CASE REPORT

1. Patient identity
Name
: Mr. Amsyah
Sex
: Male
Age
: 31 y.o
Address
: Dusun Garuda RT 001/010 Sui. Kakap
Job
: Swasta
Religion
: Islam
Patient was examined on June 10, 2014
2. Anamnesis
Main complaint :
Eye glare
History of desease :
Six days ago patients patients complain of eye glare in the left eye
when back from worked and eye starts to become red. Slowly patients
complain about loss of vision in the left eye. Then eye started has a
discharge one day ago. Sometimes it is pain.

Past clinical history :

Hypertension (-)
Diabetes Mellitus (denied) because patient never did clinical check.
Glasses wearing (-)
Others eye desease (-)
Traumatic history (-)

Family history
Hypertension (-)
Diabetes Mellitus (-)
Glasses wearing (-)

3. General Physical assestment

General condition
: Good
Awareness
: Compos mentis
Vital sign :
a. Blood Pressure
: 130/80 mmHg
b. RR
: 18/minute
c. Temperture
: 36,5C
4. Ophthalmological status
Visual acuity :
a. OD
: 6/6
b. OS
: 1/300
c. Last glasses : the patient never use glasses

OD
Ortho

OS
Eye ball position

Ortho

Eye Movement

Movement(+), ptosis (-),

Palpebra

lagoftalmos (-)
redness (-), discharge (-),

Movement (+), ptosis (-),

lagoftalmos (-)

conjungtiva

redness (+), discharge (+),

degeneration plaque (-), foreign

degeneration plaque (-), foreign

body (-), injection (-)

body (-), injection (+)

ulcer (-)

Cornea

ulcer (+)

clear, deep impression

Anterior chamber

Not Clear

Iris colour : brown, sinekia (-)

Iris/pupil

Iris colour : brown, sinekia (-)

Circular pupil, isochore

Circular pupil, isochore

Clear

Lense

Cloudy

Clear

Vitreous

Normal papil, normal blood vessel,

Fundus

normal retina, normal makula

Shadow test : negatif (-)

Intra Ocular pressure (tonometry) : -

Funduscopy : there is normal papil, normal blood vessel, normal retina,

normal macula in ocular dextra. The left eye cant be seen in funduscopy.

Visual field test: -

5. Diagnosis
Diagnose :
a. OD

: Normal eye

b. OS

: Kornea ulcer e.c fungal keratitis

DDx :

6.

OD
OS

::

1. Bacterial keratitis
2. Herpes simplex keratitis
Plan for examination
a. Slit lamp; perimetri.
b. KOH examination
c. Gram stain

d. Culture
7. Treatment
a. OD
i. Non-pharmacological
1. b. OS
i. Non-pharmacological
1. Using eye protection
ii. Pharmacological
1. For fungal keratitis: natacen 5%, ketokonazol 2x400
mg, tropin 0,5%, floxa
8. Prognosis
a. OD:
i. Ad vitam
ii. Ad functionam
iii. Ad sanactionam

: bonam
: bonam
: bonam

b. OS :
i. Ad vitam
ii. Ad functionam
iii. Ad sanactionam

: malam
: malam
: malam

CHAPTER IV
CASED EXPLANATION
A man, 31 years old, came to ophthalmologic clinic with complain six days ago
patients patients complain of eye glare in the left eye when back from worked and
eye starts to become red. Slowly patients complain about loss of vision in the left
eye. Then eye started has a discharge one day ago. Sometimes it is pain. There were
no history of eye trauma and he did not consume any drugs before.
Visual acuity is 1/300 for ocular sinistra (OS) with good projection and 6/6 for
ocular dextra(OD). From clinical assestment, there is high opacity on the left kornea
and nothing for the right eye, that cause funduscopy can not be describe for left eye.
From resume above, the diagnosis for the left eye patient lead to fungal keratitis
with kornea ulcer and. For the right eye is normal.
Fungi gain access into the corneal stroma through a defect in the epithelium,
then multiply and cause tissue necrosis and an inflammatory reaction. The epithelial
defect usually results from trauma (eg, contact lens wear, foreign material, prior
corneal surgery). The organisms can penetrate an intact Descemet membrane and
gain access into the anterior chamber or the posterior segment. Mycotoxins and
proteolytic enzymes augment the tissue damage. In the advanced countries of the
West, fungi are not a common cause of microbial keratitis. However, in the
developing countries, fungal infections are extremely common.

Farm injuries are the most important cause. Fungi cannot penetrate the intact
corneal epithelium. They need a penetrating injury or a previous epithelial defect to
enter the cornea. Topical steroid use has definitively been implicated as a cause of
increased incidence, development, and worsening of fungal keratitis. Other risk
factors to consider are foreign bodies, and immunosuppressive diseases.
Once the damaged corneal epithelium is invaded by the offending agents the
sequence of pathological changes which occur during development of corneal ulcer
can be described under four stages, viz., infiltration, active ulceration, regression
and cicatrization. Infiltration characterised by the infiltration of polymorphonuclear
and/or lymphocytes into the epithelium from the peripheral circulation
supplemented by similar cells from the underlying stroma if this tissue is also
affected. Active ulceration results from necrosis and sloughing of the epithelium,
Bowman's membrane and the involved stroma. The walls of the active ulcer project
owing to swelling of the lamellae by the imbibition of fluid and the packing of
masses of leucocytes between them. Regression is induced by the natural host
defence mechanisms (humoral antibody production and cellular immune defences)
and the treatment which augments the normal host response. Cicatrization stage
healing continues by progressive epithelization which forms a permanent covering.
The fungi which may cause corneal infections are filamentous fungi e.g.,
Aspergillus, Fusarium, Alternaria, Cephalosporium, Curvularia and Penicillium.
Yeasts e.g., Candida and Cryptococcus. (The fungi more commonly responsible for
mycotic corneal ulcers are Aspergillus (most common), Candida and Fusarium).
The most important step in the initial management of suspected fungal
keratitis is to obtain corneal material for directed smears and inoculation of media.
Smears are used to obtain rapid information about the pathogen.
Polyenes include natamycin, nystatin, and amphotericin B. Polyenes disrupt
the cell by binding to fungal cell wall ergosterol and are effective against both
filamentous and yeast forms. Azoles (imidazoles and triazoles) include
ketoconazole, miconazole, fluconazole, itraconazole, econazole, and clotrimazole.

Azoles inhibit ergosterol synthesis at low concentrations, and, at higher

concentrations, they appear to cause direct damage to cell walls. Systemic
antifungal drugs may be required for severe cases of fungal keratitis. Tablet
fluconazole or ketoconazole may be given for 2-3 weeks. Oral fluconazole and
ketoconazole are absorbed systemically with good levels in the anterior chamber
and the cornea; therefore, they should be considered in the management of deep
fungal keratitis.
Patients who do not respond to medical treatment of topical and oral
antifungal medications usually require surgical intervention, including corneal
transplantation. Approximately 15-27% of patients require surgical intervention. In
some cases, though, even corneal surgery will not restore vision, and patients will
be blind or otherwise visually impaired.