Diabetes is a worldwide epidemic disease. In recent decades it
has progressed from a disease affecting people primarily in
developed countries, to a global phenomenon. Today diabetic
retinopathy is a major cause of blindness in adult patients.
The eye is one of the target organs of this multisystemic
disease. Diabetic retinopathy is nothing more than a compromise of
the retinal microcirculation. The chronic exposure to hyperglycemia
determines a number of biochemical and consequently histological
changes
Initially, selective loss of pericytes, basement membrane
thickening, as well as a diverse number of hematologic
abnormalities, generate capillary occlusion, microaneurysm
formation, dilation and beading of retinal veins as well as retinal
ischemia.
A compromise of the endothelial barrier function allows vascular
leakage, originating retinal edema and deposition of hard
exsudates. Areas of retinal ischemia generate vasoproliferative
factors (mainly vascular endothelium growth factor - VEGF) that
later stimulate the growth of neovessels.
According to fundoscopic findings, diabetic retinopathy may be
divided in non-proliferative and proliferative diabetic
retinopathy, based on the presence of neovascularization. The most
commonly used classification scale is the International Clinical
Diabetic Retinopathy Disease Severity Scale:
No apparent retinopathy: no abnormalities
Mild Non-proliferative Diabetic Retinopathy (NPDR):
microaneurysms only
Moderate NPDR: more than just microaneurysms but
less than severe NPDR
Severe NPDR:
Any of the following:
•More than 20 intraretinal hemorrhages in each of 4 quadrants
•Definite venous beading in 2 or more quadrants
•Prominent intraretinal microvascular abnormalities (IRMA) in at
least one quadrant
And no signs of proliferative retinopathy
Proliferative Diabetic retinopathy (PDR):
One or more of the following:
•Neovascularization
•Vitreous/Preretinal hemorrhage
Neovessels in PDR are first intra-retinal with minimal fibrosis.
After this initial phase they cross the internal limiting membrane
(ILM), and migrate to the vitreous body, using it as a substrate
for further growth. These vessels are accompanied by fibrotic
changes, forming pre-retinal membranes, usually along the vascular
arcades. The final stage is characterized by an involution of the
vascular component and contraction of the fibrotic membranes.
During this cycle, several complications may arise.
PDR can be stratified according to the Diabetic Retinopathy
Study. High risk PDR was defined as any one of the following:
•Mild neovessels in the optic disc (NVD) when associated with
vitreous hemorrhage
•Moderate to severe NVD (1/4 to 1/3 of the optic disc area), with
or without vitreous hemorrhage
•Moderate neovessels elsewhere (NVE) (1/2 the optic disc area),
with vitreous hemorrhage. Treatment should be prompt in this group
of patients given the high risk of severe visual loss.
Medical management plays a primordial role in PDR. Optimal
glycemic (glycosylated hemoglobin - HbA1c < 7%) and blood
pressure control are paramount to a good outcome.
Panretinal photocoagulation (PRP) is the gold standard for
patients with severe NPDR and PDR. Laser photocoagulation aims to
destroy the ischemic areas of the retina and reduce the production
of vasoproliferative factors. Scatter laser should be avoided in
areas of vitreo-retinal traction and prominent fibrovascular
membranes since it can determine their contraction and subsequent
retinal detachment.
Vitreous hemorrhage is a common occurrence in diabetic patients
and frequently heralds the diagnosis of PDR. Blood in the vitreous
cavity and its degradation products such as hemosiderin are toxic
to retinal structures. A balance should be struck between a
conservative attitude, observing the patient regularly and surgical
intervention with pars plana vitrectomy (PPV). The Diabetic
Retinopathy Vitrectomy Study (DRVS), published in 1985,
demonstrated a superiority of early (1-6 months) surgery when
compared to late surgery ( > 1 year) in patients with diabetes
type 1. This benefit was not conclusively found for type 2
diabetics. Given the advances in vitreoretinal surgery in the last
decades we feel inclined to recommend an earlier intervention. This
should be more urgent in patients with type 1 diabetes, patients
never submitted to laser photocoagulation, patients with serious
diabetic retinopathy in the fellow eye, and patients not likely to
comply with a regular follow-up. Intraoperatively, after
vitrectomy, a thorough PRP with endolaser up to the ora serrata
should be performed.
One particular entity that demands prompt surgical intervention
is pre-macular, retro-hyaloid hemorrhage. A PPV, with induction of
posterior vitreous detachment (PVD) and clearance of the
pre-retinal blood avoids fibrosis and a subsequent dismal visual
prognosis.
Current indications for PPV in diabetic patients include:
•Dense, nonclearing vitreous hemorrhage
•Tractional retinal detachment involving or threatening the
macula
•Combined traction and rhegmatogenous retinal detachment
•Diffuse macular edema associated with a taut posterior hyaloid
•Significant recurrent vitreous hemorrhage despite maximal PRP
