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In England and Wales diabetic retinopathy is Schwickerath (1954) showed that retinal changes in
responsible for 7% of all new blind registrations diabetes mellitus may be arrested or reversed by
and up to 20% in the middle-aged (Sorsby, 1972). light coagulation. He further showed that regression
Patients with the proliferative form of the disorder could occur in newly formed vessels at retinal level
have been estimated by Deckert et al. (1967) and even though treatment was remote from the lesion.
Caird et al. (1968) to progress to blindness in 50% Okun (1968); Krill et al. (1971a, b); and Taylor and
of cases after five years. Taylor and Dobree (1970) Dobree (1970) noted regression of disc neovascularis-
noted that their patients with proliferative retino- ation occasionally when extensive xenon-arc photo-
pathy had an incidence of optic disc neovascularisa- coagulation of the diabetic retina had been
tion of 68 to 73-25 %. undertaken.
Visual prognosis is far worse if the proliferative A circumferential ablation technique using the
retinopathy involves the optic disc region (Deckert et ruby laser was described first by Aiello et al. (1969).
al., 1967); 50% of patients in this category are blind In a subsequent series (Beetham et al., 1970) 30%
within two to three years. Neovascularisation of the of patients with optic disc neovascularisation
optic disc frequently leads to vitreous haemorrhage showed significant reduction of new vessels after
and blindness (Patz and Berkow, 1968). In their treatment. James and L'Esperance (1974) treated 52
three-year study Beetham et al. (1970) showed that eyes with proliferation at the optic disc by a retinal
85% (29 patients) of untreated eyes with vitreous ablation technique with the argon laser. After
haemorrhage bled from new vessels at the optic disc. treatment 42% of eyes showed obliteration of disc
Caird et al. (1968) showed that after a vitreous neovascularisation, and 33% showed a significant
haemorrhage one-third of involved eyes were blind response.
within one year and one-third had vision which was Interim reports from a multicentre study in the
permanently impaired. Patz and Berkow (1968) United States using both xenon arc and argon laser
found that the second (good) eye in patients blind in (Diabetic Retinopathy Study Research Group, 1976)
the other eye frequently became blind through and England (British Multicentre Photocoagulation
extension of the proliferative process in a short Trial, 1977) using only xenon arc photocoagulation
period of time (50 % within one year). Meyer- indicate that photocoagulation confers real benefits
on the treated eye. This difference between treated
Address for reprints: B. L. Hercules, FRCS, 15 Chestnut and untreated eyes was enhanced by previous
Drive, Sale, Cheshire vitreous haemorrhage, as, untreated, this has a poor
555
556 B. L. Hercules, 1. 1. Gayed, S. B. Lucas, and Jiulie Jeacock
no change in the neovascularisation at the optic disc papillovitreal neovascularisation. The peripapillary
or spontaneous regression in the control eye. type can extend 3 to 4 disc diameters across the
Group 2.-Disc neovascularisation with gliosis retinal surface, and, again, can convert to the papillo-
and/or intravitreal proliferation (Figs. 4 and 5). vitreal type. Fig. 5 shows the late phase of group 2
This conforms to the later stages of epi- and peri- where the arcuate type of papillovitreal neovascu-
papillary neovascularisation described by larisation is developing.
L'Esperance. Epipapillary changes can convert Group 3.-Untreated grade 2 gradually passes
after marked glial proliferation to more widespread into this stage of massive combined disc neovascu-
Fig. 3 Fluorescein angiogram: Grade I optic disc Fig. 4 Fluorescein angiogram: Grade II optic disc
neovascularisation neovascularisation. Early stage with onset of connective-
tissue condensation in peri- and epipapillary new vessels
P < 0001). Table 2 shows that in 36% of all treated 3 showed this lack of marked improvement (see
eyes new vessels disappeared completely or almost Figs 7, 8, 9, 10, 11, 12, 13, 14).
completely. Improvement was greatest in group 1
patients, where they disappeared in 26/43 (60%) of VISUAL ACUITY
eyes. A significant improvement (95 > R > 50) In group 1 no difference could be shown by the
occurred in a further 40 % of eyes-all in groups 1 Wilcoxon test in the mean cumulative deterioration
and 2. Only 2 out of 43 eyes in group 1 (4 7%) in visual acuity between treated and control eyes.
showed no significant response, while all 10 in group In group 2 the difference ranged from very highly
Fig. 13 Fluorescein angiogram: grade II disc Fig. 14 Fluorescein angiogram: previous disc 7 months
neovascularisation before treatment after treatment, showing 50 % regression of new vessels
Peripheral retinal ablation in the treatment of proliferative diabetic retinopathy 561
significant in the first year to significant in the second control eyes in both subgroups for each year. In
and third years. In group 3 there was no significant both cases no significant difference could be
difference in mean cumulative deterioration between demonstrated (P>O 10). Examination of the result-
the treated and control eyes (Fig. 15 and Table 3). ant graphs suggested that there was no marked
Group 1 was divided on clinical grounds into divergence between the treated and control means
'active' (la) and 'quiescent' (lq) subgroups. of the quiescent group with time and that
Wilcoxon tests were then applied to the treated and this inability to demonstrate significance by the
Wilcoxon test in the active group was due to the
small sample sizes. Therefore the quiescent group
Table 2 Comparison of the response of optic (lq) was pooled, and a Mann-Whitney U-test
neovascularisation to treatment applied. This showed a significant difference between
Regression of optic disc new vessels the active (la) untreated subgroup and the pooled
Gropl) R > 95 95>R>d>0 R <50 1i quiescent group. There was, however, no significant
difference between the active ( a) treated group and
1 26 15 2 43 the pooled quiescent group (Fig. 16 and Table 4).
2 7 22 10 39
3 0 0 10 10
Total 92 1 A Control
R =0* regression
4-
C3
T = Treated
3- C = Control
C2
V A T3
units
T2
o-~c
1 1 Cl
olQ Treated
>31A Treated
0 3Tl
-1Q Pooled
0 1 2 3 years
,1 Q Control
Fig. 15 Mean cumulative deterioration in visual acuity
for control and treated eyes in all groups Fig. 16 Mean cumulative deterioration in visual acuity
I active and quiescent subgroups
for group
Table 3 Mean cumulative deterioration of visual acuity Table 4 Mean cumulative deterioration of visual acuity
(VA units)
for group 1 active and quiescent subgroups
Year Treated Control n P#
Active treated/quiescent pooled
1 0-62 0-85 39 >0-1 Year Active T n Quiescent P n P#
Group 1 2 0-24 0-83 29 >0 1
1 0-58 24 0-43 30 >0-48
3 0-08 0-92 13 >0-1 0-19
2 16 0-19 26 >0-31
1 0-63 2-34 41 <00009
3 0-0 7 -0-17 12 >0-10
Group 2 2 2-56 3-30 25 <-0005
Active control/quiescent pooled
3 1-76 2-60 10 <0-025
Year Active C n Quiescent P n P#
1 2-10 2-40 10 >0-1
1 1-17 24 0-43 30 >0-3
Group 3 2 2-60 2-90 6 >0-1
2 1-44 16 0-19 26 <0-06
3 260 340 4 t
3 2-14 7 -0-17 12 <0025
V'Wilcoxon signed ranks matched pair test (one-tail probabilities)
tlnsufficient data *Mann-Whitney U-test (one-tail probabilities)
562 B. L. Hercules, L L Gayed, S. B. Lucas, and Julie Jeacock
to have been transformed into this stage while there Caird, F. L., Burditt, A. F., and Draper, G. J. (1968).
was no progression. Treated eyes in the full-blown
Diabetic Retinopathy: further study of prognosis for
vision. Diabetes, 17, 121.
late cicatricial stage appeared to behave in the same Deckert, T., Simonsen, S. E., and Poulsen, J. E. (1967).
way as untreated eyes. It is possible that careful Prognosis of proliferative retinopathy in juvenile diabetes.
treatment of the new vessels directly may improve Diabetes, 6, 728.
prognosis for vision in this late group. Treatment of Diabetic Retinopathy Study Research Group (1976).
Preliminary report on the effects of photocoagulation
quiescent group 1 and also group 3 eyes was not therapy. American Journal of Ophthalmology, 81, 383-396.
shown to have significant deleterious effects on the James, W. A., and L'Esperance, F. A. (1974). Treatment of
eye. In view of this we would advise early treatment diabetic optic nerve neovascularization by extensive retinal
of all diabetics who are found to have neovascularisa- photocoagulation. American Journal of Ophthamology,
78, 939-947.
tion at the optic disc. Krill, A. E., Archer, D. B., and Newell, F. W. (1971a).
Treatment in all cases should be adequate, and Photocoagulation in complications secondary to branch
careful monitoring is necessary when this is vein occlusion. Archives of Ophthalmology, 85, 48.
accomplished. There are a significant number of Krill, A. E., Archer, D. B., Newell, F. W., and Chishti, M. I.
(1971b). Photocoagulation in diabetic retinopathy. 72,
patients who either achieve a less than desirable 299-321.
regression of new vessels or suffer a recurrence of Larsen, H. W. C. (1960). Diabetic retinopathy: with a
the condition. These patients should receive timely discussion of the morphological changes and the patho-
repeat treatment. genic factors. Acta Ophthalmologica, Supplement 60,42-46.
L'Esperance, F. A. (1968). An ophthalmic argon laser
photocoagulation system: design, construction and
Our thanks are due to Dr E. S. Rosen at the laboratory investigations. Transactions of the American
Manchester Royal Eye Hospital, and Dr Eva Kohner Ophthalmological Society, 66, 827-904.
at the Royal Postgraduate Medical School, Ham- L'Esperance, F. A. (1973). Argon laser photocoagulation of
diabetic retinal neovascularization. A five-year appraisal.
mersmith, for their interest and advice regarding this Transactions of the American Academy of Ophthalmology
study; to Miss M. McDermott and Mr J. Sutton and Otolaryngology, 77, 6-24.
for help in the treatment of patients, and Miss Jayne Little, H. L., Zweng, H. C., Jack, R. L., and Vassiliadis, A.
(1976). Techniques of argon laser photocoagulation of
Hughes for her work in the preparation of the paper. diabetic disc new vessels. American Journal of Ophthal-
Our thanks are also due to Mr E. Young and Mr S. mology, 82, 675-683.
Shaw for their excellent photography. Meyer-Schwickerath, G. (1954). Lichtkoagulation. Eine
methode zur Behandlung und Verhutung der Netzhaut-
ablosung. Albrecht von Graefes Archivffur Ophthalmologie,
References 156, 2-34.
Okun, E. (1968). The effectiveness of photocoagulation in
Aiello, L. M., Beetham, W. P., Balodimos, M. C., and the therapy of proliferative diabetic retinopathy (PDR).
Koncz, L. (1969). Ruby laser photocoagulation in treat- A controlled study in 50 patients. Transactions of the
ment of diabetic proliferating retinopathy preliminary American Academy of Ophthalmology and Otolaryngology,
report. In Goldberg, M. F., and Fine, S. L. (eds), Sympos- 72, 246-252.
ium on the treatment of diabetic retinopathy, Bulletin 1890, Patz, A., and Berkow, J. W. (1968). Visual and systemic
Public Health Service, pp. 437-463. prognosis in diabetic retinopathy. Transactions of the
Beetham, W. P., Aiello, L. M., Balodimos, M. C., and American Academy of Ophthalmology and Otolaryngology,
Koncz, L. (1970). Ruby laser photocoagulation of early 72, 253-258.
diabetic neovascular retinopathy. Archives of Ophthal- Sorsby, A. (1972). Incidence and Causes of Blindness in
mology, 83, 261-272. England and Wales, 1968, p. 10. HMSO: London.
British Multicentre Photocoagulation Trial (1977). Prolifera- Taylor, E., and Dobree, J. H. (1970). Proliferative diabetic
tive diabetic retinopathy: treatment with xenon-arc retinopathy: site and size of initial lesions. British Journal
photocoagulation. British Medical Journal, 1, 739-741. of Ophthalmology, 54, 11-18.