Bagian Ilmu Kesehatan Mata

Kamis, 15 juni 2017 pkl 07.00 WIB s/d

Jumat, 16 juni 2017 pkl 07.00 WIB

Residen jaga :
Jaga 2 : dr. Dian Ariani
Jaga 1 : dr. Disty Andryani
dr. Sri Tanty Fuji

Konsulen Jaga:
DR.dr. Anang Tribowo, SpM(K)
Data Dasar Permasalahan Diagnosa Penatalaksanaan
Ny Z/P/60 th/dalam kota VODS : 6/21 ph - Severe Non - Informed consent
Konsul dari PDL dengan Lensa : Proliferative - Regulasi gula darah
diagnosa Hipoglikemia + DM ODS : keruh, ST (+) diabetic sesuai TS PDL
tipe II uncontrolled + Anemia Segmen posterior: retinopathy
penyakit kronis + - Antioksidant 1
FODS ODS tab/24jam
Hipokalsemia. Yang
ditanyakan adakah tanda- Papil : bulat, batas Clinically - Pro foto fundus jika KU
tanda diabetik retinopati? tegas, warna merah Significant
normal, c/d 0,3 a/v 2:3 memungkinkan
KU : Pandangan kedua Macular
mata kabur NVD (-)
Edema ODS - Pro konsul subdivisi
RPD: Makula : RF (+) , retina
eksudat (+) Katarak Senilis
Pandangan kedua mata Imatur ODS
kabur sejak 1 tahun yang Retina: perdarahan(+),
lalu, keluhan pandangan dot (+), blot (+),flame
shape (+), eksudat (+), ICD X Terapi PDL :
berasap (+), keluhan melihat
seperti terowongan (-). 3 cotton wool spot (+), Diet DM 1700 kkal,
venous beading (+) -E10.331
hari yang lalu pasien protein 40 gr
mengeluh badan lemas dan -E11.311
IVFD D5 % gtt xv/menit
dibawa ke RSMH -H25.0
-Riwayat DM sejak 5 thn
Asam Folat 3x1 mg (po)
yang lalu tidak terkontrol obat Ca glukonas 1x 1gr (iv)
-Riwayat hipertensi (-)
- Riwayat kaca mata (-)
Pasien belum pernah berobat
ke dokter mata sebelumnya
Status Generalis
Keadaan Umum : tampak sakit ringan
Sensorium : Compos mentis
TD : 120/80 mmHg
Nadi : 70 x/menit
Respiratory rate : 20 x/menit
Temperatur : Afebris
BSS terakhir : 191
 Status Oftalmologikus
OD OS
VISUS 6/21 ph (-) 6/21 ph (-)
TIO 15,6 mmHg 15,6 mmHg
KBM Orthophoria

GBM Baik ke segala arah Baik ke segala arah

Palpebra tenang tenang
Konjungtiva tenang tenang
Kornea Jernih Jernih
BMD sedang sedang
Iris Gambaran baik Gambaran baik
Pupil Bulat, sentral, RC (+), 3 Bulat,sentral, RC (+), 3
mm mm
Lensa Keruh, ST (+) Keruh, ST(+)
 Segmen Posterior

RFODS (+)
FODS:
Papil : bulat, batas tegas, warna merah
normal, c/d 0,3 a/v 2:3 NVD (-)
Makula : RF (+), eksudat (+), perdarahan (-)
Retina: perdarahan(+), dot (+), blot (+),flame
shape (+), eksudat (+), cotton wool spot
(+), venous beading(+), NVE (-)
Jawaban Konsul Retina
Assesment :
Severe NPDR ODS + CSME ODS

Planning
Antioksidan 1tab/24jam
Pro Injeksi Anti VEGF bila sudah rawat
jalan
FOTO FUNDUS
Retinal drawing

OD OS
Terima
Kasih
7 Field
11
Signs and symptoms
The following findings indicate the presence of clinically
significant macular edema (CSME), as defined by the Early
Treatment Diabetic Retinopathy Study (ETDRS):
Retinal thickening within 500 m of the center of the fovea
Hard, yellow exudates within 500 m of the center of the fovea
with adjacent retinal thickening
At least 1 disc area of retinal thickening, any part of which is
within 1 disc diameter of the center of the fovea

Pada OCT terdapat

Retina swelling, edema kistik, dan serous retina detachment
 Flame shaped located at NFL (arrow)
Dot-Blot hemorrhage at OPL,IPL,INL
(arrowhead)
 The retinal manifestations of diabetes
mellitus are broadly classified as either
nonproliferative diabetic retinopathy
(NPDR) or proliferative diabetic
retinopathy (PDR).
Nonproliferative diabetic retinopathy
occurs when there are only intraretinal
microvascular changes, such as altered
retinal vascular permeability and eventual
retinal vessel closure. Clinically, the
hallmark of the nonproliferative phase is
microaneurysms and intraretinal
abnormalities.
 Neovascularization is not a component of
the nonproliferative phase. However, in
advanced NPDR, nonperfusion of the
retina may develop and lead to the
proliferative phase.
Proliferative diabetic retinopathy is
characterized by new vessels and
sometimes fibrous bands proliferating on
the retinal surface.
In both nonproliferative and proliferative
diabetic retinopathy, macular edema can
occur as increased retinal vascular
permeability leads to accumulation of
fluid in the retinal area serving central
vision.
pathophysiology
Chronic hyperglycemia in poorly controlled diabetes
results in biochemical alterations and altered
hemodynamics of the retinal vasculature

chronic hypoxia

Since the retina is a highly metabolic tissue dependent on

optimal oxygenation, compensatory pathways, such as
upregulation of vascular endothelial growth factor (VEGF)
protein, are targeted against this retinal hypoxia.

These efforts are futile, however, and ultimately result in

the pathologic processes of NPDR: retinal capillary
microaneurysms, vascular permeability, and eventual
vascularocclusion, or capillary closure.
microaneurysm

The retinal capillary microaneurysm usually is the first visible

sign of diabetic retinopathy.
Microaneurysms, identified clinically by ophthalmoscopy as
deep-red dots varying from 15 to 60 m in diameter, are most
common in the posterior pole.
The mechanism for the formation of microaneurysms is also
unknown. Possible mechanisms include release of a
vasoproliferative factor with endothelial cell proliferation,
weakness of the capillary wall (from loss of pericytes),
abnormalities of the adjacent retina, and increased intraluminal
pressure.
Severe nonproliferative diabetic retinopathy.
Two prominent cotton-wool spots (soft exudates) are noted on the left side
with a large blot hemorrhage between them.
Venous beading is present where the superior branch of the
superotemporal vein passes by the upper exudate.
On the right are two faint soft exudates (arrows) and many intraretinal
microvascular abnormalities.
antioxidant
Antioxidants found in vertebrates include
selenium, GSH, selenium dependent
glutathione peroxidase, non-selenium-
dependent glutathione peroxidase (g
lutathione-S-transferase), vitamin E, and
carotenoids
The highest concentration of selenium in
the human eye is present in the RPE:
100-400 ng in the RPE cells of a Single
human eye, up to 10 times more than in
the retina (40 ng)
 Indikasi Laser fotokoagulasi

NPDR + CSME
Untuk melindungi makula dan pengihatan sentral
Severe NPDR
Resiko perkembangan penyakit ke arah PDR tinggi
Early PDR
Meregresi neovaskular
PDR +CSME
Meregresi neovaskular
Advanced PDR
meregresi neovaskular, syarat: operator dapat melihat fundus
retina secara adekuat

30
Faktor Resiko
Durasi DM
Umur
Kontrol DM
Renal disease : proteinuria +
Hipertensi
Kehamilan

31
Tujuan Laser
Mengurangi edema
Menutupi jaringan iskemik
Menutupi kebocoran pembuluh darah
retina
Mencegah ablasio retina

32
Efek samping Laser
Pandangan lebih redup karena sel cone
banyak terkena
Lapang pandang menyempit
Skotoma
Kontras sensitifitas <<
Makula : masif : penglihatan warna
terganggu
Atrofi papil

33
Vitrektomi
Produk peradangan terhadap retina di
vitreus berkurang
Proses oksigenasi dan nutrisi lebih baik
Membuang traksi

34
 Mild NVD
- 1/3 disc area of NVD
Disc area (NVE)

35
FFA
Circulation of the retina and choroid
Taken after iv injection of sodium
fluorescein, an orange-red crystalline
hydrocarbon with a molecular weight of
376 daltons
2-3 ml of 25%
5ml of 10%

36
 Xantophyll Hemoglobin Melanin

Argon blue-green ++++ +++ +++

Argon green - +++ ++++

Nd-YAG green - ++++ ++++

Dye Yellow - ++++ ++++

Dye Red - + +++

Kripton red - + ++

Diode -

37
 Cotton wool spots

are ischemic infarctions of the nerve fiber layer. On

ophthalmoscopy, they are white and located superficially. On OCT,
they appear as hyperreflective, nodular or elongated lesions in the
nerve fiber layer, which can cast a shadow on the posterior layers.
Hemorrhages can be located pre-, intra- or subretinally. On ophthal-
moscopy, they are flame shaped when located in the nerve fiber
layer, and they are rounded or irregular when located in the deep
retinal layers. They are hyper- reflective on OCT and can produce a
shadow cone on the posterior layer, especially if they are located
preretinally
Microaneurysms
are 1560 mikrom in size. Histologically,
microaneurysms are hypercellular
outpouchings of the capillary wall,
subsequent also to a loss of intramural
pericytes. Typical for early changes of
diabetic retinopathy is the thickening of the
basement membrane of retinal capillaries.
 Hard exudates,

that often accompany macular edema, make it much easier to

diagnose diabetic macular edema.
They are lipid deposits located in the outer plexiform or Henle
layer of the retina.
Clinically hard exudates are yellow-white, well-defined,
intraretinal deposits. On optical coherence tomography (OCT),
they are visible as hyperreflective nodular lesions. The deposit of
the hard exudates is associated with the damage of the inner
blood-retinal barrier, i.e. the breakdown of the endothelial tight
junctions in the capillaries and microaneurysms.
Macular edema
can be associated with any severity level of
diabetic retinopathy. It is the most common
cause of visual loss in NPDR. The Early
Treatment of Diabetic Retinopathy Study
(ETDRS) investigators classified the severity
by three characteristics concerning the
relation to the center of the macula. The
macular edema is defined as clinically
significant macular edema if any of the three
features described in table 2 is present.
 Diabetic retinopathy occurs in both type 1 (also known as juvenile-
onset or insulin-dependent diabetes) and type 2 diabetes (also known
as adult-onset or noninsulin-dependent diabetes). All the features of
diabetic retinopathy may be found in both types of diabetes, but
characteristically, the incidence of the main causes of vision loss,
macular edema and retinal neovascularization is quite dif- ferent for
each type of diabetes [1].
 Diabetic retinopathy in type 1 diabetes
induces vision loss mainly due to the
formation of new vessels in the eye fundus
and development of proliferative
retinopathy, whereas in type 2 diabetes,
vision loss is most commonly due to macular
edema, and proliferative retinopathy is
relatively rare.
Introduction
Wisconsin Epidemiologic Study:
Prevalence of diabetic retinopathy :
< 5 years : 17%
- 15 years : 98%
Progression to proliverative diabeyic
retinopathy :
4 years : 11%
10 years : 30% 20% was
high risk
Introduction
Severe complication of diabetic retinopathy
Blindness
Blindness was caused by :
Vitreous haemorrhage
Retinal detachment
Neovascular glaucoma
Treatment
Goal : decrease complications of
proliferative diabetic retinopathy
Such as ;
rubeosis iridis
vitreous haemorrhage
traction retinal detachment
Laser
Indication :
NVD that at least one-fourth to one-third disc
areas in extent
NVD that is associatd with preretinal or
vitreous haemorrhage
NVE that at least one-half areas in extent and
it assiciated with preretinal or vitreous
haemorrhage
Laser
Most of argon green light is absorbed at the
level of the pigment epithelium.
Mild or moderate intensity burnt is confined
to the outer retinal layers.
An intense burn
Destroy NFL
Fibroblast proliferation scar
tissue
Rupture Bruch membrane NV
Subretina invasion
What should be avoided in laser
treatment on diabetic patients
Haemorrhage
Retinal haemorrhages

It lead to contraction of vitreous

rupture of internal limiting membran (ILM)

formation of preretinal scar tissue

Veins
It leads to venous occlusion
Larger veins burnt

Macular oedema
Recurrent vitreous haemorrhages
Fovea
Susceptible to damage by laser than opther
areas of retina
Damage central vision
Fibrous tissue and retinal traction
Stimulating further production of scar tissue

Traction on the retina

Retinal detachment
Excessive burns stimulate
proliferation of scar tissue
further detachment
Spots placed around perimeter of detached
area
Papillomacular bundle
It will not be damage if correct intensity of
laser burn
Haemorrhage and thin retina danger
White background
Optic disc
Choroidal atrophy
Hard exudate
Acute inflamatory lesions

Prevent absorption of light / reflect the ligth

inadequate burn
Laser Tissue Effect
Thermal effects.
 Pathophysiology of disease
Diabetic Retinopathies

Goal
Decrease complication
Decrease demand

Indication
PDR --- Pan retinal Photocoagulation (PRP)
CSME --- focal/grid photocoagulation
Rubeosis iridis

Considered:
Severe NPDR
 Pathophysiology of disease
Diabetic Retinopathies

Technique
CSME
 Pathophysiology of disease
Diabetic Retinopathies

Technique
PRP
Sector Scatter
moderately intense
Spot size 200 - 500 micron
duration 0.1 - to 0.2 second
spaced one burn width apart
Circumferential
Moderately intense
Spot size 200- to 500-micron
Duration 0.1 - 0.2 second
Spaced one burn width apart
360
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