Parkinson

Interesting Case: Keratoconus
Kenny Gozal
406162024
PATIENT IDENTITY
• Name : An. N P
• Age : 13 y o
• Birth : Jakarta, 5th of July 2005
• Gender : Male
• Address : Jl. Pesing Polgar 7 RT001/RW005 No. 137
• Occupation : Junior High Scool Student

• Education : Elementary
• Marital status : Single
• Religion : Muslim
• Race : Javanese
ANAMNESIS
Autoanamnesis on 09/22/2018, 11.30 o’clock at
opthalmology department, Sumber Waras
Chief Complaint: Decrease visual acuity in both

eyes
Other symptoms: Difficulties in seeing in the dark

or adapting from light to dark, a flash of lights and
sometimes appears blackspot
ANAMNESIS
History of present illness:
A 41 years old male came to ophthalmology department in Sumber Waras
Hospital complaining of decrease in both visual fields approximately 6 years ago.
The decrease of visual fields was starting from outside or peripheral to inside and
it’s getting worst. The first time he recognized was when he drove his motorbike
and had a crash because he didn’t saw the other motorbike right beside him. The
decrease in visual field is progresses each year, causing the limitation of patient
daily activities, for example; the patient can’t walk properly and often hit the wall.
Patient had a problem in seeing at night time or at dark room too. Earlier, the
patient felt a difficulty in adapting from bright place to dark place, which is took
quiet long time to adapt. Besides that, these few months, patient complaint that
sometimes he saw flash of light or dew-like shadow appearance and also dark
spot. Double vision is denied, nor blurry vision. Patient has never been to doctors
before to check his eyes, and there are no family members had the same
symptoms. Patient admit he do smoke a pack everyday.
ANAMNESIS
• Past medical history: patient had never been
suffered from eye disease, there are no systemic
disease such as hypertension and diabetic.
Patient had never been exposed to any trauma.
• Family medical history

– Mother: DM (+), HT (+), eye disease (-)
– Father: Heart disease (+), kidney disease (+), HT
(unknown), DM (unknown), eye disease (-)
PHYSICAL
EXAMINATION
• Visual Acuity:
– VOD: 6/6
– VOS: 6/6
OD OS
Lumps/nodule (-) Lumps/nodule (-)
PHYSICAL EXAMINATION Edema (-)

Hyperemia (-)
Edema (-)
Hyperemia (-)
Palpebra Ptosis (-) Ptosis (-)
Lagophthalmus (-) Lagophthalmus (-)
Ectoprion (-) Ectoprion (-)
Entropion (-) Entropion (-)
Color: transparant Color: transparant

Vascularization: conjunctiva Vascularization: conjunctiva
Bulbi injection (-), ciliary injection (-) injection (-), ciliary injection (-)
Nodule (-) Nodule (-)
Edema (-), chemosis (-) Edema (-), chemosis (-)
Conjungtiva
Hyperemia (-) Hyperemia (-)

Follicle (-) Follicle (-)
Tarsal
Papillae (-) Papillae (-)
Corpus alineum (-) Corpus alineum (-)
Color: white Color: white

Sclera
Inflammation (-) Inflammation (-)
Transparency: clear Transparency: clear

Infiltrate (-) Infiltrate (-)
Cornea
Defect (-) Defect (-)
Edema (-) Edema (-)
Depth: normal Depth: normal
Anterior
Hyphema (-) Hyphema (-)
Chamber
Hypopion (-) Hypopion (-)
Color: brown Color: brown

PHYSICAL
Synechiae (-) Synechiae (-)
EXAMINATION
Iris Iridodenesis (-) Iridodenesis (-)
Neovascularisati Neovascularisati
on (-) on (-)
Size: 3 mm Size: 3 mm
Shape: round Shape: round
Symmetrical Symmetrical
Pupil Direct light reflex Direct light reflex
(+) (+)
Indirect light Indirect light
VISUAL FIELDS
Tunnel vision
FUNDUSCOPY
EXTRAOCULAR
MUSCLES
Pergerakan bola mata ODS baik

RESUME
• A 41 years old man presented with decrease in
visual fields especially at the temporal side and
expanding to medial fields approximately 6 years
ago. Patient admitted that it getting worst causing
a limitation in daily activities. Patient also
complaining of nyctalopia and photopsia. Physical
examination revealed a decrease of visual fields
(tunnel vision). Funduscopy showed bone spicule
pigmentation at the peripheral fundus which
expanding to medial and had strike the maculae.
• DIAGNOSIS
– Retinitis Pigmentosa ODS
• DIFFERENTIAL DIAGNOSIS
– Chorioretinitis sifilis
– Vitamin A deficiency
• FURTHER EXAMINATION
– Full field ERG
– Perimetry
– Blood check for VDRL, to exclude chorioretinitis sifilis
TREATMENT
• Medical treatment:
– High dose Vitamin day; palmitate 15000 IU/day
• Non-medical treatment:
– Stop smoking
– Sunglasses which protects from UV lights
– Regular follow-up to ophthalmologist is essential to
detect treatable vision-threatening complications
such as cataracts, open-angle glaucoma and others,
also provide support and maintain contact in case of
therapeutic innovation.
PROGNOSIS
• Ad vitam : Dubia ad bonam
• Ad sanationam : Malam
• Ad functionam : Dubia ad malam

COUNSELLING, INFORMATION AND
EDUCATION:
• Explaining to the patient and family about retinitis

pigmentosa, which is an inherited disease that
slowly progressive to further visual defect and
blindness, also his current condition.
• Explaining to the patient and family that the
disease has no definitive therapy, only
supportive therapy with high dose vitamin A
routinely everyday, to slower the progress of the
disease.
CASE ANALYSIS
• Retinitis pigmentosa (RP) or pigmentary retinal dystrophy is a

inhereted diffuse degenerative disease of retina, which affects
photoreceptor initially the rod cells, and later phase
degeneration of cone photoreceptors
• Inheretion patterns: autosomal dominantly, autosomal

recessive, X-linked recessive disease  affects onset of
age and progression of disease
• RP is one of the most common fundus dystrophy disease with

the pravelence of 1 : 5000 in the world
CASE ANALYSIS
• Patophysiology: mutation or molecular defect of

more than 40 various gene of photoreceptor,
especially the mutation of outer segmen protein
of photoreceptor gene  shorter protein
synthesized  preventing a normal cascade of
phototransduction  later apoptosis of
photoreceptors
CASE ANALYSIS
• Classic symptoms:
– Nyctalopia
– Visual fields decrease/ loss  mid-peripheral to medial
– Photopsia
• Other symptoms:
– Decrease in visual acuity
• Triad signs:
– Bone-spicule pigementation
– Waxy pale optic disc
– Attenuation of arteriol
CASE ANALYSIS
• Further examination:
– Electroretinogram  test for photoreceptor electrical response
– Perimetry  visual fields
• Complocation:
• Posterior subcapsular cataracts (most commonly
found)
• Open-angle glaucoma (found in 3% population with
RP)
• Keratoconus (uncommon)
• Posterior vitreous detachment
• Blindness
CASE ANALYSIS
• Treatment:
– No specific treatment yet
– Supportive: High dose supplementation of vitamin A;
palmitate 15000 IU everyday
– Regular check up
– Sunglasses (prevention of UV lights exposure)
– Avoid smoking (especially on vitamin A
supplementation)
– Avoid retinotoxic drugs; isotretinoin, erectile
dysfunction drugs, etc
– Gene Therapy
REFERENCES
1. Bowling B. Kanski’s Clinical Ophthalmology; a systematic

approach. 8th ed. China: Heinemann Elsevier Ltd; 2016.
2. Vaughan D, Asbury T. Vaughan & Ashburry’s General

Ophthalmology. 17th ed. USA: McGraw Hill Company; 2008
3. Telander D G. Retinitis Pigmentosa. Updated April 6th 2017.

Cited: http://emedicine.medscape.com/article/1227488
THANK
YOU

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Interesting Case: Keratoconus

• Occupation : Junior High Scool Student

Chief Complaint: Decrease visual acuity in both

Other symptoms: Difficulties in seeing in the dark

• Family medical history

Lumps/nodule (-) Lumps/nodule (-)

PHYSICAL EXAMINATION Edema (-)

Color: transparant Color: transparant

Hyperemia (-) Hyperemia (-)

Color: white Color: white

Transparency: clear Transparency: clear

Color: brown Color: brown

Pergerakan bola mata ODS baik

• Ad vitam : Dubia ad bonam

• Ad functionam : Dubia ad malam

• Explaining to the patient and family about retinitis

• Retinitis pigmentosa (RP) or pigmentary retinal dystrophy is a

• Inheretion patterns: autosomal dominantly, autosomal

• RP is one of the most common fundus dystrophy disease with

• Patophysiology: mutation or molecular defect of

1. Bowling B. Kanski’s Clinical Ophthalmology; a systematic

2. Vaughan D, Asbury T. Vaughan & Ashburry’s General

3. Telander D G. Retinitis Pigmentosa. Updated April 6th 2017.

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