Diabetic Retinopathy, the role of the Optometrist!

Optom
Chronic hyperglycemia is characterized by a consistently elevated fasting blood sugar of at least 7 mmol/l (126 mg/dL) for a prolonged period to cause a systemic complication. Diabetes Mellitus is an example of chronic hyperglycemia. A Glycated hemoglobin HbA1c (the molecule of glucose in the cells of red blood cell in a period of 2 weeks to 1 month!) of more than 48 mmol/mol or 6.5% is diagnostic of Chronic hyperglycemia.
(Use of Glycated Hemoglobin (HbA1c) in Diagnosis of Diabetes Mellitus: Abbreviated report of WHO consultation, 2011)

Often times the body may develop hyperglycemia (an FBS level of at least 7mmol/l!) temporarily without inducing any body tissue damage. In other words, such elevated blood sugar level is not enough to disrupt the homeostasis of the body at that period of time and hence no metabolic imbalance complications are experienced by the body.
 Chronic hyperglycemia has been reported to cause vascular microangiopathy and hence the various complications of Diabetes mellitus viz nephropathies, retinopathies and neuropathies. Vascular supply to various parts of the body provides the necessary nutrients to the human system and also provides systemic immunity and the oxygen necessary for life while at the same time removing wastes from the system.
 Diabetes mellitus is best described as a metabolic disorder with heterogeneous etiologies which is characterized by chronic hyperglycemia and disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action (& in-action), or both.
{World Health Organization. Definition, Diagnosis and Classifications of Diabetes Mellitus and its complications. Part 1 : Diagnosis and Classification of Diabetes Mellitus. WHO/NCD/NCS/99.2 ed. Geneva, World Health Organization, 1999}.

The normal blood vessel has an enothelium lined von Willebrand factor (vWF)- a cell adhesion ligand that binds the endothelial cells with the vascular basement membrane and could be said to also reduce the tendency of blood leukocytes to aggregate on the endothelial surface. Also, the normal endothelium synthesizes Nitric oxide (NO), endothelial ADPase (which clears away platelet activator ADP {Adenosine 5'-diphosphate}) and PGI2 [postalglandin inhibitors 2] which inhibits blood leukocyte aggregation, abundance of growth factors like Vascular Endothelial Growth Factor (VEGF)and subsequent platelet activation.
In the normal state, the endothelium is in a state of homeostasis. This homeostasis could be disrupted by the presence of inflammation-inducing substance in the blood vessels or when the endothelium is been overwhelmed by oxidative stress or by direct influence of non-enzymatic absorption of glucose via the walls of the endothelium or by the effect of metabolic imbalance associated with Diabetes Mellitus or chronic hyperglycemia.
Endothelial activation is a precusor to endothelial dysfunction and subsequent atherosclerosis, retinopathies and nephropathies. Endothelial activation, secondary to the low inflammatory response, is a specific dysfunction of the endothelial intima of micro- and/or macro-vessels characterized by increased interaction of the intima with blood leukocytes and other inflammatory markers like postalglandins and complexly lead to vascular complications in Diabetes mellitus. Endothelial activation should be a primary criteria for identifying potential diabetic retinopathy complication. (Just saying!)

An injured endothelium secondary to oxidative stress on the intima, say, by blood clots or by oxidation of NO (Common in patients with chronic hyperglycemia) or from a torn thrombus or direct inhibition of endothelial homeostasis by non-enzymatic absorption of blood glucose, is characterized by an activated vWF factor, tissue factor (TF), VEGF, atherothrombus formation, subsequent activation of the fibrinogen cycle (which in Diabetics runs haywire with a poor fibrinolysis feedback!), micro- &/or macro- albuminuria etc. This leads to a cascade of complex reactions in platelet activation, adhesion, increased fibrinogen production, haphazard coagulation activations, formation of plagues in the presence of such risk factors like long term anabolic steroid use, hypercholesterolaemia, dyslipidaemia, smoking, high LDL {low density lipoprotein} cholesterol, hypertension and chronic hyperglycemia (very common in uncontrolled Diabetes Mellitus!).
Diabetic retinopathy results as a result of the endothelial insult and dysfunction.
There are two types of Diabetic retinopathy viz
(1) Wet Diabetic Retinopathy,
(2) Dry Diabetic Retinopathy.
(see  my Blog [optometry.naija] on, "Pathogenesis of Retinopathies... In a bid to understanding the challenges it poses to the primary eye care Optometrist in the Nigerian setting!" to throw more light).

But among other things, a macular involvement in either wet or dry macular degeneration secondary to Diabetes is often classified as wet Diabetic Retinopathy cos of its tendency to be visually symptomatic!

To alter the effect of hyperglycemia on the endothelium and to return homeostasis in the vascular intima, insulin presence and insulin activation process must be restored; the hyperoxides that causes oxidative stress and hence subsequently inducing oxidative breakdown of endothelium anti-platelet by triggering activation of protein kinase C isoforms, increased hexosamine pathway, glucose autooxidation, increased methyl-glyoxal, formation of advanced gyceration products (AGEs) formation, and increased polyol pathway flux through a single process of over-production of mitochondrial superoxides should be altered by 'early' consistent use of antioxidants (even without evidence of retinal vascular microangiopathy).
[Maria Mohora et al., The sources and the targets of oxidative stress in the etiology of Diabetic complications. Romanian J. Biophys., Vol. 17, Bucharist, 2007.]

That been said, it becomes the sole priority of the Nigerian Optometrist to send patients for blood sugar screening, periodic Doppler ultrasonography (reduced blood flow rate and volume tends to decrease in diabetic patients), and to do a yearly dilated funduscopy to rule out subtle 'latent' diabetic retinopathies.  Rubeosis Irides, cataract etc should be ruled out during ocular examinations. Tests to ascertain cholesterol levels should be done to rule out the role of cholesterol in the blood stream in forming plagues hence fast-forwarding atherothrombus formation in patients with chronic hyperglycemia. Co-management of diabetic morbidity with general physicians or with specialist endocrinologists in a bid to provide multi-approach system in tackling the syndrome should be our primary eye care priority.
We should emphasize on dieting, exercises, primary and secondary inhalation of smoke, hypertension control, obesity control and generally living a healthy lifestyle... It should stick to our memory that somehow obesity, comfortable living and sedentary lifestyle, with little or no exercise often provokes atherothrombus formations and could be said to trigger hexosamine pathway reaction that leads to pancreatic beta-cell destruction which begins with a resistance of insulin to circulating glucose, then glucose intolerance and finally glucose toxicity in the Islet of Langerhans... A vicious circle of chronic hyperglycemia common in type 2 diabetes becomes activated.
Type 1 Diabetes Mellitus on the other hand is an auto-immune condition that self-destructs the beta cells responsible for insulin secretion and presents with symptoms before 25 years.
For the record, Diabetes Mellitus is one of the most serious challenges to health care world-wide. According to recent projections it will affect 239 million people by 2010, doubling in prevalence since 1994. It is the 4th leading cause of blindness globally.
(Dr. David Kinschuck, Dr Robert H., Diabetic Retinopathy in primary care, Epidemiology, Pg 2., UK, 2010)

Diabetic retinopathy, especially at the advanced stage, leads to blindness. Go for diabetes screening today or get your blood sugar testing kit and watch what you eat. Happy new month.

Dr Okwudiri Victor Ezebuiroh
N/B: No financial interest is attached to this blog. It is primarily for education.