Diabetic retinopathy

Diabetic retinopathy is a frequently observed complication in both type 1 and type 2 diabetes, specially in patients with long term disease and poor glicemic control. Irreversible visual loss appears at the final stages of diabetic retinopathy and it is considered one of the most tragic of diabetic complications. It is also considered an important factor of morbidity and has a high economical impact once it is the leading cause of blindness. The pathophysiology of the retinal microvascular alterations is related to the chronic hyperglycemia that leads to the following circulatory disturbances: loss of vascular tonus, increase in vascular permeability, edema and exudation, with vascular obstruction and ischemia that stimulates neovascularization, which may lead to fibrous retraction and vitreous hemorrhages with retinal detachment. Recent studies have indicated that the strict glicemic and blood pressure controls are effective in reducing or blocking the progression of retinopathy. Up to now no pharmacological agents have shown to be effective in preventing or reducing neovascularization and visual loss. Presently, the most effective available treatment for proliferative retinopathy is laser photocoagulation. Further studies are needed to obtain new products and technologies that could effectively prevent or block retinopathy progression.     

Diabetic retinopathy

Retinopathy is present in 60% – 80% of long-term diabetics, and 5% – 10% of diabetics surviving 20 yr from the time of diagnosis will be blind, mostly from retinopathy, which is now the commonest cause of newly diagnosed blindness in the 30–65 yr age group. The mean survival time after a diagnosis of retinopathy is only 5 yr.The natural history of diabetic retinopathy is now being understood more clearly. Mild background retinopathy, characterised by microaneurysms or scattered hard exudates, may progress to maculopathy, with macular vascular pathology leading to exudates and edema at the macula; this is most common in older patients. It may also lead to proliferative retinopathy, which may progress slowly with new vessels and fibrous-tissue formation, or rapidly with widespread capillary closure and soft-exudate formation, extensive neovascularisation, hemorrhages, and blindness. The changes of diabetic retinopathy can be documented using retinal photography, and several grading methods have been devised that are useful for evaluating treatment.The cause of diabetic retinopathy is still unclear. Evidence for incriminating genetic factors, growth-hormone excess, and hypoxia associated with changes in blood flow and retinal metabolism are reviewed. Insulin responses and plasma triglyceride seem to be different in maturity-onset diabetics with retinopathy when compared with those in whom this complication is absent.Most physicians agree that good diabetic control may both lower the incidence of retinopathy and reduce the speed of its progress. While there is little evidence that drugs are ever of much value in this condition, the role of photocoagulation both by laser and xenon arc is becoming clearer with increased experience of these techniques, and the current situation is reviewed. Pituitary ablation is a very drastic method of treatment and should never be used as a desperate measure in a patient with advanced proliferative disease. It is, however, the treatment of choice in early florid retinopathy, when it proves the only chance to arrest the condition. Some new techniques of vitreous surgery are now being developed and the possible role of these in the management of patients with advanced proliferative disease is briefly reviewed.     

Diabetic retinopathy and pregnancy

Summary Diabetic retinopathy was found to be present in 12 out of a group of 67 diabetic patients supervised by us during 92 pregnancies, and 3 further pregnant diabetics were referred to us because of retinopathy. The mean duration of diabetes was 13 years (range 3–25 years). Nine patients had minimal retinopathy, 2 had background retinopathy, and the remaining 4 proliferative retinopathy. The cases with minimal retinopathy showed no progression during pregnancy. In 1 patient with background retinopathy there was deterioration. Of the 4 patients with proliferative retinopathy 1 showed regression during the pregnancy, 2 showed advance and were treated with photocoagulation (these 2 patients now have normal vision), while the patient with extensive retinitis proliferans, with retinal detachment in both eyes and previous photocoagulation remained unchanged. The prognosis during pregnancy for patients with diabetic retinopathy is reasonable and has been improved by the advent of photocoagulation.     

Diabetic retinopathy in children and adolescents

Diabetic retinopathy rarely occurs before puberty and is never proliferative in prepubescent children. On the opposite, puberty and adolescence are high-risk periods for diabetic retinopathy progression, and call for strict ophthalmologic monitoring. The period between 16 and 18 years of age is particularly critical. Progression towards florid diabetic retinopathy is to be especially feared and should be prevented in the course of adolescence, as this form can be severe and can lead to blindness. Risk factors are probably many, including diabetes duration, difficulties in achieving glycemic control due to increase in insulin requirements, low compliance to treatment, and hormonal changes related to puberty (abnormalities of the growth hormone (GH)/insulin-like growth factor-I (IGF-1) axis). Systematical diabetic retinopathy screening should be performed in adolescents, notably by non-mydriatic fundus photographs. Furthermore, the anticipation of the switch from pediatric to adult structures, together with the careful information and education of parents and children may improve visual prognosis of young diabetic patients, whose life expectancy is high.     

Contribution to retinopathy in acute pancreatitis

It is reported on 2 cases of pancreatitic retinopathy in acute pancreatitis. In the first place of the clinical symptoms there are acutely beginning bilateral vision disturbances 2 to 3 days after the onset of the disease which exist for a long time. Causally an obstruction of the precapillary and capillary parts of the vascular system of the retina, but also of the choriocapillary system by fat particles and corpuscular blood elements is discussed. With certainty still other factors play a part, for example preinjury of the vascular parts mentioned by circulating pancreatic enzymes and toxins. In patients with acute pancreatitis vision disturbances should be taken into consideration, even when these changes are very rare.     

Diabetic retinopathy and visual disability

Summary Data from blind and partial sight registers and from special surveys have been analysed to derive estimates of the number of adults in England and Wales visually disabled by diabetic retinopathy. If visual disability is defined as less than 6/18 Snellen, approximately 30 per 100.000 adults living at home are disabled by diabetic retinopathy; if defined around traditional concepts of blindness (approximately 3/60 vision or less) the estimated figure is about 20 per 100.000 total population. Annual additions to the blind register for diabetic retinopathy are about two per 100.000 total population. Weaknesses in data gathering are discussed.