RETINOPATHY

DIABETIC

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

Sasminto,Hani

Hyperglycemia

Glucose auto oxidation Sorbitol pathwayAGE formation

Oxidative Sress

Antioxidants

Lipid peroxidation Leukocyte adhesion Foam cell formation TNF a

Endothelial dysfunction NO Endothelin Prostacyclin TXA2

HypercoagulabilityFibrinolysis Coagulability Platelet reactivity

Vascular complications

Retinopathy Nephropathy Neuropathy

Good Fair Poor

Fasting blood glucose (mg/dl) 80-109 110-125 ≥126

2hpp blood glucose (mg/dl 80-144 145-179 ≥180

A1C (%) <6.5 6.5-8 >8

Total- cholesterol (mg/dl) <200 200-239 ≥240

LDL-cholesterol (mg/dl) <100 100-129 >130

HDL-cholesterol (mg/dl) >45

Triglyceride (mg/dl) <150 150-199 ≥200

Body mass index (kg/m2) 18.5-22.9 23-25 >25

Blood pressure (mmHg) <130/80 130-140/80-90 >140/90

Perkeni, 2009

KOMPLIKASI DIABETES MELLITUS

• Akut :

- Hipoglikemia

- Koma Asidosis Diabetika

- Hiperosmoler Non Ketotik

- Koma Laktat Asidosis

• Kronik :

- 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 menjadisorbitol . Bila kadar glukosa intraselular meningkat , halini akan meningkatkan pula kadar sorbitol intraselular,yang kemudian akan menghambat sintesis mio-inositolyang terdapat pada glomerular dan jaringan saraf .Penurunan kadar mio-inositol ini akan menurunkanmetabolisme fosfo-inositidin, yang kemudian akanmenurunkan aktivitas dari Na-K-ATPase danmemperburuk 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

ExudateBlot haemorrhage

Hard exudate

Haemorrhage

Vascular tortuosity Microaneurism

CWS

NVD

Pre-retinal haemorrhage

Laser burn scars

NVE

Preretinal fibrosis and tractional retinal detachment

Rubeosis iridis

PHTHISISShrunken, soft eye withopaque vascularisedcornea and no visualpotential

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, kadarlipid, dan tekanan darah yang abnormal. Pengendalianatas ketiga faktor ini terbukti mampu menurunkanrisiko 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, kadartrigliserida <150 mg/dL dan tekanan darah <130/80mmHg. (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 1PERUBAHAN REFLEK DINDING PEMBULUH ARTERI YANG MUDAH DILIHAT

GRADE 2PENINGKATAN REFLEK PEMBULUH ARTERI YANG NYATA

GRADE 3COPPER WIRE ARTERI

GRADE 4SILVER WIRE ARTERI

ATASI HIPERTENSINYA

VITREKTOMI : PERDARAHAN VITREUS