, the posterior surface of iris adheres to
the anterior capsule of lens leading to posterior synechiae formation. In
severe inflammation, due to pouring of exudate from ciliary processes,
behind the lens, an exudative membrane called cyclitic membrane may be
formed. (Khurana, 2007)
The pathological reaction in granulomatous uveitis is characterised by
infiltration with lymphocytes, plasma cells, with mobilization and
proliferation of large mononuclear cells which eventually become
epithelioid and giant cells and aggregate into nodules. Iris nodules are
usually formed near pupillary border (Koeppes nodules). Similar nodular
collection of the cells is deposited at the back of cornea in the form of
mutton fat keratic precipitates and aqueous flare is minimal. Necrosis in
the adjacent structures leads to a repairative process resulting in fibrosis
and gliosis of the involved area. (Khurana, 2007)
h. Anterior Uveitis
Though anterior uveitis, almost always presents as a combined
inflammation of iris and ciliary body (iridocyclitis), the reaction may be
more marked in iris (iritis) or ciliary body (cyclitis). Clinically it may
present as acute or chronic anterior uveitis. Main symptoms of acute
anterior uveitis are pain, photophobia, redness, lacrimation and decreased
vision. In chronic uveitis, however the eye may be white with minimal
symptoms even in the presence of signs of severe inflammation. (Khurana,
2007). External examination shows ciliary (circumcorneal) injection which
has a violaceous hue. (Kanski, 2011)

Ciliary
Miosis

Injection
due

to sphincter spasm

may predispose to the formation of posterior synechiae unless the pupil is

pharmacologically dilated. Endothelial dusting by a myriad of cells is
present early and gives rise to a dirty appearance True keratic precipitates
(KP) usually appear only after a few days and are usually nongranulomatous. (Kanski, 2011).

Endothelial
dusting by cells
Aqueous cells indicate disease activity and their number reflects
disease severity. Grading of cells is performed with a 2 mm long and 1 mm
wide slit beam with maximal light intensity and magnification. This must
be performed before mydriasis because in normal eyes cells and pigment
clumps may develop after pupillary dilatation. Worsening is defined as
either a two-step increase in the level of activity or an increase to the
maximum grade. Anterior vitreous cells indicate iridocyclitis. (Kanski,
2011).
Hypopyon is a feature of intense inflammation in which cells settle in
the inferior part of the anterior chamber (AC) and form a horizontal level.
(Kanski, 2011)

Hypopion
Posterior synechiae may develop quickly and must be broken down
before they become permanent . Low intraocular pressure (IOP) may occur
as a result of reduced secretion of aqueous by the ciliary epithelium.
(Kanski, 2011)

Extensive posterior synechiae

Fundus examination is usually normal, but should always be
performed to exclude spillover anterior uveitis associated with a posterior
focus, notably toxoplasmosis and acute retinal necrosis (Kanski, 2011).
With appropriate therapy the inflammation tends to completely resolve
within 56 weeks.The prognosis is usually very good. Complications and
poor visual prognosis are related to delayed or inadequate management.
Steroid-induced hypertension may occur but glaucomatous damage is
uncommon (Kanski, 2011).
Chronic anterior uveitis (CAU) is less common than the acute type
and is characterized by persistent inflammation that promptly relapses, in
less than 3 months, after discontinuation of treatment. The inflammation
may be granulomatous or non-granulomatous. Bilateral involvement is
more common than in AAU. Presentation is often insidious and many
patients are asymptomatic until the development of complications such as
cataract or band keratopathy. Because of the lack of symptoms patients at
risk of developing CAU should be routinely screened; this applies
particularly in patients with juvenile idiopathic arthritis. (Kanski, 2011).

External examination usually shows a white eye. Occasionally the eye

may be pink during periods of severe exacerbation of inflammatory
activity.Aqueous cells vary in number according to disease activity but
even patients with numerous cells may have no symptoms. Aqueous flare
may be more marked than cells in eyes with prolonged activity and its
severity may act as an indicator of disease activity. (Kanski, 2011). It is
due to leakage of protein particles into the aqueous humour from damaged
blood vessels. It is demonstrated on the slit lamp examination by a point
beam of light passed obliquely to the plane of iris. In the beam of light,
protein particles are seen as suspended and moving dust particles. This is
based on the Brownian movements or Tyndal phenomenon. (Khurana,
2007).

Aqueous Flare and Cells

Keratic precipitate are clusters of cellular deposits on the corneal
endothelium composed of epithelioid cells, lymphocytes and polymorphs.
(Kanski, 2011).

Keratic Precipitate
The duration is prolonged and in some cases the inflammation may
last for many months or even years. Remissions and exacerbations of
inflammatory activity are common and it is difficult to determine when the
natural course of the disease has come to an end.The prognosis is guarded
because of complications such as cataract, glaucoma and hypotony.
(Kanski, 2011).
i. Intermediate Uveitis

Intermediate uveitis affects mainly the intermediate zone of the eye

-ciliary body, principally the pars plana, peripheral retina, and vitreous.
The cause is unknown in most cases, although syphilis, tuberculosis, Lyme
disease, and sarcoidosis should be ruled out with appropriate laboratory
and ancillary testing. Multiple sclerosis should also be considered.
Intermediate uveitis is seen mainly among young adults, affects men and
women equally, and is bilateral in up to 80% of cases. (Riordan-Eva;
Whitcher, 2007)
Common complaints include painless floaters and decreased vision.
Minimal photophobia or external inflammation. Usually age 15 to 40 years
and bilateral. Vitreous cells, white exudative material over the inferior ora
serrata and pars plana (snowbank), cellular aggregates floating in the
inferior vitreous (snowballs). Younger patients may present with vitreous
hemorrhage. (Elhers, 2008)

j. Pars planitis/intermediate uveitis with snowballs

Posterior subcapsular cataract and cystoid macular edema are the most
common causes of decreased vision. In severe cases, cyclitic membranes
and retinal detachments may occur. Secondary glaucoma is rare.
Corticosteroids are used mainly to treat cystoid macular edema or retinal
neovascularization. Topical corticosteroids should be tried for 34 weeks
to identify patients predisposed to development of corticosteroid-induced
ocular hypertension. If no improvement is noted and ocular hypertension

does not develop, a posterior sub-Tenon or intraocular injection of

triamcinolone acetonide, 40 mg/mL, may be effective. Patients with
intermediate uveitis usually do well with cataract surgery. (Riordan-Eva;
Whitcher, 2007)
k. Posterior Uveitis
Posterior uveitis refers to inflammation of the choroid (choroiditis).
Since the outer layers of retina are in close contact with the choroid and
also depend on it for the nourishment, the choroidal inflammation almost
always involves the adjoining retina, and the resultant lesion is called
chorioretinitis (Khurana, 2007). Presentation varies according to the
location of the inflammatory focus and the presence of vitritis. For
example a patient with a peripheral lesion may complain of floaters
whereas a patient with a lesion involving the macula will predominantly
complain of impaired central vision (Kanski, 2011).
Blurred vision, floaters, pain, redness, and photophobia typically
absent unless anterior chamber inflammation is present (Elsher, 2008).
Various visual symptoms experienced by a patient of choroiditis are
summarised below (Khurana, 2007):
1) Defective vision. It is usually mild due to vitreous haze, but may be
severe as in central choroiditis.
2) Photopsia. It is a subjective sensation of flashes of light resulting due to
irritation of rods and cones.
3) Black spots floating in front of the eyes. It is a very common complaint
of such patients. They occur due to large exudative clumps in the
vitreous.
4) Metamorphopsia. Herein, patients perceive distorted images of the
object. This results due to alteration in the retinal contour caused by a
raised patch of choroiditis.
5) Micropsia which results due to separation of visual cells is a common
complaint. In this the objects appear smaller than they are.

6) Macropsia, i.e., perception of the objects larger than they are, may
occur due to crowding together of rods and cones.
7) Positive scotoma, i.e., perception of a fixed large spot in the field of
vision, corresponding to the lesion may be noted by many patients.
Lesions of the posterior segment of the eye can be focal, multifocal,
geographic, or diffuse. Those that tend to cause clouding of the overlying
vitreous should be differentiated from those that give rise to little or no
vitreous cells. The type and distribution of vitreous opacities should be
described. Inflammatory lesions of the posterior segment are generally
insidious in onset, but some may be accompanied by abrupt and profound
visual loss. (Riordan-Eva; Whitcher, 2007)

Retinitis
Vitreous opacities due to choroiditis are usually present in its middle
or posterior part. These may be fine, coarse, stringy or snowball opacities
(Khurana, 2007). Features of a patch of choroiditis in active stage it looks as
a pale-yellow or dirty white raised area with ill-defined edges. This results
due to exudation and cellular infiltration of the choroid which hide the
choroidal vessels. The lesion is typically deeper to the retinal vessels. The
overlying retina is often cloudy and oedematous. In atrophic stage or healed
stage, when active inflammation subsides, the affected area becomes more
sharply defined and delineated from the rest of the normal area. The
involved area shows white sclera below the atrophic choroid and black
pigmented clumps at the periphery of the lesion (Khurana, 2007).
l. Treatment

The treatment of uveitis has three main goals: to prevent visionthreatening complications, to relieve the patient's complaints and, when
feasible, to treat the underlying disease. (Babu; Rathinam, 2010)
1. Mydriatic and Cycloplegic Agents
These topical medications are used to treat the ciliary spasm that
frequently occurs with acute anterior uveitis and to break recently formed
posterior synechiae and/or prevent the development of new synechiae.
Longer acting agents, such as homatropine, scopolamine, or atropine, are
utilized to relieve ciliary spasm, whereas the shorter acting agents
(tropicamide or cyclopentolate) may play a role in preventing new
posterior synechiae formation in patients who have chronic iridocyclitis
(e.g., secondary to JIA) and minimal photophobia in whom the pupil
should be kept relatively mobile. (Yanoff, 2009)
2. Corticosteroids
Corticosteroids are the drugs of choice in most types of uveitis. They
inhibit the inflammatory process by suppressing the arachidonic acid
metabolism and activation of complement (Babu; Rathinam, 2010).
When administered systemically they have a definite role in nongranulomatous iridocyclitis, where inflammation, most of the times, is
due to antigen antibody reaction. Even in other types of uveitis, the
systemic steroids are helpful due to their potent non-specific antiinflammatory and antifibrotic effects. Systemic corticosteroids are
usually indicated in intractable anterior uveitis resistant to topical therapy
(Khurana, 2007).
In panuveitis, both topical and systemic corticosteroids are needed.
Depending upon the severity of the disease, oral prednisolone is started
in a loading dose of 1 mg/kg/day. As the inflammation subsides, tapering
of corticosteroids by 5-10 mg per week is begun within two to four
weeks of initiating therapy. Once the eye is completely quiescent, the

patient is followed on a maintenance dose ranging from 2.5-10 mg daily

of prednisolone. A reasonably long period of low-dose corticosteroids is
required as maintenance therapy in VKH(Vogt Koyanagi-Harada)
syndrome and SO.(Babu; Rathinam, 2010)
The normal response to the corticosteroid therapy may be interrupted
by recurrence of uveitis in which case the frequency of instillation of
topical drops is increased besides raising the oral corticosteroid to the
initial high-dose levels. Unilateral cases may be given a trial with
periocular injection of depot corticosteroids into the posterior subtenon
space. The side-effects and complications of topical or systemic
corticosteroids must be looked for at every follow-up visit of the patient.
These include secondary glaucoma, posterior subcapsular cataract,
increased susceptibility to infection (ocular or systemic), hypertension,
gastric ulcer, diabetes, obesity, growth retardation, osteoporosis and
psychosis. (Babu; Rathinam, 2010)
3. Antimetabolites
Indicate for sight-threatening uveitis, which is usually bilateral, noninfectious, reversible and has failed to respond to adequate steroid
therapy. Steroid-sparing therapy in patients with intolerable side-effects
from systemic steroids or those with chronic relapsing disease requiring a
daily dose of prednisolone of more than 10 mg. Once a patient has been
started on an immunosuppressive drug and the appropriate dose
ascertained, treatment should continue for 624 months, after which
gradual tapering and discontinuation of medication should be attempted
over the next 312 months. However, some patients may require longterm therapy for control of disease activity. (Kanski, 2011)
4. Vitrectomy in panuveitis
Vitrectomy for uveitis began in the late 1970s for diagnostic
purposes and for treating infections. Diagnostic vitrectomy combined

with PCR can significantly improve diagnostic yield in otherwise

idiopathic uveitis, and can frequently make a diagnosis in cases
complicated by media opacity or other features that make traditional
exam-based diagnosis difficult or impossible. Vitrectomy may be
considered as a therapeutic option when uveitis persists despite
maximum tolerable medical treatment with corticosteroids and/or other
immunosuppressants. It may also be indicated when visual loss occurs
due to complications of longstanding inflammations, such as a densely
opacified vitreous, scar tissue pulling on the ciliary body causing
hypotony, cystoid macular edema, an epiretinal membrane, a dense
posterior

lens

capsule

opacification

or

tractional

retinal

detachment.Vitrectomy removes the lodged lymphocytes in the vitreous,

inflammatory debris, immune complexes and autoantigens. It also
increases the uveal penetration of anti-inflammatory cells. Besides
providing a better access for complete removal of the cataractous lens
material along with posterior capsule, the combined approach of pars
plana lensectomy and vitrectomy allows easy performance of intraocular
maneuvers and prevents formation of cyclitic membrane. (Babu;
Rathinam, 2010)

CHAPTER III
CASE REPORT

1. Patient identity
Name
: Mr. Y
Sex
: Male
Age
: 31 years old
Address
: Sekayam, Balai Karangan
Job
: Wiraswasta
Religion
: Catholic
Patient was examined on September 22nd , 2014
2. Anamnesis
a. Chief complaint :
Pain in left eye since one day ago
b. History of disease :
Patient came to ophthalmologist with pain in left eye as major
complaint. Pain was felt by patient after his left eye, accidently, get
punctured by a small branch of tree at 10 AM yesterday. Patient was
complained about his blurred vision and watery discharge of his left
eye. Patient felt of glare when he saw in light condition.There were no
headache, nausea, and vomiting. Patient had consulted to general
practitioner and had been given some medication, such as, Cendo
Xytrol, Mefenamic Acid, and Amoxicillin. But, there was no
improvement with those medication.
c. Past clinical history :
Diabetes mellitus and hypertension history was denied by patient. There
was no ocular disease before. Wearing glasses (-).
d. Family history
Diabetes mellitus and hypertension history in family was denied by
patient.
3. General Physical assessment
General condition
: Good, with mild pain
Awareness
: Compos mentis
Vital sign :
a. Blood Pressure
: 110/80 mmHg
b. HR
: 80 x/minute
c. RR
: 24 x/minute
d. Temperature
: 36,2C
4. Ophthalmological status
Visual acuity :
a. OD
: 6/10
b. OS
: 1/300, with good light projection
OD

OS
Opacification
of lens

Corneal
erosion

injection
Hypopion

OD

Fibrin in COA

OS

Orthophoria

Eye ball position

Orthophoria

Eye Movement

Movement(+),

ptosis

(-),

Palpebra

Movement

(+),

ptosis

(-),

lagoftalmos (-), exoftalmos (-),

lagoftalmos (-), exoftalmos (-),

edema (-), blepharospasm (-)

edema (-), blepharospasm (+)

Redness

(-),

discharge

(-),

Conjungtiva

injection (-)
Clear, edema (-), infiltrate (-),

(+), injection (+)

Cornea

Ulcer (-)
Clear, deep

Redness (+), watery discharge

Hazy, edema (+), infiltrate (+),
ulcer (-), KP (-)

Anterior

Shallow, fibrin (+), hypopion (+)

chamber
Iris: brown, sinechia (-)

Iris/pupil

Iris : brown, iridodialysis (+)

Circular pupil, regular, 3 mm in

Pupil is not circular, with tears in

diameter. Direct light pupillary

iris. Direct light pupillary reflex

reflex (+), consensual reflex (+)

diminished,
diminished

consensual

reflex

Clear

Lens

Not performed

White opacification

Posterior

Funduscopy : not performed

segment

USG

normal

detachment,

no

(no

retinal

intraocular

foreign body, no fibrin)

5. Shadow test

: negative / negative

6. Visual field test

: normal / normal

7. Palpation tonometry : OS > OD

8. Resume
Patient came to ophthalmologist with pain in left eye as major complaint.
Pain was felt by patient after his left eye, accidently, get punctured by a
small branch of wood at 10 AM yesterday. Patient was complained about
his blurred vision and watery discharge of his left eye. There were no
headache, nausea, and vomiting. Patient had consulted to general
practitioner and had been given some medication, such as, Cendo Xytrol,
Mefenamic Acid, and Amoxicillin. But, patient felt that there was no eye
improvement with those medication.
Pain (+), watery (+), photophobia (+), blurred vision (+)
Visual acuity was 6/10 OD, 1/300 OS. Left palpebra seems having
blepharospasm. Cornea had a lesion cause by puncture of branch of tree
and there was edema in cornea.
9. Diagnosis
Diagnose :
a. OD

:-

b. OS

: Secondary glaucoma et causa traumatic cataract

Anterior uveitis

DDx :

OD

:-

OS

: Primary close angle glaucoma and keratitis

10. Plan for examination

a. Flourescein test
b. Tonometry
c. Gonioscopy
11. Treatment
a. Atropine eye drops (Cendo tropin), 3 times a day
b. Prostaglandine analog eye drops (latanoprost), 2 times a day
c. Antibiotic (Flouroquinolone) eye drops, every hours
d. Systemic corticosteroid (methyl prednisolone), once a day
e. Asetazolamide per oral, 3 times a day
f. KCl 600 mg (Electrolyte) per oral, 3 times a day
12. Prognosis
a. OD:
i. Ad vitam
: dubia ad bonam
ii. Ad functionam
: dubia ad bonam
iii. Ad sanactionam
: dubia ad bonam
b. OS :
i. Ad vitam
ii. Ad functionam
iii. Ad sanactionam

: dubia ad bonam
: dubia ad bonam
: dubia ad bonam

CHAPTER IV
DISCUSSION
A man, 31 years old, works as a laborer. Patient complains pain in his left eye
since one day ago after his eye was get punctured by branch of tree. The patient
felt blurred vision in his left eye, there is redness in konjungtiva, photophobia, and
watery discharge of his left eye. Fever history was denied by patient. From the
ophthalmic examination, the visual acuity of right eye is 6/10, and left eye is
1/300 with good light projection. Eyelids of both eyes are normal, but the left
eyes lid is tend to blink and close. Conjunctiva of the left eye has subconjunctival
injection with no bleeding. Cornea of the left eye has infiltrate, defect, and edema.
The anterior chamber of the left eye is shallow and containing some fibrins,
meanwhile the right eyes anterior chamber is shallow and clear. Iris is brown in
color, but there is a tears due to the injury in the left eye. Pupil is anisochore, the
right pupil has regular circular shaped with 3 mm in diameters. The left eyes
pupil is irregular due to the tears in iris. Direct light reflex and consensual reflex
for right eye are positive, but diminished in the left eye. The lens is opaque in the
left eye and clear in the right eye. Funduscopy is not performed in left eye due to
hazy cornea and white opacification of the lens. In USG examination, there is no
fibrin or mass founded (clear), and no retinal detachment in vitreous of left eye. In
palpation of both eyes, it is found that the left eyes intraocular pressure (IOP) is
slightly higher than the right eye.
Painfull sensation, which felt by patient, is caused by stimulation of the
trigeminal nerve. Cornal edema, increasing intraocular pressure, and inflammation

or infection in uvea will affect the trigeminal nerve and produce pain sensation.
The patient also complaint about photophobia. Photophobia is intimately, likely
inextricably, linked to pain sensation. The trigeminal nerve and its nuclei are the
primary mediators of pain sensation to the head. The conjunctiva, cornea, sclera,
and uvea (iris, ciliary body, and choroid) are densely innervated with trigeminal
fibers, and exquisitely sensitive to pain. Any painful stimulus to these areas (e.g.
iritis, uveitis) invariably causes photophobia.
Blurry vision can be caused by the refractive media defect such as cornea or
the lens, from uvea tract like iris, cilliar corpus, choroid, or the retina. In this case,
patient has some problems with the visual refractive media. It is hazy cornea
(shows that there is edema in cornea), and white opacification of lens (traumatic
cataract). These conditions can cause disrupting of the refraction media and
finally, it can hampered the light to retinal.
The patients left eye is red because of subconjunctival and cilliary
injection. Subconjunctival injection is dilatation of posterior conjunctiva artery.
Ciliar injection is dilatation of pericorneal blood vessel (a. cilliar anterior) that can
be caused by inflammation in the cornea, corneal ulcer, corpus alienum,
inflammation in the uveal tract, glaucoma, endophtalmitis or panophtalmitis.
From the ophthalmologic examination, the visual acuity is 6/10 for OD and
1/300 for OS. Visual acuity can decrease because of defect in the cornea, opacity
in the lens, inflammation in the uveal tract, retinal impairment, etc. The visual
acuity in the patients left eye decreasing suddenly can be caused by defect in the
cornea like keratitis or corneal ulcer, or from the uveal tract. Since the patient
didnt complain about any discharge from his eye, it can caused by inflammation
in uveal tract such as anterior uveitis. Uveitis is inflammation of the iris (iritis,
iridocyclitis), ciliary body (intermediate uveitis, cyclitis, peripheral uveitis, or pars
planitis), or choroid (choroiditis). Anterior uveitis is iritis and iridocyclitis. Uveitis
can cause by corneal infection, systemic infection like syphilis, tuberculosis,
systemic immunological disease like sarcoidosis, Vogt-Koyanagi-Harada, arthritis
rheumatoid, and trauma, etc.

Cornea of the left eye has infiltrate, defect and edema. It can be caused by
there is inflammation in the cornea. In anterior uveitis, the infiltrate can be caused
by chronic inflammation resulting debris in the anterior chamber that stick to the
inner surface of the corneal endothelium and make keratic precipitate. The defect
in the cornea is possibly the port of entry of the branch of tree that can cause
inflammation to the iris (anterior uveitis) . The anterior chamber is opaque and
shallow in the left eye can caused by accumulation of inflammatory cell, debris or
fibrin.
Iris of both eyes is brown, but there is a tearing of the left eyes iris. The iris
is adherent to the lens in several places as a result of inflammation, causing an
irregular, fixed pupil. The adhesion may alter the sphincter pupils muscle
movement. So the pupil will be anisochore.
Cataract can cause blurred vision but the patient didnt complaint about
blurred vision in the left eye or white eye before so the most possible cause for
the opacity of the lens in the patient is trauma. The lens becomes white soon after
the entry of a foreign body or penetrating trauma, since interruption of the lens
capsule allows aqueous and sometimes vitreous to penetrate into the lens
structure. Trauma does not result in rupture of the capsule, may cause an anterior
and/or posterior subcapsular cataract or both. Initially, fluid influx causes swelling
and thickening of the lens fibers. Later the fibers become less swollen; the anterior
subcapsular region whitens and may develop a characteristic flower-shaped
pattern, or an amorphous or punctate opacity.
Secondary glaucomas are caused by other ocular diseases or factors such as
inflammation, trauma, bleeding, tumors, medication, and physical or chemical
influences. The differential diagnosis of secondary glaucoma is primary close
angle glaucoma. The symptoms which appear in this patient are general symptoms
of glaucoma. But primary close angle glaucoma can be diagnose when there is no
another underlying ocular disease or factor which induce the glaucoma.
The differential diagnose for OS is keratitis. Keratitis can caused by viral,
bacterial, or fungal infection with or without trauma before. The symptom is the
patient feel usually blurred, there is watery or purulent discharge, change in

corneal surface related to cause, there is cilliar injection and conjunctival

injection, the pupil is normal or myosis but the pupil still reactive to the light. In
the patient, there is no discharge, and the pupil is irregular and doesnt reactive to
the light so keratitis can be disregard. And for the traumatic cataract the
differential diagnose is senile cataract and traumatic lens dislocation. Since the
opacity of the lens happened after the patient stabbed by wire, the senile cataract
can be disregard. Small perforation caused by penetrating injury will close
immediately because of ephitelial proliferation so the opacity only in the small
area like found in the patient. Lens dislocation can occur after a trauma and can be
no symptom if the dislocation is partial but if the lens floating in the vitreous the
patient will have blurred vision and red eye. Iridodonesis, a quivering of the iris
when the patient moves the eye, is a common sign of lens dislocation and is due to
the lack of lens support. This is present both in partially and in completely
dislocated lenses. But in the patient, iridodonesis cant be find.
The non medicamentous treatment in this patient is close the eye with
bandage when the patient work to avoid exposure to dust, wood, foreign body, and
ultraviolet light. Medical treatment which given to this patient are atropine (cendo
tropin) eye drops, prostaglandin analog (latanoprost) eye drops, antibiotic
(levofloxacin) eye drops, oral steroid, oral asetazolamide (glaukon), and oral
KSR. Mydriatic agent (atropine) is given to promote comfort by relieving spasm
of the ciliary muscle and pupillary sphincter, and to break down recently formed
posterior synechiae. Atropine can decrease the inflammation of the eye too.
Prostglandin analog (latanoprost) is used to decreased the intraocular pressure by
facilitating the aqueous humor outflow. Antibiotic (levofloxacin) is given to heal
the bacterial infection (uveitis) of the eye. Systemic steroid is used to decrease the
inflammation. Corticosteroid has the function to reduce the inflammation of the
eye by inhibit cyclo-oxygenase and lipoxygenase pathways, decrease complement
level, migration of lymphocytes, production of vasoactive amines and interleukin,
circulating monocytes and macrophage activity. Oral steroid is chosen than steroid
eyedrop because there is defect in cornea. If topical steroid is given to corneal
defect, it can disturb the healing process and fungi can easily grow, which can

destroy the corneal structure. Oral asetazolamide is used to decrease the aqueous
humor production. Asetazolamide can block anhidrase carbonic enzyme which
make diuresis, decrease secretion of aquoeus humor up to 60% and decrease the
intraocular pressure. Because asetazolamide is a diuretic drug, it could disturb the
electrolyte balance in the body, so KSR is given to avoid this effect.

CHAPTER V
CONCLUSION

A 31 years old man complain pain in his left eye since one day ago after
his eyes got punctured by small branch of tree. Ophthalmologic examination show
subconjunctival and cilliar injection, irregular pupil, not reactive to light, tears in
iris, opacity of the lens, fibrin and hypopion in anterior chamber. Anterior
chamber looks shallow, and with palpation tonometry, the left eye has slighlty
higher pressure than right eye. The therapy include non-medicamentous (use
bandage to avoid exposure to foreign body, dust, and UV) and medicamentous
(mydriatic agent [atropine], prostaglandin analog [latanoprost], antibiotic
[levofloxacin], systemic corticosteroid [methyl prednisolone], asetazolamide, and
KSR for the left eye).

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