RETINOPATHY DIABETIC

Dhian, Putri, Ulfa, Aan, Diah, Hanri, Agri, Rini, Nadira, Sasminto,Hani

Hyperglycemia
AGE formation

Glucose auto oxidation

Sorbitol pathway Antioxidants

Oxidative Sress
Lipid peroxidation Leukocyte adhesion Foam cell formation TNF a Endothelial dysfunction NO Endothelin Prostacyclin TXA2 Vascular complications
Hypercoagulability Fibrinolysis Coagulability Platelet reactivity

Retinopathy

Nephropathy

Neuropathy

Good
Fasting blood glucose (mg/dl)
2hpp blood glucose (mg/dl

Fair
110-125
145-179

Poor
126
180

80-109
80-144

A1C (%)
Total- cholesterol (mg/dl)

<6.5
<200

6.5-8
200-239

>8
240

LDL-cholesterol (mg/dl)
HDL-cholesterol (mg/dl) Triglyceride (mg/dl) Body mass index (kg/m2) Blood pressure (mmHg)

<100
>45 <150 18.5-22.9 <130/80

100-129

>130

150-199 23-25 130-140/80-90

200 >25 >140/90

Perkeni, 2009

KOMPLIKASI DIABETES MELLITUS

Akut : Kronik :

- Hipoglikemia - Koma Asidosis Diabetika - Hiperosmoler Non Ketotik - Koma Laktat Asidosis

- Mikroangiopati : - Nefropati D M - Retinopati DM - Kardiomiopati DM - Neuropati DM - Makroangiopati : - PJK - CVA - Ulkus/ ganggren - Neuropati DM - Rentan Infeksi : - TB Pulmo, dll.

 MIKROANGIOPATI OKULER
KELAINAN RETINA PROGRESIF AKIBAT

GANGGUAN MIKROVASKULER YANG DISEBABKAN HIPERGLIKEMIA KRONIK

 PENYEBAB UTAMA KEBUTAAN PADA USIA

PRODUKTIF DI NEGARA BERKEMBANG Penderita DM 25x lebih mudah terkena kebutaan (KOMNAS Diabetes Amerika) 90% PENDERITA DIABETES MENGALAMI RETINOPATI SETELAH 20 TAHUN PREVALENSI RETINOPATI DIABETIKA 30% PREVALENSI KEBUTAAN AKIBAT RETINOPATI 5% (usia 20-65 th) RD pada DM tipe 1 40% RD pada DM tipe 2 20% Pasien yg di dx DM pada usia <30 th insiden RD setelah 10 th 50% Pasien yg di dx DM pada usia >30 th 90%
Lang, Ophthalmology, 2nd. Ed.2006

 DIABETES MELITUS MENYEBABKAN KELAINAN :

KERATOKONJUNGTIVITIS SICCA, XANTHELASMA, MYCOTIC ORBITAL INFECTIONS, PERUBAHAN REFRAKSI SEMENTARA, KATARAK, GLAUKOMA, NEUROPATI OPTIK, KELUMPUHAN OCULOMOTOR

 Teori Enzim katalisis aldose reduktase .

Enzim ini akan mengkatalisa perubahan glukosa menjadi sorbitol . Bila kadar glukosa intraselular meningkat , hal ini akan meningkatkan pula kadar sorbitol intraselular, yang kemudian akan menghambat sintesis mio-inositol yang terdapat pada glomerular dan jaringan saraf . Penurunan kadar mio-inositol ini akan menurunkan metabolisme fosfo-inositidin, yang kemudian akan menurunkan aktivitas dari Na-K-ATPase dan memperburuk kerusakan mikrovaskular .

 Vasoproliferative Factors Currently intense interest exists in vasoproliferative

factors released by the retina itself, retinal vessels, and the retinal pigment epithelium, which are felt to induce neovascularization. Vascular endothelial growth factor (VEGF), which inhibits the growth of the retinal endothelial cells in vitro, has been implicated in diabetic retinopathy. Considerable evidence suggests that VEGF has a direct role in the proliferative retinal vascular abnormalities that are found in diabetes. Animal models have demonstrated that VEGF expression correlates with the development and regression of neovascularization.[13] The concentration of VEGF in aqueous and vitreous directly correlates with the severity of retinopathy.[14] Angiogenesis is a complex process; many other growth factors and cytokines have been implicated in the development of diabetic retinopathy.

 Platelets and Blood Viscosity

Diabetes is associated with abnormalities of platelet function. It has been postulated that platelet abnormalities or alterations in blood viscosity in diabetics may contribute to diabetic retinopathy by causing focal capillary occlusion and focal areas of ischemia in the retina which, in turn, contribute to the development of diabetic retinopathy.[15]

 Duration of DM
Control of DM. Will not prevent but delays Hypertension

Renal Disease Pregnancy

Obesity, hyperlipidemia, smoking, anemia

 Background /Non Proliferative

Diabetic maculopathy Pre-proliferative

Proliferative End-stage diabetic eye disease

Microaneurism

Exudate

Blot haemorrhage

Hard exudate

CWS

Haemorrhage

Vascular tortuosity

Microaneurism

NVD

NVE

Pre-retinal haemorrhage

Laser burn scars

Preretinal fibrosis and tractional retinal detachment

Rubeosis iridis

PHTHISIS Shrunken, soft eye with opaque vascularised cornea and no visual potential

 ASIMPTOMATIK UNTUK JANGKA LAMA

STADIUM LANJUT DG EDEMA MAKULA/

VITREOUS HEMORRHAGE VISUS TURUN MENDADAK

 PEM. FUNDUS DG PUPIL DIDILATASI

OFTALMOSKOPI, FOTO FUNDUS, FFA

 VASCULAR RETINAL DISEASE

Radiation retinopathy Hypertensive retinopathy

Retinal venous obstruction (central retinal vein

occlusion (CRVO), branch retinal vein occlusion (BRVO)) The ocular ischemic Syndrome Anemia Leukemia Coats disease Idiopathic juxtafoveal retinal telangiectasia Sickle cell retinopathy

 LASER: Light

Amplification by the Stimulated Emission of Radiation

Focal Grid

Panretinal

photocoagulation

 mengendalikan faktor risiko, yaitu kadar gula, kadar

lipid, dan tekanan darah yang abnormal. Pengendalian atas ketiga faktor ini terbukti mampu menurunkan risiko dan memperlambat progresivitas retinopati DM. (Garg S, Davis RM. Diabetic retinopathy screening update. Clinical Diabetes. 2009;27(4):140-5) Target optimal yang harus dicapai adalah kadar HbA1c <7%, kadar low-density lipoprotein (LDL) <100 mg/dL, kadar high-density lipoprotein >50 mg/dL, kadar trigliserida <150 mg/dL dan tekanan darah <130/80 mmHg. (American Diabetes Association. Standards of medical care in diabetes - 2010. Diabetes Care. 2010;33(Suppl1):S11-61.)

Microaneurysm Retinal hemorrhages Retinal lipid exudates Cotton-wool spots Capillary nonperfusion Macular edema Neovascularization.

Vitreous hemorrhage Retinal detachment Neovascular glaucoma Premature cataract Cranial nerve palsies

 No retinopathy or BDR with normal vision

See yearly, or sooner if vision deteriorates

Refer to ophthalmologist
BDR with macular changes BDR with decrease in vision

Pre-proliferative retinopathy
Proliferative retinopathy

 KONTROL GD DELAY RETINOPATHY

RUBEOSIS IRIDIS - IRREVERSIBLE

 RETINOPATI YANG TERJADI PADA PENDERITA

HIPERTENSI

 VASOKONTRIKSI FOKAL/ LUAS PD ARTERIOLE

CROSSING PHENOMEN COPPER WIRE & SILVER WIRE

PERDARAHAN EKSUDAT: CWS, STAR FIGURE (LANJUT)

 GRADE 0 : NORMAL
GRADE 1 : PENYEMPITAN ARTERI MUDAH

DILIHAT GRADE 2 : PENYEMPITAN ARTERI NYATA, IRREGULARITAS SETEMPAT GRADE 3 : GRADE 2 + PERDARAHAN RETINA DAN ATAU EKSUDAT GRADE 4 : GRADE 3 + PAPIL EDEM

GRADE 0 NORMAL GRADE 1 PERUBAHAN REFLEK DINDING PEMBULUH ARTERI YANG MUDAH DILIHAT GRADE 2 PENINGKATAN REFLEK PEMBULUH ARTERI YANG NYATA

GRADE 3 COPPER WIRE ARTERI

GRADE 4 SILVER WIRE ARTERI

 ATASI HIPERTENSINYA
VITREKTOMI : PERDARAHAN VITREUS