We thank Professor McLeod for his interest in our paper, “Vitrectomy with Silicone Oil Infusion in Severe Diabetic Retinopathy”[1] and value the opportunity to address some of the issues he has raised.[2]

Professor McLeod notes that surgical success can be judged only if the retina has remained attached for a minimum of six months from the last retinal procedure. He notes that 10 (43%) of 23 eyes in our report had follow-up of only one or two months. Tables 1-5 list the results in 17 (74%) eyes on which we have follow-up of at least six months (mean = 9.3 months). Of the six patients on whom we do not have at least six months follow-up, two have left the United States, and the whereabouts of four are unknown. The follow-up of these six patients ranged from one to four months after surgery.

Table 1 Surgical Indications

*TRD, traction retinal detachment; VH, vitreous hemorrhage; TRRD, traction-rhegmatogenous retinal detachment; 
FS, fibrinoid syndrome; NVG, neovascular glaucoma.

The composition of the subgroup with at least six months follow-up strongly resembles the composition of the entire group of 23 eyes.[1] For example, the indications for surgery are almost identical in their representation (Table 1). The average complexity score in this subgroup was 4.5, which is the same as that of the entire cohort. Additional details regarding this cohort of 17 eyes are as follows. In eight (47%) eyes, silicone oil infusion (SOI) was part of the initial operation during primary vitrectomy. In nine (53%) eyes, SOI was done after previously failed vitrectomy. Preoperatively, 11 (65%) eyes were phakic, and six (35%) were pseudophakic. Eight (73%) of 11 phakic eyes underwent lensectomy, and five (29%) of these were left aphakic. Four (67%) of the pseudophakic eyes underwent intraocular lens removal and were left aphakic. Different intraocular procedures were performed at the time of surgery. Scleral buckles were placed in two (12%) eyes. Epiciliary dissection was done in two (12%) eyes, one of which had preoperative hypotony. Membrane peeling was done in all eyes. A Baerveldt valve was placed in one (6%) eye, and a peripheral relaxing retinectomy was necessary in one (6%) eye. Silicone oil (SO) was removed in two (12%) eyes at five and eights months after surgery, respectively, without complication. SO was removed due to migration into the anterior segment with corneal touch in one eye and due to cataract progression in the second eye. As one might expect, in all these aspects, this cohort of 17 eyes with at least six months follow-up resembles the overall cohort of 23 eyes on which we reported.[1]

Table 2 Anatomic results of vitrectomy, membrane peeling, and silicone oil infusion.

The anatomic results of surgery among eyes with at least six months follow-up are quite similar to those of the entire cohort although a lower reattachment rate occurred among eyes undergoing surgery after having failed previous vitrectomy (Table 2). After a single operation employing pars plana vitrectomy with membrane peeling (PPV) and SOI, the retina was fully attached in 12 (71%) of 17 eyes with at least six months follow-up. In the eight eyes that were operated for the first time with primary SOI, the retina was attached in seven (88%) eyes. In the nine eyes that underwent SOI after previously failed vitrectomy, the retina was attached in five (56%). The difference in the reattachment rate between these two groups was not statistically significant (Fisher’s exact test, p = 0.18) as was the case in the cohort of 23 eyes.[1]

Among eyes with at least six months follow-up, three of the five eyes with recurrent detachment underwent repeat PPV and SOI. The retina was reattached in two (40%) eyes. The third eye developed hypotony despite complete retinal attachment five months after SOI and underwent repeat surgery with additional SOI and epiciliary dissection but became phthisical. The remaining two patients declined additional surgery. Therefore, with multiple operations employing PPV and SOI, the final anatomic success rate at last follow-up was 14/17 (82%), which is close the final anatomic success rate (20/23 (87%)) we reported previously.[1]

Table 3 Visual outcome.

With longer follow-up, visual results were not as good as we reported initially (Table 3). Among eyes with at least six months follow-up (and as noted in our initial report[1]), two (9%) had no light perception at last follow-up (neither underwent scleral buckling). Both eyes had preoperative vision of light perception. Loss of light perception was due to retinal and optic nerve ischemia in each case. Preoperatively, the visual acuity of all patients ranged from light perception to less than counting fingers at one foot. Six months or more after surgery, three (18%) of 17 eyes had vision: less than or equal to 5/200. Among the entire cohort of 23 eyes, five (22%) had vision: less than or equal to 5/200.

Table 4 Regression of rubeosis iridis and neovascular glaucoma.

Rubeosis iridis was present preoperatively in seven (30%) of 23 eyes, three of which had neovascular glaucoma (NVG). The rate of NVG regression among eyes with at least six months follow-up was the same as in the entire cohort (Table 4). The rate of rubeosis iridis regression was greater than we reported initially (i.e. 3/7 (43%)) due to continued regression of rubeosis during the longer period of follow-up (Table 4). Of the three eyes with NVG, one eye underwent Baerveldt valve placement with normalization of the postoperative intraocular pressure. Five months after surgery, however, the eye developed hypotony. Subsequently, the valve was removed, and the eye underwent additional SOI. As noted above, however, the eye became phthisical. As reported initially, the NVG regressed after surgery in the second eye, and the third eye had NVG regression but no light perception postoperatively due to ischemia. As noted in our initial report, only one eye developed de novo rubeosis iridis.[1] Among the 17 eyes with at least six months follow-up, six (35%) had intraocular pressure: less than or equal to 5 mmHg. In our initial report, five (23%) of 23 eyes had intraocular pressure: less than or equal to 5 mmHg.[1] Three of these six eyes had persistent retinal detachment, which we presume to be the cause of the hypotony. Among eyes with at least six months follow-up, the remaining 11 (65%) had intraocular pressure ranging from 6-48 mm Hg, with four patients taking anti-glaucoma medications.

Table 5 Prevalence of complications.

Intraoperative complications were not different among eyes with at least six months follow-up vs. the entire cohort of 23 eyes (Table 5). Postoperative complications differed in that there was an increased prevalence of cataract, hypotony, and silicone oil in the anterior chamber over time, which is not surprising.

Table 6 Condition of fellow eye.

Professor McLeod suggests that in addition to using data from eyes with at least six months follow-up, one should use the status of the fellow eye to judge surgical success. At the time of surgery, all fellow eyes had proliferative diabetic retinopathy (in addition to other vision threatening conditions) and had undergone full panretinal photocoagulation (Table 6). Among patients with traction retinal detachment in the fellow eye, two underwent fellow eye surgery, and one patient refused surgery (Table 6). Six (29%) of 21 fellow eyes were pseudophakic. Among the six fellow eyes with visual acuity Professor McLeod points out that only seven (30%) of 23 eyes in our series had retinal breaks (either pre-existing or intraoperative), and he asks what the rationale for silicone oil use was in the remaining 16 eyes. It is not our habit to use silicone oil routinely for re-operation of eyes with proliferative diabetic retinopathy. We usually manage such cases with membrane dissection, extensive laser photocoagulation, and gas tamponade, when indicated.[3] The average case complexity score in a series of more than 150 eyes with severe diabetic retinopathy on which we operated using modern surgical techniques was 3.7.[3] In this series, the average complexity score was 4.5, which was significantly greater.[1] We felt that silicone oil was needed in all these cases due to the severe nature of the proliferative diabetic retinopathy as well as specific features of the case.

Specifically, rubeosis iridis was present in seven (30%) eyes, despite previous application of substantial panretinal photocoagulation, and silicone oil was used to compartmentalize the eye and inhibit progression of rubeosis iridis (Table 4). Among six (26%) eyes with retinal breaks, silicone oil tamponade was used due to the extensive nature of the retinal breaks. Normally, we use intraocular gas for this purpose.[3] Five (22%) eyes had traction retinal detachment and anterior hyaloidal fibrovascular proliferation, and silicone oil was used to help maintain a more normal intraocular pressure and forestall the development of phthisis. In two (9%) eyes with the fibrinoid syndrome, silicone oil was used to prevent the development of transvitreal fibrous sheets, which we feared might foster recurrent retinal detachment (Tables 1 and 2). Two eyes (9%) had no light perception in the fellow eye, and silicone oil was used to provide more rapid visual rehabilitation (Table 6). One eye (4%) had recurrent vitreous hemorrhage, and silicone oil was used to help maintain media clarity postoperatively.

Professor McLeod observes that silicone oil continues to be used during diabetic vitrectomy despite the attendant anterior and posterior segment complications. He suggests that wide-angle viewing systems, heavy liquids, endolaser, and long-acting gases enable one to manage posterior retinal breaks and retinectomies. Professor McLeod asks, “What is the appropriate use of silicone oil in the diabetic eye in the modern era?” He suggests that in cases where breaks can be managed with gas tamponade and rubeosis can be reversed with retinal reattachment and laser photocoagulation, the use of silicone might be “gratuitous”. Professor McLeod suggests that appropriate uses of silicone might include patients with posturing difficulties or patients in whom there is a need for early visual rehabilitation.

We recognize that the conclusions of our study are limited because it is a nonrandomized retrospective study without a control group. Thus, we cannot identify the “virtuous” indications for the use of silicone oil in the setting of severe proliferative diabetic retinopathy based on these data. Without the use of silicone oil, for example, rubeosis iridis might have regressed, and the retina might have remained attached in eyes exhibiting the fibrinoid syndrome. Nonetheless, the data from our study are consistent with the notion that silicone oil is an acceptable and useful tool in the management of eyes with severe complications of proliferative diabetic retinopathy. Our experience suggests, but does not prove, that silicone oil tamponade improves the prognosis in some otherwise unsalvageable cases. Among 11 (48%) of 23 eyes in this series, silicone oil was used initially at the time of repeat vitreous surgery. Short-term retinal reattachment was achieved in eight (73%) of these eyes. Among these 11 eyes, nine had follow-up of at least six months, and retinal reattachment was maintained in five (56%) of these nine with a single operation. Overall, 10 eyes failed initial PPV with or without SOI, underwent repeat PPV and SOI, and had at least six months follow-up. Retinal reattachment without phthisis was achieved in seven (70%) of these eyes. Since the initial vitrectomies employed modern surgical techniques, these results indicate that even in the modern surgical era, use of silicone oil can improve anatomic (and functional) outcome in selected cases.

References

(1) Castellarin A, Grigorian R, Bhagat N, Del Priore L, Seery C, Zarbin MA. Vitrectomy with silicone oil infusion in severe diabetic retinopathy. Br J Ophthalmol 2003; 87(3):318-21.

(2) McLeod D. Silicone oil in diabetic vitrectomy [electronic response to Castellarin A et al. Vitrectomy with silicone oil infusion in severe diabetic retinopathy] bjphthalmol.com 2003 http://bjo.bmjjournals.com/cgi/eletters/87/3/318#130

(3) Grigorian R, Castellarin A, Del Priore L, Fegan R, Zarbin MA. Epiretinal membrane removal in diabetic eyes: comparison of viscodissection with conventional methods of membrane peeling. Br J Ophthalmol 2003; in press.

Hello, My name is Nicole Galvan and I have a beautiful son named Walter N. Edwards III. His nickname is Tre and he means the world to me. If it was not for his presence in the world, I do not no where I would be at today. I have a very large family encircling both my fathers' as well as my mothers' side. On my mothers' side of the family we have a condition known as "nystagmus", that is known to be carried by "only" the women in our family. It is known that this "disorder" Was inherited to us by my great-great grandfather, who had one green eye and one blue eye. Also the women who carry this have a certain type of blood type as well. We have noticed a pattern that the disorder skips from every other person. To our family this is quite normal and yet something that noone has been able to quite understand or researched to that matter. When I had my first, and only, son a year ago on December 17th of 2003, the first week he was home my mother kept telling me, he is gonna have the "dancing eyes". I kept telling her, no he is not, for in my heart I did not want him to suffer from that disorder. For to our family it is something unique and common, but to other people of the world, who are unaware of this, it is a "weird" thing to look at. When the disorder became noticeable, I thought, what can I do to help my child? So now I am writing you, or any other doctor or affiliation that you are connected to, to try and help me. I know that there are ways to help this condition, but it is not known to the less fortunate. This is a plea, to help one person enjoy his life better. Like I said he just turned a year. I have been thoroughly researching nystagmus, and even magnesium and intravenous thiamin is a key factor to help my son, but it is so expensive. I have heard about voluntary surgeory for this but I do not know who to contact. In this article that I read today about surgery being done in the early 1900's and how there is corrective surgery for the head movement, that means that there is somtheing that can be done. Yet the local doctors always conlude that there is no cure and there is no corrective surgery. Not to get off the subject, but just like there "is" a cure for aids for the fortunate, there is a cure for this. I am asking for any kind of help, maybe something you can refer me to as to getting a funding set up for my son. I will dedicate my life and my time to this. I am just asking for a little miracle, and with the help of god himself, maybe my son can get this condition fixed now so he can lead an active life. I thank you sincerely for even taking the time out to read this. Thank You So Much.

Dear Editor

We read with great interest the article by Kello et al.[1] on the causes of severe visual impairment and blindness in children in schools for the blind in Ethiopia. The authors have to be congratulated for the hardhitting and well written article. A current concern for people involved in pediatric eye care is the emergence of what is probably the third epidemic of retinopathy of prematurity (ROP) in developing countries.[2,3] It is therefore significant that no case of ROP was found in the population screened in this study. Several factors could account for this:
1. The very low or nil prevalence of ROP in countries such as Ethiopia, where the study was carried out, is most probably due to lack of intensive care facilities for premature infants and their low survival rates.
2. The variation in the incidence of ROP between ethnic groups could also account for this, with the available evidence suggesting that African-American infants are less prone to severe outcome ROP than white infants.[4,5]
3. However, it is also important to note that the article mentions that children with mental retardation were not examined owing to the admission criteria of the blind schools that precludes their admission. This too could have accounted for the gross underestimation of the prevalence of ROP as suggested by Jacobson et al.[6] In addition, these children with mental handicap could be suffering from cerebral palsy and would have been at high risk for ROP due to the higher incidence of retinal vascular anomalies associated with both cerebral ischaemia and prematurity.[7]
4. A large number of infants had phthisis bulbi (51 cases). In children with bilateral phthisis bulbi, there is a possibility that an unknown proportion developed the condition secondary to endstage ROP.

In conclusion, if improvement in perinatal care occurs in Ethiopia, the overall numbers of children with ROP would increase as is seen in other developing countries like India with infant mortality rates (IMRs) between 10-60 per 1000 live births3. Lack of ophthalmologists experienced in the management of ROP could be effectively circumvented by introduction of a digital retina camera technology to improve access to subspecialty care[8] for cases requiring treatment. As a lower cost option, screening infants under 1200 g alone might be more cost effective [9] and could be the first step, with modification of the screening guidelines made later, consequent to research undertaken within the country itself.

References

(1) A B Kello and C Gilbert. Causes of severe visual impairment and blindness in children in schools for the blind in Ethiopia. Br J Ophthalmol 2003;87:526-530.

(2) Wheatley CM, Dickinson JL, Mackey DA, Craig JE, and Sale MM. Retinopathy of prematurity: recent advances in our understanding. Arch Dis Child Fetal Neonatal Ed 2002;87: F78-82.

(3) Gilbert C, Rahi J, Eckstein M, et al. Retinopathy of prematurity in middle-income countries. Lancet 1997;350: 12-4.

(4) Schaffer DB, Palmer EA, Plotsky DF, et al. Prognostic factors in the natural course of retinopathy of prematurity. Ophthalmology 1993; 100: 230-7.

(5) Saunders RA, Donahue ML, Christmann LM, et al. Racial variation in retinopathy of prematurity. Arch Ophthalmol 1997;115: 604-8.

(6) Jacobson L, Fernell E, Broberger U, et al. Children with blindness due to retinopathy of prematurity: a population-based study. Perinatal data, neurological and ophthalmological outcome. Dev Med Child Neurol 1998; 40: 155-9.

(7) Pennefather PM, and Tin W. Ocular abnormalities associated with cerebral palsy after preterm birth. Eye 2000;14: 78-81.

(8) Schwartz DS, Harrison SA, Ferrone PJ, Trese MT. Telemedical evaluation and management of retinopathy of prematurity using a fiberoptic digital fundus camera. Ophthalmology 2000;107: 25-8.

(9) Lee SK, Normand C, McMillan D, et al. Evidence for changing guidelines for routine screening for retinopathy of prematurity. Arch Pediatr Adolesc Med 2001;155: 387-95.

Dear Editor

In the article presented by Wickham and associates,[1] the authors compared vitrectomy and gas for treating inferior break retinal detachments with vitrectomy, gas and scleral buckle. The study showed no significant difference in the final outcome between the two groups. While vitrectomy and gas for inferior break retinal detachments appears promising, there are several issues that we would like to raise.

First, the surgery was performed by either a registrar, fellow or consultant. These surgeons may have varying degrees of experience and the inconsistency may affect the rate of successful surgical outcome. Second, additional tears were treated with cryotherapy or laser. As shown by Bonnet M et al,[2] the post-operative proliferative vitreoretinopathy (PVR) rate could be as high as 25.8% in patients treated with cryotherapy as compared to 2.2% in the laser group. It is unclear what the relative distribution of patients who underwent cryotherapy in the two groups was and this may have been a confounding factor in the study. Third, patients underwent an air/gas exchange with either SF6 or C3F8. As C3F8 had a much longer duration of tamponade than SF6, the use of one agent over another may have lead to a difference in the success rate.

The study excluded patients with PVR grade C. However, for those with grade A or B, a scleral buckle was planned before the operation. This could lead to a selection bias where potentially more difficult cases were scheduled into the scleral buckle group. This may be a contributing factor for a higher rate of post-operative PVR (20%) and epiretinal membrane formation in this group, compared to a rate of 5-10% reported previously.[3 -4] The underlying vitreo-retinal pathology rather than the placement of the scleral buckle may have been a major reason behind the high PVR rate noted in this group.

The authors stated that the main reasons for performing vitrectomy and gas without scleral buckle was to avoid the possible complications of scleral buckle, namely, longer operating time,[5] exposure, refractive change, diplopia and anterior segment ischaemia.[6-10] Perhaps, in the interest of readers, the authors can provide us with the information if any of these complications developed during the study.

The high rate of final reattachment reported in the study is encouraging. We believe that vitrectomy and gas alone is an effective method to treat selected cases of retinal detachments with inferior retinal breaks. A controlled, randomized, prospective study, comparing the outcome in properly matched groups and with meticulous attention to surgical methods [11] will help address some of the above issues and help elucidate further if the procedure without the use of scleral buckle will benefit patients with inferior break retinal detachment.

We would like to commend the authors for conducting this very nice study on an important topic that may provide a better alternative treatment. We wish that the issues that we raise will help broaden the discussion on the topic.

Yolanda Y.Y. Kwong, MRCS C.W. Tsang, MRCS Wico W. Lai, MD, FACS Dennis S.C. Lam, FRCS, FRCOphth Hong Kong, People¡¦s Republic of China

The Corresponding Author has the right to grant on behalf of all authors and does grant on behalf of all authors, an exclusive licence (or non exclusive for government employees) on a worldwide basis to the BMJ Publishing Group Ltd and its licensees, to permit this article (if accepted) to be published in BJO and any other BMJPG products and to exploit all subsidiary rights, as set out in our licence (http://bjo.bmjjournals.com/misc/ifora/licenceform.shtml)

References

(1) Wickham L, Connor M, Aylward GW. Vitrectomy and gas for inferior break retinal detachments: are the results comparable to vitrectomy, gas, and scleral buckle? Br J Ophthalmol 2004;88:1376-1379.

(2) Bonnet M, Guenoun S. Surgical risk factors for severe postoperative proliferative vitreoretinopathy in retinal detachment with grade B PVR. Graefes Arch Clin Exp Ophthalmol 1995;233(12):789-91

(3) Charteris DG, Sethi CS, Lewis GP, Fisher SK. Proliferative vitreoretinopathy ¡V developments in adjunctive treatment and retinal pathology. Eye 2002;16:369-374.

(4) The Retina Society Terminology Committee. The classification of retinal detachment with proliferative vitreoretinopathy. Ophthalmol 1983;90:121-125.

(5) Hakin KN, Lavin MJ, Leaver PK. Primary vitrectomy for rhegmatogenous retinal detachment. Graefes Arch Clin Exp Ophthalmol 1993;231:344-6.

(6) Findall RJ, Norton EW, Curtin, et al. Reduction of extrusion and infection following episcleral silicone implants and cryopexy in retinal detachment surgery. Am J Ophthalmol 1971;71:835-7.

(7) Hayashi H, Hayashi K, Nakao F, et al. Corneal shape changes after scleral buckling surgery. Ophthalmology 1997;104:831-7.

(8) Domniz Y, Cahana M, Avni I. Corneal surface changes after pars plana vitrectomy and scleral buckling surgery. J Cataract Refract Surg 2001;27:868-72.

(8) Fison PN, Chignell AH. Diplopia after retinal detachment surgery. Br J Ophthalmol 1987;71:521-5.

(10) Kwartz J, Charles S, Mc Cormack P, et al. Anterior segment ischaemia following segmental scleral buckling. Br J Ophthalmol 1994;78:409-10.

(11) P Leaver. Expanding the role of vitrectomy in retinal reattachment surgery. Br J Ophthalmol 1993;77:197.