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.

Dear Editor,

We thank Barnes et al for their interest in our study and for affording us the opportunity to correct some misinterpretations that others may also have made regarding our paper.

We agree entirely that histological examination of the complete excision surface as suggested by Mohs would be the ideal one should aim at and that it would be superior to conventional bread loaf histological sectioning. We dispute that this is realistically possible in inhomogeneous and exceedingly mobile eyelid tissues unless they are fixed prior to excision as in the chemosurgery that Mohs originally described.

Trying to cut a complete 2mm thick saucer of tissue through fresh skin, orbicularis, tarsal plate, orbital septum and fat and then transferring it without distorting the relative tissue orientation is a challenge that few are equal to. It might have been helpful if Barnes et al had shared their practical experience of the technique with us in their letter.

That the risk of BCC recurrence relates to the tumour type is not in dispute and is indeed born out in our results. But it is helpful of Barnes et al to remind other readers of this fact. Histological subtype was not specified in the greater portion of our series as our histopathologists only pass comment when BCCs are infiltrative or unusual in other respects. We apologise for not stating this explicitly as it has clearly led to some misunderstanding.

However there is no justification for Barnes et al's assumption that the 'non-specified' tumours were small because 72% were managed by direct closure. We have clearly failed to get over a most important point. Direct closure under tension is not only possible in much larger lid defects than conventionally taught but also gives far superior functional and cosmetic results. As such we urge others to use this method of repair more widely.

That 76% of our tumours occurred on the lower lid should not come as a surprise to anyone as it is a well recognised fact. It does not suggest that our series is in any way biased.

That our series differs from the selected series in the Australian Mohs database is self evident. We described our experience with an unselected consecutive series of 223 secondary and tertiary periocular Basal Cell Carcinomas (BCC) referrals to a UK regional Oculoplastic service. Our case mix should therefore be representative of that in other similar UK units and our results are therefore more relevant to them than those of the high risk biased Australian Mohs series and our results can be used as an audit benchmark. Although we have used conventional non-Mohs treatment, we achieved a very low recurrence rate.

We fully support that full histological margin control, as in Mohs micrographic surgery, is the best treatment option in recurrent, high risk cases. Our study shows that careful non-Mohs BBC excision remains a valuable, safe and cost effective option. Our technique offered the patients with primary non-infiltrative BCC excellent cure rates and functional and cosmetic outcomes with no recurrence over 5 years follow up.

Correspondence to:
V T Thaller, FRCOphth
The Royal Eye Infirmary
Apsley Road
Plymouth
PL4 6PL
UK
vladimir.thaller@phnt.swest.nhs.uk

Editor,
We read Tanner et al's paper on the predictive value of vitreous pigment (Schaffer's sign) for retinal breaks in posterior vitreous detachment1 with great interest. Based on their figures, patients who have a negative Schaffer's sign had a 1% chance of having a retinal tear or hole and a 0.5% chance of having a lesion for which prophylaxis was thought to be appropriate. Thus Schaffer's sign has a negative predictive value of 99% in their series. They go on to recommend that if vitreous pigment is present then the patient should be referred for urgent vitreoretinal opinion while those with no pigment should be referred on a less urgent basis. We would like to put these findings in perspective. The incidence of retinal breaks in patients aged 10 years or more who do not have any history of ocular disease is 6-14%.[1] Retinal breaks have been found in 37/250 (14.8%) of autopsy eyes with posterior vitreous detachment by Foos.[2] The incidence of retinal detachment is approximately 12/100,000 of the general population per year.[3] This suggests that less than 0.2% people with a retinal break eventually have a detachment of the retina. This value may be higher in patients with a symptomatic posterior vitreous detachment; however it is reasonable to conclude that only a minority of retinal breaks will go on to cause a retinal detachment. Prophylactic treatment of retinal breaks by laser or cryotherapy is not without complications; also detachments can occur in eyes that have had prophylactic treatment.[4] Byer has reported that retinal breaks in unoperated eyes with posterior vitreous detachment can be followed up without treatment, with only a minority progressing to retinal detachments.[5] We have a test that has a negative predictive value of 99%. We know that only a minority of patients who have a retinal tear or hole actually benefit from prophylactic treatment. Can we still justify referring all patients with a posterior vitreous detachment and no vitreous pigment for a specialist examination or even a follow-up examination in the light of this knowledge? The appropriate recommendation would be that all patients presenting with posterior vitreous detachment, no vitreous pigment and no retinal tears or holes at initial examination can be safely discharged with an explanation of the warning symptoms which should prompt the patient to return to the ophthalmologist.

References
1. Byer NE. Clinical study of retinal breaks. Trans Am Acad Ophthalmol Otolaryngol 1967;71:461-73.
2. Foos RY. Posterior vitreous detachment. Trans Am Acad Ophthalmol Otolaryngol 1972;76:480-97.
3. Haiman MH, Burton TC, Brown CK. Epidemiology of retinal detachment. Arch Ophthalmol 1982;100:289-92.
4. Schroeder W, Baden H. Retinal detachment despite preventive coagulation. Ophthalmologe 1996;93:144-8.
5. Byer NE. What happens to untreated asymptomatic retinal breaks, and are they affected by posterior vitreous detachment? Ophthalmology 1998;105:1045-9.