The hallmark of proliferative diabetic retinopathy (PDR) is neovascularization. Retinal ischemia is thought to play a major role in this process. New vessels originate as endothelial proliferations, which pass through defects in the internal limiting membrane of the retina and become attached to the posterior vitreous cortex. (The absence of the internal limiting membrane at the optic disc may explain the frequency of neovascularization at this site.) The vitreous then serves as a scaffold for new vessel and fibrous tissue growth. PDR is associated with several serious complications:

  • The new vessels are structurally abnormal. They leak fluid and are prone to hemorrhage – either into the vitreous or into the potential space between the internal limiting membrane and the rest of the retina (often termed preretinal or subhyaloid haemorrhage).
  • Contracting fibrovascular membranes exert traction on the underlying retina, causing tractional and/or rhegmatogenous retinal detachment.
  • Widespread retinal ischemia can result in new vessels at the iris, leading to neovascular glaucoma (of which diabetes is one of several causes).


Complications of PDR can cause sudden and severe loss of vision. Less catastrophic hemorrhage or retinal detachment can produce floaters, blots or flashing lights in the visual field. Patients may experience ocular pain, photophobia and decreased vision with neovascular glaucoma.


Significantly, visual acuity may be normal in the presence of vision-threatening PDR. When complications occur, acuity may be reduced to hand movements or worse. The iris is examined for NVI and neovascular glaucoma prior to dilatation. (The pupils of diabetic patients often have a slow or poor response to mydriatics.) In diabetic patients, PDR is defined as one or more of:

  • any definite neovascularization, or
  • preretinal or vitreous hemorrhage.

In addition, neovascularization is described as new vessels on the disc (NVD, on or within 1 disc diameter of the optic nerve head), new vessels elsewhere (NVE), or in the iris (NVI, rubeosis iridis). NVE are less likely to bleed than NVD. Other critical signs relate to the presence of complications of PDR and the indications for surgery:

  • Preretinal hemorrhage is often oval- or crescent-shaped. Vitreous hemorrhage diffuses through the vitreous cavity and may obscure the retina. In eyes without hemorrhage, a detached posterior vitreous suggests that vitreous hemorrhage is less likely to occur.
  • Significant fibrosis increases the risk of retinal detachment, and may obscure the macula. Tractional retinal detachment has a shiny surface, which is concave towards the pupil. The retinal surface with rhegmatogenous retinal detachment is dull, and undulates with shifting subretinal fluid.
  • Early NVI may be easily missed without magnification. The vessels usually grow radially from the pupillary margin towards the corneal angle.


As with DR in general, the incidence of PDR correlates best with the duration of diabetes. Over a period of 10 years, approximately 10 percent of patients with Type 2 diabetes may develop PDR.


Prompt treatment of PDR with high-risk characteristics improves the prognosis for vision.

See Also and Management

See: Diabetes – Proliferative Retinopathy Management.

Figure 1.

Extensive neovascularisation around the optic disc, with exudation & haemorrhages temporally

Figure 2.

Appearance following panretinal laser photocoagulation: resolution of neovascular vessels; retinal atrophy & irregular pigmentation.

Diabetes – Proliferative Retinopathy Assessment