77
the strong support of a well-organised trial to the advocates of photocoagulation clinical in diabetic retinopathy. Confined to patients with vasoproliferative changes in at least one eye or severe non-proliferative changes in both eyes, the trial confirms the grim prognosis for vision in eyes so affected. Taking the group as a whole, however, it strongly suggests that photocoagulation will approximately halve the risk of catastrophic visual loss. 1732 patients with the retinal changes described above but with visual acuity of 20/100 or better in both eyes were enrolled in a 15-centre study, directed by an executive committee headed by Dr MATTHEW DAVIS, coordinated by the University of Maryland, and generously financed by the U.S. Department of Health, Education and Welfare. One randomly selected eye of each patient was subjected to treatment with xenon-arc or argonlaser photocoagulation (also chosen randomly); the other, untreated eye was observed as the control. Aimed, focal coagulation of surface new vessels, including those on the optic disc when the laser was used, or extensive scatter coagulation of the retina ("pattern bombing" or "retinal ablation") were employed. An important end-point in the two-year analysis was "severe visual loss", defined as visual acuity less than S/200 at two or more consecutive, four-monthly follow-up visits. It occurred in 9.4% of untreated eyes and in 4. 1% of treated eyes, a difference very highly unlikely to have arisen by chance. Some evidence of visual recovery in these badly affected eyes was recorded about twice as often in treated as in untreated eyes. Analysis of the initial appearance of the eyes from retinal photographs supported the clinical view that severe visual loss was likely when neovascularisation was classified as moderate or severe (particularly when it involved the optic disc) and most likely of all when these changes were accompanied by fresh hæmorrhage. Treatment effects were so striking in these most vulnerable groups that the trial organisers have felt constrained to modify the protocol and recommend treatment for control eyes. In a large number of eyes with neither neovascularisation nor haemorrhage, presumably the fellow eye of one more severely affected which qualified the patient for the trial, the cumulative rate of severe visual loss over two years was only 2-1% in untreated and 2-9% in treated eyes. Inevitably with a destructive treatment like photocoagulation, there was a price to be paid for prevention of severe visual loss. Minor losses of acuity (2-4 lines of test type) were more frequent in treated than in untreated eyes, though after two years the difference was very small (13.0% versus 10.5%). There was also some sacrifice of visual field, more so with the xenon-arc than with the argon-laser treatment.
logy’O gives
THE LANCET
Photocoagulation for Diabetic Retinopathy beam of intense white light from the first used in the treatment of diabetic retinopathy by MEYER-SCHWICKERATH in 1959.1 Since then, many thousands of diabetics have been treated by this comparatively simple technique, and modifications employing monochromatic, coherent laser emission-notably, the green-light argon laser2 useful for its very narrow beam and its preferential absorption by red-cell hæmoglobin— are still being evaluated. Despite widespread application of this treatment and some strong advocacy,3-S the varied manifestations and the episodic, unpredictable progression of diabetic retinopathy have made it difficult to define the indications and assess the value of the treatment. Serious visual disability due to diabetic retinopathy is a leading cause of blindness among middle-aged people in Britain6 and a few years ago was estimated by the Committee on Blindness of the British Diabetic Association to be the cause of visual loss in about 1500 people a year in the U.K.Pituitary ablation, the sole active form of treatment for which some advantage had been shown,9was applicable only to a small, highly selected subgroup of younger, reasonably fit diabetics with retinopathy sufficiently advanced to justify a procedure itself carrying a substantial risk to health and life but not so far advanced that retinal changes were irreversible. Otherwise, apart from last-ditch attempts to slow progression of retinopathy by rigorous improvement of metabolic "control" of the diabetes, the clinician could do little but wait for the inevitable succession of events-in younger patients, usually repeated hæmorrhage, retinovitreous vasoproliferation, and fibrosis and in older patients, advancing maculopathy-that would usher in blindness. A preliminary, two-year report in the April, 1976, issue of the A -merican Journal of OphthalmoTHE
narrow
xenon arc was
1. Meyer-Schwickerath, G. Bucherei Augenarztes, 1959, 33, 1. 2. L’Esperance, F. A. Trans. Am. Ophthal. Soc. 1968, 66, 828. 3. Dobree, J. H., Taylor, E. Trans. Ophthal. Soc. U.K. 1968, 85, 313. 4. Okun, E., Johnston, G. P. in The Treatment of Diabetic Retinopathy (edited by M F. Goldberg and S. L. Fine); p. 523. U.S.P.H.S. Publication no. 1890, Washington D.C., 1969. 5. Rubinstein, K., Myska, V. Br. J. Ophthal. 1972, 56, 1. 6 Sorsby, A Rep. publ. Hlth med. Subj. no. 28, 1972. 7. Report on Diabetic Blindness in the United Kingdom. British Diabetic Association, 1969. 8 Lundbæk, K., Malmros, R., Anderson, H. C., et al. Excerpta med. int. Congr. Ser. 172 (edited by J. Ostman). Amsterdam, 1969. 9. Kohner, E. M, Joplin, G. F., Cheng, H., Blach, R., Fraser, T. R. Trans. Ophthal. Soc. U.K. 1972, 92, 79.
10. Diabetic 383.
Retinopathy Study
Research
Group. Am. J. Ophthal. 1976, 81,
78
There were, however, hints that the xenon arc was also more effective than the argon laser in preserving vision. Some would take that paradox to support the argument that the more substantial retinal ablation also removes more of the source of a
pathogenic
factor which drives the
onwards. In the older,
usually non-insulin-dependent
betic, vasoproliferative retinopathy is and it is the
retinopathy dia-
uncommon
extensive variants of "background" retinopathy which threaten vision. An interim report on the results of a small multicentre trial, sponsored by the British Diabetic Association,11 was restricted to older patients with diabetic maculopathy. In 76 patients with both eyes roughly equally affected with retinal hxmorrhages, exudates, and macular oedema with visual acuity of 6/9 or less, or with circinate hard exudate involving the macular region with vision better than 6/9, a randomly selected eye from each patient was submitted to xenon-arc photocoagulation applied locally to lesions lateral to the macula, more generally to all visible lesions, or to the centre of circinate exudates. More control eyes (18) than treated eyes (8) deteriorated to blindness over a follow-up period of up to three years. The mean slowing effect of treatment on the rate of deterioration of visual acuity was statistically significant but small, with no obvious trend to increase with passing time and most evident in patients with intermediate degrees of visual deficit at baseline. The design of this trial was good but its scale hardly adequate to answer its primary questions. So we now seem to have a simple, low-risk treatment which will, in the short term at least, delay visual deterioration in diabetic retinopathy in patients with retinal neovascularisation, especially when this is more than slight and when it is accompanied by retinal haemorrhage, and also perhaps in older patients with maculopathy. In "ordinary" background retinopathy risk to vision is low and uninfluenced by photocoagulation. To take advantage of this new information (and to react promptly to further developments) we should consider redeploying our clinical resources. A first step should be the repeated, systematic ophthalmoscopic screening of patients under adequate conditions of mydriasis, and at intervals determined by the retinal appearance and by the type and duration of diabetes. A for verification questionable lesions stage should probably include fluorescein retinal angiograms which show up small tufts of new vessels which may escape ordinary clinical examination. Referral of patients with treatable lesions to an ophthalmologist with access to a photocoagulator should follow without delay, and treatment by aimed photocoagulation, retinal ablation, or both (and to include new vessels on the disc where the 11. Interim
Report of
more
a
Multicentre Controlled
Study. Lancet, 1975,
ii,
1110.
argon laser is available) should be performed. A planned schedule of follow-up observations and additional coagulation completes the schema. Where all of this cannot be done within a single hospital, ad-hoc district, area, or even regional ar-
rangements should be made. We
overlook the anxiety of the patient for his vision as he observes the increased interest and activity centred on his eyes. Nor must we sweep into this system patients with retinopathy unsuitable for treatment. For simple background retinopathy we can and need do little but observe and improve diabetic control. When extensive retinal or pre-retinal fibrosis is already present, photocoagulation may accelerate contraction and hasten retinal detachment. Very occasionally vitreous haemorrhage may occur soon after treatment, especially if large venous channels are too closely approached. Diabetic retinopathy is the most readily visible and clinically eloquent manifestation of a process which is progressing in other tissues and organs, not least the renal glomerulus. Enthusiasm for photocoagulation, a destructive process and clearly not the end of the road in the treatment of diabetic retinopathy, should not deflect more general efforts to prevent diabetic microvascular disease. This aspiration may well defy fulfilment until we have made a deeper penetration into the continuing mystery of the causation of diabetic microangiopathy.
The Future of
must not
Community
Medicine
THE specialty of community medicine emerged in Britain from a union of the Todd Commission on Medical Education, the Hunter Working Party, and the reorganisation of the National Health Service. A turbulent infancy and childhood aré almost inevitable since each of the three parents has different expectations of the child. And already we are hearing the cries of doom and disaster. Before and even after Todd, medical students seldom opted for careers in public health or community medicine, and there is concern that the quality of entrant to the specialty is poor. This week Dr HEATH and Dr PARRY (p. 82) put forward some ideas on the future of community medicine and they make a valuable contribution in the
emphasis they put on proper manpower planning. Perhaps the figures they cite, with their promise of rapid promotion for the able, will encourage more doctors to choose this sphere. HEATH and PARRY do, however, seem to overlook some of the serious problems which community medicine has to tackle. The first
role and identity. The Hunter working party slightly confused the issue by concentrating on management aspects. In fact, only concerns
the strong support of a well-organised trial to the advocates of photocoagulation clinical in diabetic retinopathy. Confined to patients with vasoproliferative changes in at least one eye or severe non-proliferative changes in both eyes, the trial confirms the grim prognosis for vision in eyes so affected. Taking the group as a whole, however, it strongly suggests that photocoagulation will approximately halve the risk of catastrophic visual loss. 1732 patients with the retinal changes described above but with visual acuity of 20/100 or better in both eyes were enrolled in a 15-centre study, directed by an executive committee headed by Dr MATTHEW DAVIS, coordinated by the University of Maryland, and generously financed by the U.S. Department of Health, Education and Welfare. One randomly selected eye of each patient was subjected to treatment with xenon-arc or argonlaser photocoagulation (also chosen randomly); the other, untreated eye was observed as the control. Aimed, focal coagulation of surface new vessels, including those on the optic disc when the laser was used, or extensive scatter coagulation of the retina ("pattern bombing" or "retinal ablation") were employed. An important end-point in the two-year analysis was "severe visual loss", defined as visual acuity less than S/200 at two or more consecutive, four-monthly follow-up visits. It occurred in 9.4% of untreated eyes and in 4. 1% of treated eyes, a difference very highly unlikely to have arisen by chance. Some evidence of visual recovery in these badly affected eyes was recorded about twice as often in treated as in untreated eyes. Analysis of the initial appearance of the eyes from retinal photographs supported the clinical view that severe visual loss was likely when neovascularisation was classified as moderate or severe (particularly when it involved the optic disc) and most likely of all when these changes were accompanied by fresh hæmorrhage. Treatment effects were so striking in these most vulnerable groups that the trial organisers have felt constrained to modify the protocol and recommend treatment for control eyes. In a large number of eyes with neither neovascularisation nor haemorrhage, presumably the fellow eye of one more severely affected which qualified the patient for the trial, the cumulative rate of severe visual loss over two years was only 2-1% in untreated and 2-9% in treated eyes. Inevitably with a destructive treatment like photocoagulation, there was a price to be paid for prevention of severe visual loss. Minor losses of acuity (2-4 lines of test type) were more frequent in treated than in untreated eyes, though after two years the difference was very small (13.0% versus 10.5%). There was also some sacrifice of visual field, more so with the xenon-arc than with the argon-laser treatment.
logy’O gives
THE LANCET
Photocoagulation for Diabetic Retinopathy beam of intense white light from the first used in the treatment of diabetic retinopathy by MEYER-SCHWICKERATH in 1959.1 Since then, many thousands of diabetics have been treated by this comparatively simple technique, and modifications employing monochromatic, coherent laser emission-notably, the green-light argon laser2 useful for its very narrow beam and its preferential absorption by red-cell hæmoglobin— are still being evaluated. Despite widespread application of this treatment and some strong advocacy,3-S the varied manifestations and the episodic, unpredictable progression of diabetic retinopathy have made it difficult to define the indications and assess the value of the treatment. Serious visual disability due to diabetic retinopathy is a leading cause of blindness among middle-aged people in Britain6 and a few years ago was estimated by the Committee on Blindness of the British Diabetic Association to be the cause of visual loss in about 1500 people a year in the U.K.Pituitary ablation, the sole active form of treatment for which some advantage had been shown,9was applicable only to a small, highly selected subgroup of younger, reasonably fit diabetics with retinopathy sufficiently advanced to justify a procedure itself carrying a substantial risk to health and life but not so far advanced that retinal changes were irreversible. Otherwise, apart from last-ditch attempts to slow progression of retinopathy by rigorous improvement of metabolic "control" of the diabetes, the clinician could do little but wait for the inevitable succession of events-in younger patients, usually repeated hæmorrhage, retinovitreous vasoproliferation, and fibrosis and in older patients, advancing maculopathy-that would usher in blindness. A preliminary, two-year report in the April, 1976, issue of the A -merican Journal of OphthalmoTHE
narrow
xenon arc was
1. Meyer-Schwickerath, G. Bucherei Augenarztes, 1959, 33, 1. 2. L’Esperance, F. A. Trans. Am. Ophthal. Soc. 1968, 66, 828. 3. Dobree, J. H., Taylor, E. Trans. Ophthal. Soc. U.K. 1968, 85, 313. 4. Okun, E., Johnston, G. P. in The Treatment of Diabetic Retinopathy (edited by M F. Goldberg and S. L. Fine); p. 523. U.S.P.H.S. Publication no. 1890, Washington D.C., 1969. 5. Rubinstein, K., Myska, V. Br. J. Ophthal. 1972, 56, 1. 6 Sorsby, A Rep. publ. Hlth med. Subj. no. 28, 1972. 7. Report on Diabetic Blindness in the United Kingdom. British Diabetic Association, 1969. 8 Lundbæk, K., Malmros, R., Anderson, H. C., et al. Excerpta med. int. Congr. Ser. 172 (edited by J. Ostman). Amsterdam, 1969. 9. Kohner, E. M, Joplin, G. F., Cheng, H., Blach, R., Fraser, T. R. Trans. Ophthal. Soc. U.K. 1972, 92, 79.
10. Diabetic 383.
Retinopathy Study
Research
Group. Am. J. Ophthal. 1976, 81,
78
There were, however, hints that the xenon arc was also more effective than the argon laser in preserving vision. Some would take that paradox to support the argument that the more substantial retinal ablation also removes more of the source of a
pathogenic
factor which drives the
onwards. In the older,
usually non-insulin-dependent
betic, vasoproliferative retinopathy is and it is the
retinopathy dia-
uncommon
extensive variants of "background" retinopathy which threaten vision. An interim report on the results of a small multicentre trial, sponsored by the British Diabetic Association,11 was restricted to older patients with diabetic maculopathy. In 76 patients with both eyes roughly equally affected with retinal hxmorrhages, exudates, and macular oedema with visual acuity of 6/9 or less, or with circinate hard exudate involving the macular region with vision better than 6/9, a randomly selected eye from each patient was submitted to xenon-arc photocoagulation applied locally to lesions lateral to the macula, more generally to all visible lesions, or to the centre of circinate exudates. More control eyes (18) than treated eyes (8) deteriorated to blindness over a follow-up period of up to three years. The mean slowing effect of treatment on the rate of deterioration of visual acuity was statistically significant but small, with no obvious trend to increase with passing time and most evident in patients with intermediate degrees of visual deficit at baseline. The design of this trial was good but its scale hardly adequate to answer its primary questions. So we now seem to have a simple, low-risk treatment which will, in the short term at least, delay visual deterioration in diabetic retinopathy in patients with retinal neovascularisation, especially when this is more than slight and when it is accompanied by retinal haemorrhage, and also perhaps in older patients with maculopathy. In "ordinary" background retinopathy risk to vision is low and uninfluenced by photocoagulation. To take advantage of this new information (and to react promptly to further developments) we should consider redeploying our clinical resources. A first step should be the repeated, systematic ophthalmoscopic screening of patients under adequate conditions of mydriasis, and at intervals determined by the retinal appearance and by the type and duration of diabetes. A for verification questionable lesions stage should probably include fluorescein retinal angiograms which show up small tufts of new vessels which may escape ordinary clinical examination. Referral of patients with treatable lesions to an ophthalmologist with access to a photocoagulator should follow without delay, and treatment by aimed photocoagulation, retinal ablation, or both (and to include new vessels on the disc where the 11. Interim
Report of
more
a
Multicentre Controlled
Study. Lancet, 1975,
ii,
1110.
argon laser is available) should be performed. A planned schedule of follow-up observations and additional coagulation completes the schema. Where all of this cannot be done within a single hospital, ad-hoc district, area, or even regional ar-
rangements should be made. We
overlook the anxiety of the patient for his vision as he observes the increased interest and activity centred on his eyes. Nor must we sweep into this system patients with retinopathy unsuitable for treatment. For simple background retinopathy we can and need do little but observe and improve diabetic control. When extensive retinal or pre-retinal fibrosis is already present, photocoagulation may accelerate contraction and hasten retinal detachment. Very occasionally vitreous haemorrhage may occur soon after treatment, especially if large venous channels are too closely approached. Diabetic retinopathy is the most readily visible and clinically eloquent manifestation of a process which is progressing in other tissues and organs, not least the renal glomerulus. Enthusiasm for photocoagulation, a destructive process and clearly not the end of the road in the treatment of diabetic retinopathy, should not deflect more general efforts to prevent diabetic microvascular disease. This aspiration may well defy fulfilment until we have made a deeper penetration into the continuing mystery of the causation of diabetic microangiopathy.
The Future of
must not
Community
Medicine
THE specialty of community medicine emerged in Britain from a union of the Todd Commission on Medical Education, the Hunter Working Party, and the reorganisation of the National Health Service. A turbulent infancy and childhood aré almost inevitable since each of the three parents has different expectations of the child. And already we are hearing the cries of doom and disaster. Before and even after Todd, medical students seldom opted for careers in public health or community medicine, and there is concern that the quality of entrant to the specialty is poor. This week Dr HEATH and Dr PARRY (p. 82) put forward some ideas on the future of community medicine and they make a valuable contribution in the
emphasis they put on proper manpower planning. Perhaps the figures they cite, with their promise of rapid promotion for the able, will encourage more doctors to choose this sphere. HEATH and PARRY do, however, seem to overlook some of the serious problems which community medicine has to tackle. The first
role and identity. The Hunter working party slightly confused the issue by concentrating on management aspects. In fact, only concerns
