We thank Dr Bhatt for his letter and his interest in our study.[1]
1. We completely agree with him that the steroid induced rise in
intraocular pressure as the one of the most frequently encountered side-
effects of intravitreal triamcinolone acetonide can be of major concern.
In a recent study, an increase intraocular pressure after an intravitreal
injection of 25 mg triamcinolone acetonide...
We thank Dr Bhatt for his letter and his interest in our study.[1]
1. We completely agree with him that the steroid induced rise in
intraocular pressure as the one of the most frequently encountered side-
effects of intravitreal triamcinolone acetonide can be of major concern.
In a recent study, an increase intraocular pressure after an intravitreal
injection of 25 mg triamcinolone acetonide was found in about 50% of the
eyes injected.[2] In the majority of them, intraocular pressure could be
normalized by topical antiglaucomatous medication without development of
glaucomatous changes of the optic nerve head. About 1% of the eyes,
however, had to undergo filtering surgery since intraocular pressure was
elevated to values higher than 40 mm Hg despite maximal medical treatment.
It has remained unclear yet, whether frequency and amount of the rise in
intraocular pressure are dependent on the dosage of triamcinolone
injected. It may be a topic of future studies.
The question of the best dosage of intravitreal triamcinolone
acetonide as treatment of exudative age-related macular degeneration has
not been answered, yet, let alone the question whether intravitreal
triamcinolone acetonide is at all helpful for therapy of exudative age-
related macular degeneration. Recently, Gillies and colleagues published
the one-year results of their randomised clinical trial of a single dose
of intravitreal triamcinolone acetonide for neovascular age-related
macular degeneration.[3] Using a dosage of 4 mg triamcinolone acetonide,
they found that a single dose of intravitreal triamcinolone had no effect
on the risk of loss of visual acuity during the first year of the study in
eyes with classic choroidal neovascularization, despite a significant
antiangiogenic effect found 3 months after treatment. The experiences of
Gillies and coworkers may be reason to use a higher dosage of
triamcinolone acetonide in a treatment trial of exudative age-related
macular degeneration.
2. Without doubt, intravitreal steroids increase cataract formation
and lead to earlier cataract surgery. The possible phototoxicity of
ultraviolet radiation after cataract surgery, however, may not be reason
not to inject triamcinolone acetonide intravitreally since phototoxicity
may take a relatively long time to develop, and because some intraocular
lenses can provide some protection against phototoxicity by filtering the
ultraviolet radiation.
3. The authors completely agree with Dr Bhatt, that one of the
mechanisms by which intravitreal triamcinolone may possibly be helpful in
the treatment of exudative age-related macular degeneration is its anti-
inflammatory effect. Another reason could be a direct anti-
angioproliferative effect which has been found in in-vitro studies on
bovine retinal endothelial cells (own data). The authors also agree with
Dr. Bhatt that repetitive injections of triamcinolone acetonide may be
necessary as has been suggested.[4]
References
(1) Jonas JB, Kreissig I, Degenring R. Intraocular pressure after
intravitreal injection of triamcinolone acetonide. Br J Ophthalmol 2003;87:24-7.
(2) Jonas JB, Kreissig I, Degenring R. Intraocular pressure after intravitreal injection of triamcinolone acetonide. Br J Ophthalmol 2003;87:24-7.
(3) Gillies MC, Simpson JM, Luo W, et al. A randomised clinical trial of a single dose of intravitreal triamcinolone acetonide for neovascular age-related macular degeneration: one-year results. Arch Ophthalmol 2003; 121:667-73.
(4) Jonas JB, Kreissig I, Degenring RF. Repeated intravitreal injections of
triamcinolone acetonide as treatment of progressive exudative age-related
macular degeneration. Graef Arch Clin Exp Ophthalmol 2002;240:873-4.
My experience with ketamine anaesthesia in paediatric ophthalmic surgery in a semi-rural setting is very positive. It provides a viable alternative to more expensive and infrastructure-intensive anaesthesia procedures, and
is more than sufficient to complete most ophthalmic procedures.
Reference
(1) M S Pun, J Thakur, G Poudyal, R Gurung, S Rana, G Tabin, W V Good, and S Ruit. Ketamine...
My experience with ketamine anaesthesia in paediatric ophthalmic surgery in a semi-rural setting is very positive. It provides a viable alternative to more expensive and infrastructure-intensive anaesthesia procedures, and
is more than sufficient to complete most ophthalmic procedures.
Reference
(1) M S Pun, J Thakur, G Poudyal, R Gurung, S Rana, G Tabin, W V Good, and S Ruit. Ketamine anaesthesia for paediatric ophthalmology surgery. Br J Ophthalmol 2003;87:535-537.
The comment of Seal et al.[1] on the report by Radford et al.[2] on the incidence of acanthamoeba keratitis highlighted a number of points of interest when interpreting the results of a surveillance project carried out through the British Ophthalmological Surveillance Unit (BOSU).
The correspondence describes the study as a questionnaire survey.
This is incorrect; cases were asc...
The comment of Seal et al.[1] on the report by Radford et al.[2] on the incidence of acanthamoeba keratitis highlighted a number of points of interest when interpreting the results of a surveillance project carried out through the British Ophthalmological Surveillance Unit (BOSU).
The correspondence describes the study as a questionnaire survey.
This is incorrect; cases were ascertained through prospective
population-
based active surveillance. This methodology has been shown to be
effective
in trials, identifying up to twice as many cases as passive methods [3,4]
and has been evaluated in ophthalmology.[5] Furthermore, they also
imply
that the BOSU has some authorship rights over the report. This is also
incorrect. The BOSU provides a methodological framework for assessing
the
incidence and clinical features of rare eye conditions. Cases are
identified through our surveillance system and notified to independent
research groups who contact the reporting ophthalmologist directly to
collect information about the reported case. The BOSU does not collect
any
information about the patients and as such does not have any claims to
ownership of the data or request to be listed as the author in any
subsequent publications.
Seal et al. do highlight the likelihood of underascertainment in
this study. This
is
a recognised source of potential bias and when possible the BOSU does
encourage researchers to ascertain cases through an additional
independent
source to allow the incidence to be estimated using capture-recapture
analysis. In the event of this being unavailable they should make
efforts
to estimate ascertainment and identify possible sources of error.
Radford
et al did this through comparison with microbiological and pharmacy
records at selected centres.
The assertion by Seal et al. that the ascertainment for this study
should mirror
the response rate achieved during the study period by the BOSU reporting system is inaccurate. Any incidence rate reported by a surveillance
project must be considered as a minimum rate and it is wrong to assume
that the correction should be proportional to the level of non-response.
Despite no reliable independent source to assess ascertainment existing
for this study, a subsequent survey of reporting ophthalmologists
indicated that they had reported 93% of cases of acanthamoeba keratitis
to
the BOSU.[5]
Case ascertainment achieved through the BOSU is not directly linked
to response rate, and can differ between conditions. Barriers to
participation in the surveillance scheme have been reported.[5] In
addition, difficulties with the interpretation of the case definition,[6]
management by non-consultant ophthalmologists or reluctance by
participating ophthalmologists to report certain conditions could be
relevant. Whilst we appreciate that some errors in estimation of
incidence
are inherent active surveillance through the BOSU continues to provide
the
best opportunity for the epidemiological investigation of rare eye
conditions.
References
(1) Seal DV Beattie TK Tomlinson A Fan D Wong E, Acanthamoeba
Keratitis. Br J Ophthalmol 2003 87(4):516.
(2) Radford CF, Minassian DC, Dart JKG. Acanthamoeba keratitis in
England
and Wales: Incidence, outcome and risk factors. Br J Ophthalmol 2002; 86(5):536-42.
(3) Thacker SB Redmond S, Berkelman RL, A controlled trial of
disease
surveillance strategies. Am J Prev Med 1986:2:345-350
(4) Vogt RL, LaRue D, Klaucke DN, Jillison DA, Comparison of an
active and
passive surveillance system of primary care providers for hepetitis,
measles, rubella, and salmonellosis in Vermont. Am J Pub
Health 1983:73:795-797.
(5) Foot BG, Stanford MR, Rahi J, Thompson JR. The British
Ophthalmological Surveillance Unit: An Evaluation of the First 3 Years. Eye 2003;17:9-15
(6) Foot BG Stanford MR. Questioning Questionnaires. Eye 2001;15(6):693-4.
Sinha et al. describing ten eyes of nine patients who had a myopic refractive error and had previously undergone retinal detachment surgery underwent LASIK surgery.[1]
All of them received a scleral buckle and encirclage at least six months before LASIK surgery. The LASIK
surgery could be completed in eight eyes but in two eyes it was aborted
intraoperatively because of inadequate suction se...
Sinha et al. describing ten eyes of nine patients who had a myopic refractive error and had previously undergone retinal detachment surgery underwent LASIK surgery.[1]
All of them received a scleral buckle and encirclage at least six months before LASIK surgery. The LASIK
surgery could be completed in eight eyes but in two eyes it was aborted
intraoperatively because of inadequate suction secondary to extensive
conjunctival scarring. This report is of interest, as there is hardly any
similar information in the literature. Since all the eyes received a
scleral buckle and encirclage before, why did the suction only fail in the
two eyes? Did they receive multiple retinal detachment surgery before?
Did the number of quadrants buckled and the size of the scleral buckle
implanted matter? This additional information certainly will shed more
light into this clinical problem.
The authors used hansatome microkeratome (Chiron Vision, Claremont,
CA, USA) to create a hinged flap. This hansatome has only one suction
port to hold the conjunctiva. Maybe those microkeratomes, like the one
from Nidek, that have more than one suction ports would give better
suction and extra safety especially in these eyes with conjunctival
scarring. Inadequate suction can lead to serious complications like thin
flap as reported by the authors. The authors used the hansatome head
cutting a 180 µm flap and reported a wide range of thickness of the flap
from 110 – 170 µm. However, the method of measurement was not reported.
Corneal flap thickness can be measured by subtracting the intraoperative
corneal bed pachymetry measurement from intraoperative total corneal
pachymetry.[2] In addition, intraoperative pachymetry can give us a better
idea of ‘residual stromal thickness’, which is particularly important in
these eyes that the development of postoperative keratectasia is a real
concern. I agree with the authors that other refractive procedures like
photorefractive keratectomy are good options in suitable candidates in
this scenario.
The authors read with interest the comments made by Dr Arevalo and
colleagues.[1] We certainly agree that new breaks may develop in the
vitreous base region within 2 clock hours of the scleral wound. Because
of this, we advocate the use of encircling scleral buckles (3.5-5 mm wide)
as opposed to segmental scleral buckles in patients undergoing primary
open-globe injury repair.
The authors read with interest the comments made by Dr Arevalo and
colleagues.[1] We certainly agree that new breaks may develop in the
vitreous base region within 2 clock hours of the scleral wound. Because
of this, we advocate the use of encircling scleral buckles (3.5-5 mm wide)
as opposed to segmental scleral buckles in patients undergoing primary
open-globe injury repair.
We agree that placing an encircling scleral buckle to support the
posterior edge of the vitreous base does require more skill than simply
closing an open-globe wound. However, we have found that with adequate
training, encircling scleral buckles can usually be placed after open-
globe injury repair in 15-30 minutes.
The timing of vitrectomy in cases of ocular trauma is controversial.
We also try to wait at least 1-2 weeks before performing a vitrectomy, if
necessary, in order to minimize the risks of very early (potential
bleeding, inflammation and poor visualization) and very late (cellular
proliferation) vitrectomy.
We agree that a prospective randomized clinical trial is needed to
better delineate the role of primary encircling scleral buckle placement
at the time of open-globe injury repair.
Reference
(1) Arevalo JF, Fernandez CF, Mendoza AJ. Primary scleral buckle placement during repair of posterior segment open globe injuries [electronic response to JG Arroyo et al. A matched study of primary scleral buckle placement during repair of posterior segment open globe injuries] bjophthalmol.com 2003 http://bjo.bmjjournals.com/cgi/eletters/87/1/75#147
Schueler and associates describe their experience with thermochemotherapy (TCT) in bilateral retinoblastoma.[1] The reported results of transpupillary thermotherapy used in combination with chemotherapy are encouraging, with 86-96% tumor control.[2,3] In the current series, however, local recurrence occurred in 38%.
The dosage of carboplatin used in the current series was 10 mg/Kg BW, which is lower...
Schueler and associates describe their experience with thermochemotherapy (TCT) in bilateral retinoblastoma.[1] The reported results of transpupillary thermotherapy used in combination with chemotherapy are encouraging, with 86-96% tumor control.[2,3] In the current series, however, local recurrence occurred in 38%.
The dosage of carboplatin used in the current series was 10 mg/Kg BW, which is lower than the standard dosage of 18.6-mg/Kg BW.[4] Lower dose of carboplatin, the key drug in the chemotherapy regimen for retinoblastoma, could have influenced the higher recurrence rate.
The authors mention that they treated submacular tumors with TCT. However, in our experience, tumors located in the macular area are better treated initially with chemotherapy for 3-6 cycles in order to achieve maximum possible reduction in tumor size before considering thermotherapy. Chemo reduced macular tumors tend to shrink away from the fovea towards one of the major arcades or the optic nerve, thus exposing the foveal region. Residual tumor beyond 3-6 cycles of chemotherapy could be treated with thermotherapy. A smaller scar thus produced may optimize residual central vision.
The high mean total duration of thermotherapy in the current series is probably because of a smaller spot size of 0.4 mm. The diode laser (Iris Medical Inc, Mountain View, Ca, USA) with an operating microscope adapter allows for a spot size of 0.8,1.2,and 2.0 mm.[3] The relatively newer large spot indirect ophthalmoscope delivery system provides a 1.2mm spot size.[3] A larger spot size will indeed reduce the duration of thermotherapy and allow for a more uniform coverage. Corneal, iris and lens complications are minimized with better convergent beam optical systems currently available.
We believe that with higher dose of carboplatin, staggered thermotherapy for submacular tumors, use of better optical systems for delivery and a larger spot size for thermotherapy, and judicious selection of cases, the tumor regression and vision salvage with TCT could be further optimized.
References
(1) Schueler AO, Jurklies C, Heimann H et al. Thermochemotherapy in hereditary retinoblastoma. Br J Ophthalmol 2003; 87:90-95.
(2) Lumbraso L, Doz F, Urbeita M et al. Chemothermotherapy in the management of retinoblastoma. Ophthalmology 2002; 109:1130-1136
(3) Shields CL, Santos CM, Diniz W et al. Thermotherapy for retinoblastoma. Arch Ophthalmol 1999; 117:885-893.
(4) Shields CL, Honavar SG, Shields JA et al. Factors predictive of recurrence of retinal tumors, vitreous seeds, and subretinal seeds following chemoreduction for retinoblastoma. Arch Ophthalmol 2002; 120:460-464.
Kotter et al. refer to some problems, such as fabrication of authorship, data and ethical transgressions,[1] in our article published in The Lancet[2] on February 19, 2000. However, they do so without knowing the current facts about an ongoing process. They cite accusations that rely on an unfinalised investigation from the year 2000. As we are now in 2003, I do feel that I have to present updated cor...
Kotter et al. refer to some problems, such as fabrication of authorship, data and ethical transgressions,[1] in our article published in The Lancet[2] on February 19, 2000. However, they do so without knowing the current facts about an ongoing process. They cite accusations that rely on an unfinalised investigation from the year 2000. As we are now in 2003, I do feel that I have to present updated correct information.
Before I do that, however, I would like to note that the best scientific evidence against fabrication of the results, is its reproducibility by other groups. The results of Kotter et al. show the beneficial effect of interferon in Behcet's disease just as our results did,[2] and our results are being increasingly reproduced.
The fact that the accusations were made on the basis of an unfinalised investigation was clear in the editorial [3] and letter [4] written about our article in The Lancet [2] at the time. The editor of The Lancet stated that: "... further investigations are in progress"3 and the Dean of our medical school stated that "... the issue will be finalised ... in a court of law". [4]
I would like to report on the decisions made by courts of law during the three-year-period since then.
First of all, during ongoing inquires about the article,[2] it was established without doubt by an investigating commission that all my coauthors had already known that their names were included as coauthors before the article was published. None of the coauthors had objected to the inclusion of his/her name at the time. It was not until after two months after the publication that some of the coauthors claimed that they were unaware of inclusion of their names. It is noteworthy that they did so only after an ethical inquiry was embarked upon. The issue of fabricated authorship was brought to a court, accusing me of forging signatures. The Court unambiguously declared my innocence at its first session on the matter on April 3, 2003, concluding that there was no forging of signatures and that it cannot be imagined that the coauthors had been unaware of the article given the totality of the circumstances surrounding the issue.[5] This conclusion is supported independently by decisions of two other separate administrative courts.[6,7] As attested by those court decisions, there is no fabrication of authorship.
I was also accused of possible fabrication of the patients.[4] However, in a declaratory action taken by another court, it was definitely established that all 135 patients mentioned in The Lancet article2 were officially registered at the Hacettepe University Medical School.[8]
At the same time, the highest administrative court, The State Council of Turkey issued a stay order against any administrative act due to the claimed ethical transgressions,[9] in favour of me. This decision was further approved at a plenary session held at The State Council of Turkey with the involvement of members from all administrative chambers of the Court.[10]
Kotter et al. are unintentionally perpetuating incorrect accusations about me in the Journal.[1] I am hoping the impropriety of those accusations is clear in light of all the independent court decisions I describe above. Judicial decisions should be respected by everyone who believes in upholding the supremacy of law. It is my natural right to response and the readers of the Journal deserve to be informed by updated correct information.
There is no indication that either authorship or the results reported in The Lancet article [2] were fabricated. Besides judicial decisions, the best scientific evidence that the data are not fabricated is its reproducibility by other groups, as I mentioned at the beginning. It is well shown in the literature that our results [2] are being increasingly reproduced, and I am happy to see that. In our clinic, we have been using interferon in Behcet's disease since early 1990s and we are among the first groups to use it in this disease. We published our preliminary results previously.[11-12] The main problem in Behcet's disease is to prevent serious complications such as vascular thrombotic attacks, ocular involvement and their recurrences.[13] Conventional drugs and corticosteroids have very little if any effect on the course of such complications. The first two years of the disease is the most critical period and the disease generally runs a more severe course in patients in whom the disease is diagnosed at an age less than 30.[14-16] I believe that as interferon usage is increased, ocular complications of Behcet's disease will be minimised as well as extraocular manifestations. I suggest that the earlier we begin interferon, the better it is.
References
(1) Kotter I, Zierhut M, Eckstein, et al. Human recombinant interferon alfa-2a for the treatment of Behcet's disease with sight threatening posterior or panuveitis. Br J Ophthalmol 2003;87:423-31.
(2) Demiroglu H, Ozcebe OI, Barista I, et al. Interferon alfa-2b, colchicine, and benzathine penicillin versus colchicine and benzathine penicillin in Behcet's disease: a randomised trial. Lancet 2000;355:605-9.
(3) Horton R. Retraction: Interferon alfa-2b ... in Behcet's disease. Lancet 2000;356:1292.
(4) Sayek I. Behcet's disease: flaws in research integrity of randomised trial. Lancet 2000;356:1351.
(5) Turkish Republic, Ankara 3rd Court of General Criminal Jurisdiction; file no: 2003/256, decision no: 2003/335.
(7) Turkish Republic, Ankara 3rd Administrative Court; file no: 2000/1121.
(8) Turkish Republic, Ankara 2nd Civil Court of First Instance; file no: 2002/66 different work..
(9) 12th Chamber of The State Council of Turkey; file no: 2002/883.
(10) Plenary session, The State Council of Turkey, no: 2002/340.
(11) Caliskan S, Eldem B, Demiroglu H, et al. Interferon alpha-2b in the treatment of ocular Behcet's disease. Middle East J Ophthalmol 1995;3:94-9.
(12) Dundar S, Demiroglu H, Ozcebe O, et al. Alpha interferon in Behcet's disease. Hematol Rev 1996;9:285-90.
(13) Demiroglu H, Yalcin S, Buyukasik Y, et al. Vascular thrombotic problems in Behcet's disease. Acta Haematol 1997;98:172.
(14) Demiroglu H, Barista I, Dundar S. Assessing the risk of deep vein thrombosis in Behcet's disease. Thromb Res 1996;84:297-8.
(15) Demiroglu H, Barista I, Dundar S. Risk factor assessment and prognosis of eye involvement in Behcet's disease in Turkey. Ophthalmology 1997;104:701-5.
(16) Bardak Y. Effects of age and sex on Behcet's disease. J Rheumatol 1999;26:1008-9.
We read with great interest the manuscript by Li et al. about staining of the internal limiting membrane (ILM) and epiretinal membrane (ERM) with trypan blue (TB).[1] We would like to comment one aspect of this manuscript, when the authors claimed that a good staining of both the ILM and the ERM was achieved with TB. We disagree that ILM is stained by TB, and propose that TB only stains the ERM, but...
We read with great interest the manuscript by Li et al. about staining of the internal limiting membrane (ILM) and epiretinal membrane (ERM) with trypan blue (TB).[1] We would like to comment one aspect of this manuscript, when the authors claimed that a good staining of both the ILM and the ERM was achieved with TB. We disagree that ILM is stained by TB, and propose that TB only stains the ERM, but not the ILM.
The authors affirm "ILM staining" with TB as they observed histologically the presence of ILM in four eyes with macular holes stage III and IV. In one of those eyes, immunohistochemistry was performed, and an epiretinal membrane was observed. The other 3 cases, immunohistochemistry examination was not made because of insufficient tissue. Most of the stage III and IV macular holes are known to be associated with an epiretinal membrane,[2] and probably an ERM would be seen in addition to the ILM in those 3 cases if immunohistochemistry for glial elements were performed. Therefore, we believe that TB stained the ERM associated with the macular holes, but not the ILM. In their study, staining with TB of 7 patients with
idiopathic epiretinal membrane was successfully performed. ERM of proliferative vitreoretinopathy is also reported to be well stained by TB.[3] We speculate that TB has binding affinity to some of the glial cell elements of the highly cellular ERMs, either those associated with macular holes or not.
Indocyanine green (ICG) is another new dye for intraocular staining, that gained wide acceptance among retina surgeons in the last few years.[4] In contrast to the cellular affinity of TB, ICG stains well the acellular ILM, because of the fast binding of ICG to collagen proteins of the ILM. ERM tends to stain negatively by ICG, because the hydrophilic ICG does not penetrate cell membranes easily.[5]
TB staining seems to be a good alternative to ICG staining in the surgical management of macular diseases. Further studies are warranted about the intraocular kinetics of that dye.
References
(1) Li K, Wong D, Hiscott P, et al. Trypan blue staining of internal limiting membrane and epiretinal membrane during vitrectomy: visual results and histopathological findings. Br J Ophthalmol 2003;87:216-19.
(2) Tornambe P, Augustin AJ: Macular holes. Review of the current status of knowledge of pathogenesis and treatment methods. Ophthalmologe 2002;99:601-08.
(3) Feron EJ, Veckeneer M, Parys-Van Ginderdeuren R, et al. Trypan blue staining of epiretinal membranes in proliferative vitreoretinopathy. Arch Ophthalmol2002;120:141-4.
(4) Schmidt JC, Meyer CH, Rodrigues EB, et al. Staining of internal limiting membrane in vitreomacular surgery: A Simplified technique. Retina 2003 In Press.
(5) Forster RE, Petersen MR, Da Mata AP, et al. Negative indocyanine green staining of epiretinal membranes. Retina 2002;22:106-7.
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)...
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.
First of all let me congratulate the authors for their work on
exudative ARMD. But there are still some issues which need to be
brought into account:
1. Some published studies show that even 4.0 mg of intravitreal
triamcinolone has significant side effects in terms of increased IOP and
more so for eyes which needed the second dose of the triamcinolone, with
a few of them even needing a filtratio...
First of all let me congratulate the authors for their work on
exudative ARMD. But there are still some issues which need to be
brought into account:
1. Some published studies show that even 4.0 mg of intravitreal
triamcinolone has significant side effects in terms of increased IOP and
more so for eyes which needed the second dose of the triamcinolone, with
a few of them even needing a filtration surgery. In this particular
study however 25mg of Triamcinolone has been used which may cause even
more increased elevation of IOP. This issue is an important one as many
of our ARMD patients have co-existing chronic open angle glaucoma with a
compromised blood supply of the optic nerve head. With the intravitreal
steroids induced rise in IOP, we may tilt the balance on the wrong side
thereby taking their peripheral vision along-with the central loss due
to the ARMD. [1,2,5]
2. The effect of intravitreal steroids in the progression of
cataract is
not very much emphasized in various studies. If earlier cataract surgery
in treated ARMD patients is required, this has theoretical implications
in terms of ultraviolet light exposure, one of the environmental factors
implicated in ARMD. If there is no long term benefit for preventing the
progression of ARMD with the steroids then why should we increase the
chances of cataract in these patients thereby rendering their retinas
more vulnerable to damage caused by the UV radiation?[2]
3. Various in-vitro studies suggest that down-regulation of
inflammatory
markers and changes in the endothelial cell permeability are probably
the
modes of action of triamcinolone in exudative ARMD, but all these
actions
are probably only for the duration when the steroids are in high
concentration in the vicinity. To maintain high concentrations
triamcinolone should be injected repeatedly and probably that is the
reason the improvement fades with time in many patients. Moreover none
of the studies published so far have been long enough to actually give a
fair idea about the long term outcome. The longest duration for which
the follow up has been done is 18 months. [3,4]
We need data from multicenter, placebo-controlled trials on a much larger population with long-term follow-up to establish the efficacy of the drug and assess possible side effects and complications. Until then we should probably reserve this therapy for those cases where
there is recurrence after laser treatment.[5]
References
(1) Danis RP, Ciulla TA, Pratt LM, Anliker W. Intravitreal triamcinolone acetonide in exudative age-related macular degeneration. Retina 2000; 20(3):244-50.
(2) Challa JK, Gillies MC, Penfold PL, Gyory JF, Hunyor AB, Billson FA. Exudative macular degeneration and intravitreal triamcinolone: 18 month follow up. Aust N Z J Ophthalmol. 1998 Nov;26(4):277-81.
(3) Penfold PL, Gyory JF, Hunyor AB, Billson FA. Exudative macular
degeneration and intravitreal triamcinolone. A pilot study. Aust N Z J
Ophthalmol 1995 Nov;23(4):293-8.
(4) Jonas JB, Kreissig I, Degenring R. Intraocular pressure after
intravitreal injection of triamcinolone acetonide. Br J Ophthalmol 2003 Jan;87(1):24-7.
(5) Ranson NT, Danis RP, Ciulla TA, Pratt L. Intravitreal
triamcinolone in subfoveal recurrence of choroidal neovascularisation
after laser treatment in macular degeneration.
Br J Ophthalmol 2002 May; 86(5):527-9.
Dear Editor
We thank Dr Bhatt for his letter and his interest in our study.[1]
1. We completely agree with him that the steroid induced rise in intraocular pressure as the one of the most frequently encountered side- effects of intravitreal triamcinolone acetonide can be of major concern. In a recent study, an increase intraocular pressure after an intravitreal injection of 25 mg triamcinolone acetonide...
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My experience with ketamine anaesthesia in paediatric ophthalmic surgery in a semi-rural setting is very positive. It provides a viable alternative to more expensive and infrastructure-intensive anaesthesia procedures, and is more than sufficient to complete most ophthalmic procedures.
Reference
(1) M S Pun, J Thakur, G Poudyal, R Gurung, S Rana, G Tabin, W V Good, and S Ruit. Ketamine...
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First of all let me congratulate the authors for their work on exudative ARMD. But there are still some issues which need to be brought into account:
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