Ophthalmology spot diagnosis : Rubeosis Iridis

 

Definition: Neovascularization of iris

Pathophysiology: Causes that lead to retinal hypoxia triggers release of vasoproliferative factors include vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF) and others

rubeosis iridis neovascular glaucoma

Etiology:

1. Diabetic Retinopathy

2. Retinal Vascular Occlusive Diseases

  • Central Retinal Vein Occlusion (CRVO)
  • Ischaemic Hemiretinal Vein Occlusion

3. Ocular Ischaemic Syndrome

  • Carotid Artery Occlusive Disease
  • Takayasu’s Syndrome
  • Carotid-Cavernous Fistula
  • Giant Cell Arteritis
  • Wyburn-Mason syndrome
  • Strabismus Surgery
  • Ocular Radiation

4. Tumours

  • Uveal Melanomas
  • Metastatic Choroidal Tumours
  • Medulloepithelioma
  • Hypoxic Retinoblastoma
  • Pigmented Ciliary Adenocarcinoma
  • Metastatic Malignant Lymphoma

5. Others

  • Uveitis
  • Retinal Vasculitis
  • Coat’s Disease (Retinal telangiectasia)
  • Eales’ Disease (Periphlebitis retinae)
  • Sarcoidosis
  • X-linked Retinoschisis
  • Chronic Retinal Detachment
  • Retinopathy of Prematurity (ROP)
  • Systemic Cryoglobulinaemia

Important causes:

  1. Proliferative Diabetic Retinopathy (PDR)
  2. Central Retinal Vein Occlusion (CRVO)
  3. Sickle cell retinopathy
  4. Chronic iridocyclitis
  5. Retinoblastoma

Grading of rubeosis iridis:

  • 0 : No iris neovascularization
  • 1 : Less than 2 quadrants of NV at iris pupillary zone
  • 2 : More than 2 quadrants of NV at iris pupillary zone
  • 3 : Grade 2 + less than 3 quadrants of NV at iris ciliary zone and/or ectropion uveae
  • 4 : More than 3 quadrants of NV at iris ciliary zone and/or ectropion uveae

Findings:

  1. Abnormal iris vessels
  2. Perform gonioscopy to assess presence of angle neovascularization
  3. May have elevated IOP (neovascular glaucoma)

Rubeosis Iridis and Neovascular glaucoma:

The disease develops in 3 stages:

1. Neovascularization of the iris (NVI)

2. Secondary open angle glaucoma (SOAG): The NVI extend to involve the angle, and are accompanied by fibrosis, blocking the trabecular meshwork and  causing ocular hypertension, and SOAG.

3. Secondary angle closure glaucoma (SACG): Myofibroblasts within the fibrovascular tissue proliferate and contract, forming peripheral anterior synechiae (PAS), and secondary angle closure, with resulting intra-ocular pressure rise.

100 days glaucoma: Neovascular glaucoma (NVG) secondary to ischemic CRVO

Treatment:

  1. Ischemia: Panretinal Photocoagulation (PRP)
  2. IOP control: Glaucoma drainage implant (e.g. Molteno’s tube)

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