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Home , Diabetic retinopathy, Retinopathy, Rubeosis iridis

PROGRESSION OF DIABETIC AND RUBEOTIC FOLLOWING SURGERY

1 2 1 S. A. SADIQ , A. eRA TTERJEE and S. A. VERNON Nottingham and Manchester

SUMMARY retinopathy following cataract surgery over a There has been recent interest in the progression of prolonged time period compared with the fellow which initially had a similar level of retino­ following extracapsnlar cataract l 2 extraction (ECCE) especially with vitreous loss. It is pathy. , Recently two cases have been reported of well known that diabetic retinopathy progresses after rapid progression of retinopathy in the immediate intracapsular cataract extraction (ICCE) but was post-operative period with rubeosis developing thought to be less common after ECCE. We present 7 within a few weeks of surgery in the operated eye 3 patients with symmetrical non-proliferative diabetic only. retinopathy who underwent ECCE with intraocular We present 7 cases of diabetics who progressed to (IOL) implantation. These patients ranged in age aggressive neovascularisation or rubeosis leading to from 56 to 69 years; 2 were -dependent diabetics rubeotic glaucoma and severe visual loss within a few (100M) and 5 non-lOOMs. developed weeks of surgery. These patients were managed by quickly between post-operative outpatient visits despite general ophthalmologists in centres where there good diabetic control and a static retinal picture in the were no consultants with an interest in fellow eye. Visual loss following the onset of rubeosis (except one), and nor were these patients referred to was severe, with 3 patients needing cyclocryotherapy a recognised diabetic specialist when complications and eventually having no perception of light. The rapid arose. onset of rubeosis between post-operative outpatient visits leads us to suggest much shorter periods between reviews than is current practice and the consideration of routine panretinal photocoagulation in the immediate CASE REPORTS post-operative period in diabetics with worsening Case 1 retinopathy after ECCE and IOL. Possible causes of A 65-year-old West Indian man with a 26 year the increase in neovascularisation and rubeosis are history of non-insulin-dependent diabetes mellitus discussed. The most important message highlighted by (non-IDDM) presented in August 1989 with a right these case histories is that the surgery and follow-up of (VA) of 6/36 and a left VA of 6/60. He diabetic patients undergoing surgery should be under­ was found to have bilateral posterior subcapsular and taken by an ophthalmologist with an interest in cortical . Fundal examination revealed diabetes. Where there is no recognised diabetic retinal exudates at the right macula, and two incomplete specialist in a unit, then early referral to such an circinate rings around the left macula. There were no ophthalmologist is recommended when complications new vessels (NV) in either eye. Focal laser was not arise. performed for the left circinate rings as it was felt that the fundal view was inadequate. There have been reports of complications of cataract He underwent an uncomplicated left extracapsular surgery in diabetics, and of progression of diabetic cataract extraction (ECCE) with implantation (IOL) in November 1989. Four months l 2 From: Queen's Medical Centre, Nottingham; Royal Eye post-operatively his V A was 6/60 in the right eye and Hospital, Manchester, UK. Correspondence to: Mr S. A. Sadiq, Depart­ 6/18 in the left with new spectacles. The intraocular ment, Queens Medical Centre, Nottingham NG7 2UH, UK. pressure (lOP) was 20 mmHg in each eye. Fundal

Eye (1995) 9, 728-732 © 1995 Royal College of Ophthalmologists CATARACT SURGERY IN DIABETES 729 examination revealed right-sided and a Case 3 left incomplete circinate ring inferior to the macula. A 56-year-old woman with non-IDDM was first seen At this stage, the consultant felt that the retinopathy in 1981 with a VA of 6/9 and lOPs of 16 mIIlHg in did not merit laser treatment, but the patient was both ; both fundi showed background retino­ placed on the waiting list for right ECCE. pathy only. The situation was stable until 1986 when In May 1990 the patient presented with a 1 month the V As had reduced to 6/36 in the right eye and history of the left eye being increasingly painful and 6/12 in the left due to increasing cataract. In October . The left VA had reduced to counting fingers 1986 she underwent an uncomplicated right ECCE (CF), and was very injected with rubeosis iridis and with IOL. One month post-operatively the right VA an lOP of 44 mmHg. Fundal examination showed the had improved only to 6/36 due to a thickened left venous system not to be engorged, and there posterior capsule and early maculopathy, although were no NVs. Gonioscopy showed early NVs in the a FFA was not requested. Two months post­ drainage angle. He underwent an urgent left operatively the right lOP was found to be elevated panretinal photocoagulation (PRP) with only 677 at 30 mmHg (left lOP was 18 mmHg) and burns due to a poor view. A month later his left VA vessels were noted on the thickened posterior was no perception of light (NPL) with frank rubeosis capsule. Both fundi showed macular exudates. iridis and corneal oedema, with an lOP of 70 mmHg Treatment was started with timolol drops 0.5% b.d. despite treatment with timolol, betamethasone and which reduced the right lOP to under 21 mmHg. atropine drops, and acetazolamide systemically. He In February 1987 a right macular laser photo­ was in pain and underwent left inferior half coagulation was performed for the maculopathy, cyclocryotherapy, later followed by superior half whilst pilocarpine drops and acetazolamide tablets cyclocryotherapy. After this his left eye became pain­ were added to try to control the lOP. By March 1987 free with a VA of NPL and an lOP around 40 the right VA was CF and rubeosis of the right mmHg. was noted, whilst the left VA was 6/24. Over the next During this period the right VA had worsened to year the right lOP varied between 20 mmHg and 22 CF due to increasing cataract. Right again mmHg whilst the left lOP varied between 14 mmHg revealed a maculopathy, but there were no retinal or and 16 mmHg. Fundal examination revealed bilat­ disc NVs. Understandably, he was not keen. to eral maculopathy, worse in the right eye. proceed with right ECCE. In March 1988 the right VA decreased to hand movements (HM) due to vitreous haemorrhage. The right lOP was 30 mmHg with a rubeotic iris. The left Case 2 VA was 6/36, with an lOP of 14 mmHg and A 69-year-old man with non-IDDM presented in unchanged maculopathy. The right eye underwent August 1987 with a right VA of 6/60 and left VA of three episodes of laser PRP (1043 burns) in April 6/18. Fundus examination revealed bilateral early and May 1988. The right lOP remained elevated at diabetic maculopathy. He underwent argon laser 30 mmHg despite medical treatment and so a right photocoagulation to a left circinate ring in November cyclocryotherapy was performed in June 1988, which 1987 but the left V A decreased to CF due to resulted in a post-operative right lOP below 20 increasing maculopathy by February 1988. A year mmHg. later the right VA had also reduced to CF due to a Over the next 2 years the right eye had a further combination of posterior subcapsular cataract and four episodes of vitreous haemorrhage due to disc maculopathy. In June 1990 he underwent an NVs, leaving a residual vision of CF. uncomplicated right ECCE with IOL. Post-opera­ tively the V A improved only to 6/60 in the right eye. The lOPs were 10 mmHg in the right eye and 14 mmHg in the left. Fundal examination revealed the Case 4 bilateral maculopathy, but with no NVs. A fundal A 57-year-old man with a 25 year history of IDDM angiogram (FFA) was not obtained. In presented in June 1990 with a gradual reduction of September 1990 he returned to the casualty depart­ VA in both eyes over the previous 2 years. He was ment with a right VA of CF and an injected eye. The hypertensive and his regular medication consisted of right was oedematous with an inflamed atenolol, cyclopenthiazide and insulin. His V A was anterior chamber and an lOP of 38 mmHg in the CF in both eyes and lOPs were 18 mmHg in the right right eye and 14 mmHg in the left. Right iris rubeosis eye and 15 mmHg in the left. He had bilateral was seen but there were no retinal NVs. posterior subcapsular cataract, but there was no The lOP responded partially to medical treatment diabetic retinopathy in either eye. as an inpatient, but 2 weeks after admission the He underwent right ECCE under local anaesthesia patient became unwell and was referred to the in August 1990, which was complicated by posterior diabetic ward where he later died. capsule rupture requiring anterior and 730 S. A. SADIQ ET AL. insertion of an anterior chamber IOL. Post-opera­ CF, the right iris was rube otic and the cornea was tively the right V A improved to 6/12 after refraction. oedematous. lOPs at this stage were 55 mHg in the No retinopathy was noted. A year later he under­ right eye and 12 mmHg in the left eye. He underwent went uncomplicated left ECCE with posterior right cyclocryotherapy which made the right eye chamber IOL. At this stage, his right VA was 6/24 comfortable. By June 1991 the right VA was NPL. and left VA was 6/12, and lOPs were 9 mmHg in the In October 1992 the left vision had reduced to 6/60 right eye and 11 mmHg in the left eye. due to increasing cataract, and the patient underwent In October 1991 he presented with a 3 month uncomplicated left ECCE with posterior chamber history of reduction in the right VA to CF. The left IOL which improved the left vision to 6/24. Post­ VA was 6/18. The right eye showed rubeosis of the operatively, the left lOP was 18 mmHg, and fundal iris. lOPs were 8 mmHg in the right eye and 16 examination revealed background diabetic retino­ mmHg in the left. No diabetic retinopathy was seen pathy without any NVs. However, by December in either eye, although the right fundal view was 1992 the left lOP had risen to 25 mmHg, and hazy. He underwent two sessions of right PRP (1965 although no iris vessels were seen, NVs were found burns) in the following 6 months and this resulted in in the drainage angle and on the left . He a reduction in the iris rubeosis. In June 1992 his VA underwent a left PRP (858 burns) which resulted in was 6/18 in the right eye and 6112 in the left. lOPs regression of the disc NVs, leaving a VA of 6/18 in were 25 mmHg in the right eye and 14 mmHg in the his left and only eye. In January 1993 the left lOP left. No diabetic retinopathy was seen in either eye was 25 mmHg and early disc cupping was noted. He and he was started on timolol drops 0.5 % b.d. to the underwent a left trabeculectomy which unfortunately right eye with good effect. failed, and medical treatment was reinstituted. He underwent two further episodes of left PRP for mild recurrence of the disc NVs with a good result. At his Case 5 latest clinic visit the right eye was comfortable, and A 64-year-old man with a 15 year history of non­ his VA was NPL in the right eye and 6/18 in the left IDDM treated with metformin was referred for eye. lOPs were 40 mmHg in the right eye and 18 diabetic retinopathy . His VA was 6/18 in mmHg in the left eye. There were no NVs in the left the right eye and 6/9 in the left eye, and lOPs were 21 fundus. mmHg in both eyes. He had right-sided posterior subcapsular cataract. Fundal examination revealed bilateral background diabetic retinopathy. In the Case 6 following 2 years he required laser treatment for A 66-year-old man with a 1 year history of non­ circinate rings: on one occasion to the right eye and IDDM and treated with gliclazide, on three occasions to the left eye. metformin and nifedipine retard, presented in Four years after presentation, the right V A was September 1993 with a reduction in left vision. His further reduced to CF due to increasing cataract. The VA was 6/12 in the right eye and CF in the left eye, left VA was 6/12 and the lOPs were 19 mmHg in and his lOPs were 21 mmHg in each eye. He had a both eyes. Fundal examination revealed bilateral moderate left cataract and there was no evidence of background retinopathy with regression of circinate diabetic retinopathy in either eye. In January 1994 he rings. He underwent planned right ICCE and underwent an uncomplicated left ECCE and IOL. anterior- chamber IOL in October 1988. Although One month post-operatively the left vision was 6/60 there was an lOP spike on the first post-operative unaided and the left eye was quiet, with an lOP of 15 day, this settled with conservative treatment. Three mmHg. The left fundus revealed some cystoid weeks later, the right VA had improved to 6/36, macular oedema but no retinopathy, although a whilst the left VA was 6/18. lOPs were 34 mmHg in FFA was not performed. When seen in April 1994, the right eye and 20 mmHg in the left eye, and the the V A was 6/9 in the right eye and CF in the left patient was commenced on timolol drops to the right eye. The left lOP had risen to 40 mmHg and the left eye. Fundal examination revealed some macular anterior chamber was quiet. The patient was found exudates in the right eye, but there was no evidence to have early rubeosis of the left iris. Gonioscopy of neovascularisation. The left eye showed back­ revealed NVs in the drainage angle. The left optic ground diabetic retinopathy at that time. Over the disc showed early thinning of the inferior rim, but next ;3 months the right lOP continued to be raised, there were no signs of neovascularisation. There was and so systemic acetazolamide was added; this persistent cystoid macular oedema. He was started reduced the right lOP to under 20 mmHg until on carteolol drops and underwent a left PRP (760 November 1989, when he presented with right-sided burns), following which the left lOP was initially due to a vitreous haemorrhage. His lOPs under 20 mmHg without any topical therapy. Two were 40 mmHg in the right eye and 20 mmHg in the months later it had again risen to 40 mmHg, and so left eye. In March 1990 the right visual acuity was carteololl % b.d. was restarted. At his last clinic visit, CATARACT SURGERY IN DIABETES 731 his VA was 6/12 in the right eye and 6/60 in the left forward migration of any retinal angiogenic factor eye. lOPs were 18 mmHg in the right eye and 23 and also reduce the backward flow of an agent mmHg in the left eye. There was no diabetic postulated to cause post-operative cystoid macular retinopathy in either eye. oedema. This would explain the increased complica­ tions following intracapsular surgery or in cases Case 7 where posterior capsule rupture occurs. A 57-year-old man presented in March 1991 with an We recommend that, where dense cataract 8 year history of non-IDDM controlled with precludes visualisation of the fundus, cataract gliclazide. His VA was 6/6 in both eyes, lOPs were surgery should be undertaken although with a 18 mmHg in each eye, and there were early bilateral guarded prognosis, as assessment and treatment of cortical cataracts. Both fundi showed mild back­ any retinopathy may otherwise be impossible. ground diabetic retinopathy in the form of Since surgery may lead to aggravation of diabetic microaneurysms and dot haemorrhages. There were retinopathy it is preferable to delay surgery in a no exudates, or NVs. In July 1993 patient with background diabetic retinopathy for as he underwent a right macular grid photocoagulation long as he or she is able to cope with their daily for oedema. By June 1994 his VA had deteriorated activities, although IDDM patients may require to 6/60 in the right eye and 6/18 in the left eye, and he earlier surgery if the cataract is interfering with underwent an uncomplicated right ECCE with IOL accurate administration of their medication. This has under local anaesthesia. However, at 3 weeks post­ become less of a problem since the introduction of operatively he was thought to be developing early insulin pens where insulin does not have to be drawn rubeosis although the lOP remained normal at 20 up by the patient. mmHg. The right posterior pole showed some Patients with pre-operative diabetic retinopathy macular oedema, but there were no signs of NVs. should be advised that the visual prognosis for He was booked for PRP but failed to attend for this. cataract extraction is worse than it would be if no When seen at 11 weeks he had developed frank retinopathy were present. Those with early or rubeosis with an lOP of 40 mmHg in the right eye. moderate cataract and diabetic retinopathy, particu­ The left lOP was 18 mmHg. His VA at this stage was larly proliferative, should be treated pre-operatively, CF in the right eye and 6/24 in the left eye. The right with cataract extraction being performed when macula revealed some oedema and the disc was pale, neovascularisation has receded. If cataract precludes but there were no discs NVs. adequate laser treatment, then this can be performed immediately after cataract extraction with an indirect laser system while the patient is still on the operating DISCUSSION table or early on in the post-operative period. There have been previous reports of increases in Particular care should be taken to maintain an diabetic retinopathy following cataract surgery.4,5 intact posterior capsule during surgery to retain its However, reports of rubeotic glaucoma following barrier effect against forward diffusion of any cataract surgery in diabetics are few and involve angiogenic factor, or backward movement of a 5 small numbers.3,4 Jaffe et al. showed that cataract postulated agent causing cystoid macular oedema. extraction was highly associated with asymmetrical The key message we would like to highlight from progression of non-proliferative retinopathy, with these case reports is that the surgery and follow-up of progression in 74% of operated eyes. No patient had these patients should be undertaken by an ophthal­ progression in the unoperated eye alone. mologist with an interest in diabetes. In such a Our cases repeat this finding, all showing progres­ setting, the optimum use can also be made of sion of retinopathy in the operated eye only and for those patients who rapid progression of the proliferative changes leading seem to be running into problems, so that significant to rubeosis iridis and neovascular glaucoma within a changes are identified at an early stage and few months of surgery (range 1-18 months). appropriate treatment given. Where there is no Possible mechanisms of progression of diabetic recognised diabetic retinal specialist in a unit, then retinopathy and rubeosis remain to be determined. early referral to such a specialist is recommended Surgical trauma may contribute to the breakdown of before complications progress. the blood- barrier leading to increases in 5 Key words: Cataract surgery, Diabetes, Glaucoma, Retinopathy, macular oedema, haemorrhages and exudates. Rubeosis. Successful phacoemulsification causes less surgical trauma and less post-operative inflammation. It REFERENCES would seem the best method of cataract surgery in 1. Jaffe OJ, Burton TC. Progression of nonproliferative diabetic patients, although as yet no controlled study diabetic retinopathy following cataract extraction. Arch has investigated this. OphthalmoI1988;106:74S. An intact posterior capsule may protect against 2. Pollack A, Dotan S, Oliver M. Progression of diabetic 732 S. A. SADIQ ET AL.

retinopathy after cataract extraction. Br J Ophthalmol placement of a posterior chamber lens in patients with 1991;75:547. diabetic retinopathy. Ophthalmology 1993;100:730-8. 5. Jaffe GJ, Burton TC, Kuhn E, Prestcott A, Hartz A. 3. Prasad P, Setna PH, Dunne JA. Accelerated ocular Progression of non-proliferative retinopathy and visual neovascularisation in diabetics following posterior outcome after extracapsular cataract extraction and chamber lens implantation. Br J Ophthalmol intraocular lens implantation. Am J Ophthalmol 1990;74:313--4. 1992;114:448-56. 4. Benson WE, Brown GC, Tasman W, McNamara JA, 6. Alphar 11. Cataract extraction and diabetic retinopathy. Vander JF. Extracapsular cataract extraction and Am Intraocular Implant Soc 1984;10:433.