Akhtar Jamal Khan  ( Akhtar`s Eye Hospital, Rashid Minhas Road, Gulshan-e-Iqbal, Karachi. )

Of 3000 diabetic patients screened, 780 were diagnosed to have retinopathy. The incidence of the complication was higher in the age group of 51 years and above, and of diabetes (76.7%) (JPMA 41: 49, 1991).

The average life of diabetic patients has been prolonged with the advent of antidiabetic drugs. Unfor­tunately, the incidence of diabetic retinopathy has increased many folds. In a nonselective randomized population based study in 1959 at Liaquat Medical College, Hyderabad, the incidence of diabetes was 1.7% in patients below 40 and 3% in above 40 years age group¹. In another survey at Karachi in 1986, it increased to 7.66%¹. The present study was conducted to determine the incidence of retinopathy both proliferative and back­ground type, and see the effect of the duration of diabetes on the patients.

An IBM personal computer was used to compile the data of 3,000 diabetic patients examined. Ml patients underwent a prdiminary examination, including exter¬nal ocular tests, recording of visual acuity and the best corrected visual acuity. Intraocular pressure was recorded by applanation tonometry. Fundus examina¬tions by indirect ophthalmoscope as well as with slit lamp and fundus lens were done routinely. For per¬manent record, coloured photographs by Topcon Fun¬dus Camera were taken in all cases where changes due to diabetes were noted either in the anterior or posterior segment. Fluorescein angiography was carried out only for macular oedema. Diabetic retinopathy was further classified into background type of diabetic retinopathy (BDR) and proliferative diabetic retinopathy (PDR).

Three thousand diabetics were included in the study of which 780 (26%) had retinopathy. Four hundred and nine (52%) were males and 371 (48%) females. Six hundred and seventeen (79%) cases had background, and 163 (2 1%) proliferative retinopathy. Of the 409 male diabetics the incidence of it increased alarmingly with the prolongation of the duration  retinopathy rose from 0.7% in the 2 1-30 year age group to 66.1% in the age group 51 years and above while the incidence in the female population was 1.1% in the age group 21-30 years and 54.2% in the age group of 51 years onward (Table I).

A remarkable correlation was observed between the duration of diabetes and retinopathy. Of 780 patients with retinopathy 182 (23.3%) had diabetes for 1-5 years and 598 (76.7%) for 6-16 years. The effect of duration of diabetes on the development of retinopathy is similar in both sexes (Table II).

The two common hypotheses for pathogenesis of diabetic retinopathy are (i) high blood pressure and low intraocular pressure (I.O.P) ³ and (ii) hypoxia leading to production of vasoproliferative substances^4,5 ­Stefansson et al³ observed that high blood pressure and low I.O. P. were present in a majority of their patients with diabetic retinopathy. In contrast those diabetics, who had low blood pressure and high intraocular pressure, did not develop diabetic retinopathy. The auther also observed that if the diabetic patients who had low blood pressure with diabetic retinopathy, developed glaucoma, the progress of diabetic retinopathy was retarded or stopped. Therefore, they opined that high blood pressure and low intraocular pressure were the main causes of diabetic retinopathy, rather than hypoxic retina, as suggested by others^4-7. The initial changes in the capillary cell population, which include endothelial proliferation on the venous side and generalized pericyte damage, are possibly related to the capillary venous dilation linked with the initial increase in blood flow⁸. The first sign of diabetic retinopathy is therefore an increased permeability to fluorescein dye as measured by fluorophotometer^9-12. In diabetics there is an increase in hemoglobin A1c and decrease in 2-3 diphosphoglycerate (2-3 DPG) which increases the affinity of Hb for oxygen. Thus oxygen release is affected. The total oxygen consumption of the diabetic retinaincreases by 10-12% above the normal^13,14, so it is believed that these two factors, i.e. increased consumption and decreased availability of oxygen, lead to tissue hypoxia state. Constant high blood pressure, prolonged hyper­glycaemia, increased Hb Aic and decreased 2-3 DPG cause hindrance in dissociation of oxygen, from Jib molecule and on the other hand increased consumption of oxygen by diabetic retina causes an imbalance be­tween supply and demand. This probably leads to venous capillary dilation surrounded by capillary closure. Another factor which plays an important role in the pathogenesis of loss of retinal pericytes and thickening of basement membrane is aldose reductase¹⁵. Hohman¹⁶ grew human retinal capillary pericytes in tissue culture and demonstrated presence of aldose reductase in these pericytes. In various population based studies conducted in different parts of the world, including Australia^17,18, Denmark¹⁹, Iceland²⁰ and United States²¹ it was estab­lished that the prevalence of diabetic retinopathy varies between 24 and 70%. However the reason for large variations in the prevalence of total (24% to 70%) and proliferative (4.5% to 22%) retinopathy, may be due to the fact that these studies were not performed under the same conditions²² (Table III). According to a study conducted in Sweden24. the prevalence of retinopathy in insulin-treated diabetics of  40 years of age or younger was 66% and in orally treated diabetic patients of all ages it was 17%. There was an increasing prevalence of retinopathy in all age groups with longer duration of diabetes. Background retinopathy was present in 31% subjects and proliferative in 13%.22. The results of our study are comparable to the figures quoted by other investigators. A higher age group and a long duration of diabetes influence the develop­ment of the retinal changes. The pathogenesis is yet to be determined.

1. Khan, N. Oration 1987, a clinical study of diabetes mellitus over 40 years. Karachi, Pakistan Academy of Medical Sciences, 1987, p. 4.
2. Kban, A.J> Diabetic retinopathy. Pakistani. Ophthalmol., 1989; 5: 53.
3. Stefansson, E., Landers, M.B. and Wolbarsht, ML. The role of oxygen and vasodilation in diabetic retinopathy, in diabetic renat.retinal syndrome. Prevention and Management Edited by E.A. Friedman and F.A. L’Esperance, New York, Grune & Stratton, 1981, p.117.
4. Ditzel, LI. Afflnity hypoxia as a pathogenetic factor of microangiopathy with particular reference to diabetic retinopathy. Act.a Endocinol., 1980; 238 (Suppl): 39.
5. Wise, G.N. Retinal neovascularization. Trans. Am. Ophthalmol. Soc., 1956; 54: 729.
6. Ditzel, LI. and Standl, E. The problem of tissue oxygenation in diabetes mellitus. Acts Med. Scand., 1975; 579 (Supple) : 49.
7. Ditzel, LI. The problem of tissue oxygenation in diabetes mellitus. Acta Med. Scand., 1975; 578(Supple): 69.
8. Cunha-Vas, J.G. Diabetic retinopathy. Human and experimental studies. Trans. Ophthal­mol. Soc. UK., 1972; 912: 11.
9. Cunha-Vas, J.G., Figo G.M. de Abreu, J.F.R. and Campos, AJ. Early breakdown of the blood retinal barrier in diabetes. Br. LI. Ophthalmol., 1975; 59: 649.
10. Cunha-Vas, 3G., Goldberg, M.F., Vygantas, C. and North, 3. Early detection of retinal involvement in diabetes by vitreous fluorophotometry. Ophthalmology, 1979; 86: 264.
11. Cunha-Vas, J.G., Fonseca, J.R., de Abreu, J.F. and Ruas, M.A. Studies on retinal blood floso II. Diabetic retinopathy. Arch Ophthalmol., 1978; 96: 809.
12. Cunha-Vas. J.G., Fonseca, J.R., de Abreu, J.F. and Ruas, M.A. Follow-up study by vitreous fluorophotometry of early retinal involvement in diabetics. Am. J. Ophthalmol., 1987; 86: 467.
13. White. P. Endocrine manifestations in juvenile diabetes. Arch. Intern. Med., 1939; 63:39.
14. Horstmann, P. The oxygen consumptions in diabetes mellitus. Acts Med. Scand., 1951; 139: 326.
15. Kinoshita. 3K. Aldose reductase in the diabetic eye. XLIII. Edward Jackson memorial lecture. Am. 3. Ophthalmol., 1986; 102: 685.
16. Hohman, T.C., Nishimura, C., Robinson, W.G. Jr., Kador, P.F. and Kinoshita,3.H. Aldose reductasc in cultured human and canine retinal capillary pericytes. ARVO Abstracts. Supplement to Invest. Ophthalmol. Via Sci Philadelphia, Lippincott, 1986, p. 328
17. Heriot, W.J., Borger, i.P., Zimmet, P., King. H., Taylor, R. and Raper. L.R. Diabetic retinopathy in a natural population. AusL J. Ophthalmol., 1983; 11: 175.
18. Mitchell, P. The prevalence of diabetic retinopathy; a study of 1300 diabetics from Newcastle and Hunter Valley. Aust. 3. Ophthalrnol., 1980; 8: 241.
19. Nielsen, N.y. Diabetic retinopathy. I. The course of retinopathy in insulin-treated diabetics. A one year epidemiological cohort study of diabetes mellitus. The island of Falster, Denmark. Acts Ophthalmol., 1984; 62: 256.
20. Danielsen, R.. Jonasson, F. and Helgason, T. Prevalence of retinopathy and proteinuria in type 1 diabetics in tceland. Acta Med. Scand., 1982; 212: 277.
21. Klein, R, Davis, M.D., Mosws, S.E., Klein, B. and DeMets, D.L The Wisconsin epidemiologic study of diabetic retinopathy. A comparison of retinopathy in younger and older onsetdiabetic persons, in Comparison of type land II diabetes. Edited by M. Vranic, C.H. Hollenbery and G. Steiner. New York, Plenum Press, 1985, p. 321.
22. Klein, R., Klein, B.E.K., Moss, S.E., Davis, M.D. and DeMets, D.L. The Wisconsin Epidemiologic Study of Diabetic Retinopathy. II. Prevalence and Risk of Diabetic Retinopathy when age at Diagnosis is less than 30 years. Arch Ophthalmol., 1984; 102: 520-526.
23. Klein, R., Klein, B.E.K., Moss, SE., Davis, M.D. and DeMets, D.L: The Wisconsin Epidemiologic Study of Diabetic Retinopathy. III. Prevalence and Risk of Diabetic Retinopathy when age at Diagnosis is 30 or more years. Arch Ophthalrnol., 1984; 102: 527-532.
24. Jerneld, B. and Algverc, P. Relationship of duration and onset of diabetes to prevalence of diabetic retinopathy. Am. 3. Ophthalmol., 1986; 102:431.