We have been conducting high volume cataract surgery (hospital-based
with full fledged ophthalmic facilities) in rural parts of Maharastra
state in India, conducting about 4000 to 5000 thousand sutureless
cataract extractions with lens implantations in last 5 years.
Patients with mature cataract with vision not more than finger counting
at
5 feet are selected. They all undergo routine eye exams and...
We have been conducting high volume cataract surgery (hospital-based
with full fledged ophthalmic facilities) in rural parts of Maharastra
state in India, conducting about 4000 to 5000 thousand sutureless
cataract extractions with lens implantations in last 5 years.
Patients with mature cataract with vision not more than finger counting
at
5 feet are selected. They all undergo routine eye exams and physical
check ups pre-operatively. We use a frown incision 7 to 7.5mm (white
mature or dark brown cataracts don't get expressed with the
viscoelastics method for incisions smaller then this). Post-op
refraction is done after 6 weeks; the average cylinder is about 1.5 D at
90 degrees.
Unfortunately, we don't have any method to compile this data. Also
follow-up after the final refraction is very poor. I would be grateful
if you could suggest a means to compile this data and utilize it in the
future. We would welcome any suggestions from you.
We appreciate the comments of Sridhar et al. regarding our letter:
“The role of corticosteroids in fungal keratitis: a different view”
published in your journal [1]. The authors comment on our recommendation
for a gradual tapering of corticosteroids in cases where steroids were
used for the treatment of initially misdiagnosed fungal corneal
infections.
We appreciate the comments of Sridhar et al. regarding our letter:
“The role of corticosteroids in fungal keratitis: a different view”
published in your journal [1]. The authors comment on our recommendation
for a gradual tapering of corticosteroids in cases where steroids were
used for the treatment of initially misdiagnosed fungal corneal
infections.
As mentioned in our cases report the use of corticosteroids in fungal
corneal ulcers is a subject of active debate [2,3]. There is no evidence
that in cases of corneal infections treated with effective antifungals and
steroids the penetration of fungus is made worse even if the antifungals
are considered in vitro fungistatic. Dr Sridhar et al. brings to our
attention the well known theoretical problems of corticosteroids in fungus
infections that prompted us to immediatelly discontinue the steroids.
Despite theoretical disadvantages we need to emphasize that stopping
steroids made corneas perforate creating a much greater apparent problem
than these theoretical considerations of which we were quite aware.
The point of our letter is that the cessation of steroids in fact
caused acute severe worsening and perforation of the cornea. We think that
in cases of severe fungal infections, as these we tried to treat, the
cautious use of steroids with immediate tapering and close monitoring of
ulcer progression could halt the infectious process and benefit the
patient until the antifungal treatment will be effective. Any other use of
steroids in fungal corneal infections could increase the fungal load and
is not clearly justified.
References
(1) Peponis V, J B Herz JB, and H E Kaufman HE The role of
corticosteroids in fungal keratitis: a different view. Br J Ophthalmol
2004; 88: 1227
(2) Pineda R, Dolhman CH. The role of steroids in the management of
Acanthamoeba keratitis, fungal keratitis and epidemic
keratoconjunctivitis. Int Ophthalm Clin. 1994;34(3):19-31.
(3) Schreiber W, Olbrisch A, Vorwerk CK, et al. Combined topical
fluconazole and corticosteroid treatment for experimental Candida albicans
keratomycosis. Invest Ophthalm Vis Sci. 2003;44:2634-43.
Editor,
We read with interest the article by Culliance and Cleary on the method of prevention of visual field defects after macular hole surgery. In their series, one group of 82 eyes received conventional pars plana vitrectomy surgery with mechanical induction of posterior vitreous detachment (PVD) around the optic disc followed by complete posterior cortical vitreous removal. Twenty-two percent of these...
Editor,
We read with interest the article by Culliance and Cleary on the method of prevention of visual field defects after macular hole surgery. In their series, one group of 82 eyes received conventional pars plana vitrectomy surgery with mechanical induction of posterior vitreous detachment (PVD) around the optic disc followed by complete posterior cortical vitreous removal. Twenty-two percent of these eyes had certain postoperative visual field defect. On the contrary, another group of 20 eyes received pars plana vitrectomy with peeling of the posterior hyaloid
confined to the macular area with sparing of the peripapillary region. None of them had any postoperative visual field loss. The authors proposed that vitreopapillary traction around the optic nerve head during the mechanical separation of the posterior hyaloid is responsible for the
formation of the observed postoperative inferotemporal visual field defects. The microcirculation at the optic nerve head may be damaged during the induction of PVD as the posterior cortical vitreous is most adherent at the superonasal aspect of the optic disc.[1] However, we are
concerned about the standardisation of the method of removing the remaining peripheral cortical vitreous in these two groups of eyes, as peripheral vitreous may act as a protective cushion from dehydration during fluid/air exchange. Yan et al[2] had shown that no significant
correlation was found between iatrogenic detachment of vitreous cortex and postoperative visual field defect, but all patients who had postoperative visual field defect had undergone fluid/air exchange in their series.
Similarly, Ohji et al[3] had demonstrated that using humidified air for fluid/air exchange in macular hole surgery could prevent postoperative visual field defect. Others had demonstrated that the visual field defect
was dependent upon the site of the air infusion port.[4] [5] All these reports suggest that air dehydration of the peripheral retina may be a very important factor in causing postoperative visual field defect after macular hole surgery.
In conclusion, we congratulate Culliance and Cleary on their study describing the prevention of visual field defects after macular hole surgery by limited posterior hyaloid peeling. However, the exact mechanism behind this success needs further evaluation.
1. Katz B, Hoyt WF. Intrapapillar and peripapillary hemorrhage in young patients with incomplete posterior vitreous detachment. Signs of vitreopapillary traction. Ophthalmology 1995;102:349-54.
2. Yan H, Dhurjon L, Chow DR, et al. Visual field defect after pars plana vitrectomy. Ophthalmology 1998;105:1612-6.
3. Ohji M, Nao-IN, Saito Y, et al. Prevention of visual field defect after macular hole surgery by passing air used for fluid-air exchange through water. Am J Ophthalmol 1999;127:62.
4. Takenaka H, Maeno T, Mano T, et al. Causes of visual field defects after vitrectomy. Nippon Ganka Gakkai Zasshi 1999;103(5):399-403.
5. Welcj JC. Dehydration injury as a possible cause of visual field defect after pars plana vitrectomy for macular hole. Am J Ophthalmol 1997;124:698-9.
I read with interest the World View article by Ezegwui et al.[1]
entitled: "The Causes of Childhood blindness: results from schools for
the blind in South Eastern Nigeria". Childhood blindness has profound
consequences not only for the individual but for the family and
community. Approximating the average life span at 60 years, the man-year
loss caused by childhood blindness is roughly six-fold, which...
I read with interest the World View article by Ezegwui et al.[1]
entitled: "The Causes of Childhood blindness: results from schools for
the blind in South Eastern Nigeria". Childhood blindness has profound
consequences not only for the individual but for the family and
community. Approximating the average life span at 60 years, the man-year
loss caused by childhood blindness is roughly six-fold, which directly
or indirectly is an economic burden on society. Therefore, during the
present era of Vision 2020, the Right to Sight publication on childhood
blindness is highly warranted.[2] The present authors, too, are to be
congratulated for this yeoman endeavor. In their discussion, it is very
rightly pointed out that a large number of children can be examined
within a short time by a standard method with low financial costs.[1]
Way back in 1999, we carried out a survey in only available school for
blind in Eastern Nepal. Though the aim of the survey and method of
examinations were similar to the present report, the causes of severe
visual impairment(SVI)/blindness(BL) were found to be different. In our
study, 41.25% had a retinal lesion. Either avoidable (38.75%) or
treatable (including avoidable) diseases were evident in 46.25% of eyes.
Lenticular problem constituted only 4% of the eyes. On the basis of our
experience, together with the present study and previous reports in
literature,[3-8] it seems there is a geographical variation among health
care systems with regard to the causes of SVI/BL. Both avoidable
blindness and treatable eye disease in children should be taken into
consideration.
Thus, it should be our goal to establish Paediatric Ophthalmology units
at all tertiary eye care centres, and to strengthen the primary eye care
system. Also, we should aim to establish more special schools for blind
for blind shildren.
References
(1) I R Ezegwui, R E , U F Ezepue Causes of childhood blindness: results
from schools for the blind in south eastern Nigeria. B J
Ophthalmol 2003;87:20-3
(2) Gilbert C, Foster A. Childhood blindness in the context of vision
2020-the right to sight. Bull World Health Organ
2001;79:227-32
(3) Chirambo MC, Benezra D. Causes of blindness among students in blind
school institutions in a developing country. Br J Ophthalmol
1976;60:665-8.
(4) Worlde-Gebriel Z, Gebru H, West CE. Causes of blindness in children
in the blind schools of Ethiopia. Trop Geogr Med
1992;44:135-41.
(5) Schwab L, Kagame K. Blindness in Africa: Zimbabwe schools for the
blind survey. Br J Ophthalmol 1993;77:410-2.
(6) Gilbert CE, Wood M, Waddel K, et al. Causes of childhood
blindness in East-Africa:results in 491 pupils attending 17 schools for
the blind in Malawi, Kenya
and Uganda. Ophthalmic Epidemiol 1995;2:77-84
(7) Umeh RE, Chukwu A, Okoye O, et al. Treatable causes of
blindness in a school for the blind in Nigeria. Commun Eye Health
1997;10:14-15.
(8) Rahi JS,Gilbert CE, Foster A,MinassianD.Measuring the burden of
childhood blindness. B J Ophthalmol 1999;83:387-8.
We read with interest the article by Ebner et al [1] investigating the
efficacy of periocular triamcinolone for the treatment of Thyroid Associated
Ophthalmopathy (TAO) and the presence of ocular or systemic adverse effects also
previously published in 2001 [2]. The study used patients with TAO of less than
6 months duration previously untre...
We read with interest the article by Ebner et al [1] investigating the
efficacy of periocular triamcinolone for the treatment of Thyroid Associated
Ophthalmopathy (TAO) and the presence of ocular or systemic adverse effects also
previously published in 2001 [2]. The study used patients with TAO of less than
6 months duration previously untreated, and assumed that the activity of the TAO
would be equal.
However large differences are apparent in both the demographics (a 78 year
old presenting with new onset TAO, and the use of an 11 year old child both
raised interesting scientific and ethical questions.) and the area of diplopia
at baseline suggesting baseline activity was not equal between groups. No
mention was made of either smoking or systemic medications used, both of which
are factors affecting the activity of TAO, and the subsequent measurement of the
potential systemic adverse effects of intraorbital triamcinolone. The main
measure of the local effect of triamcinolone was the area of single vision
obtained on a Goldmann perimeter, but the use of a 2-IV size light and the
measurement of “summation of angular points” is unclear.
The standard Goldmann nomenclature generally used designates a Roman numeral
for target size, and a combination of a number and letter to signify target
brightness and intensity. A 2-IV suggests a 4.51mm diameter light was used but
the brightness and intensity measure are not evident. The optimal size is a spot
subtending an angle of 2° to help discern the point of diplopia; a size IV only
subtends an angle of 0.86°and maybe to small to discriminate accurately. The
summation of angular points method to assess the area of single vision on the
graph obtained does not seem logical. Why not calculate the area within the
graph? No history of either prior strabismus or suppression seems to have been
elicited from the patients that would have a large effect on the results.
Both graphs shown demonstrate a large number of point readings taken
superiorly with only relatively few inferiorly, making the graph area a less
reliable measure. A more suitable method may have been a baseline independent
orthoptic assessment with serial Lees screen or Lister perimeter measurements,
and the adoption of Bagolini’s glasses to minimise suppression. The effects of
triamcinolone locally were measured with exophthalmometry, optic disc appearance
(normal, papilloedema, atrophy), ocular motility assessment and intraocular
pressure (IOP). The authors demonstrated in fig.3 an example of improved
cosmesis obtained but failed to measure this during the study, with perhaps
serial photographs [4]. Exophthalmometry values were not published, but any
change was stated to be not statistically significant.
The authors failed to explain why they thought the significant difference
between the areas of no diplopia demonstrated between the treatment and control
group were not supported by either a significant change in either proptosis or
extra ocular muscle diameter (except superior rectus) both of which are good
clinical indicators of TAO activity. Systemically the effect of triamcinolone
was measured by recording the body weight, blood pressure and various blood
tests at baseline, week 10 and week 24. Single point measurement of these
variables is unlikely to provide statistically significant information
especially when confounding factors such as systemic medications taken are
unknown.
References
(1) Ebner R, Devoto M,Weil D et al. Treatment of thyroid associated
ophthalmopathy with periocular injections of triamcinolone. Br J Ophthalmol
2004;88:1380-1386.
(2) Ebner R, Devoto M,Weil D et al. Tratamiento de la oftalmopatia asociada a
distiroidismo con triamcinolona periocular . Arch Oftalmol Bs As 2001;76:55-66.
(3) Dickinson AJ, Perros P, :Controversies in the clinical evaluation of
active thyroid associated thyroid orbitopathy. Clin Endocrinol 2001;55:283 -303.
Editor,
We read with interest the Newsdesk piece in the March 2000 issue of the journal, commenting on recent studies indicating a conceptual shift in the understanding of the molecular basis of differential susceptibility to
organ-specific autoimmune diseases. However, we were disappointed that the Newsdesk piece was restricted to studies of the animal model of multiple sclerosis and not that of uveitis....
Editor,
We read with interest the Newsdesk piece in the March 2000 issue of the journal, commenting on recent studies indicating a conceptual shift in the understanding of the molecular basis of differential susceptibility to
organ-specific autoimmune diseases. However, we were disappointed that the Newsdesk piece was restricted to studies of the animal model of multiple sclerosis and not that of uveitis. In a paper published in 1997[1] we demonstrated that ocular-specific antigens (S-Antigen
[arrestin] and interphotoreceptor retinoid-binding protein [RBP]), that are targets for pathogenic autoimmune processes, are expressed in the thymus of certain animals. Furthermore, we found that animals which
express S-antigen or IRBP in their thymus are resistant to experimental autoimmune uveoretinitis induced by the corresponding molecule, whereas the absence of thymic expression correlates with susceptibility.
1. Egwuago CE, Charukamnoetkanok P, Gery I. Thymic expression of autoantigens correlates with resistance to autoimmune disease. J Immunol 1997;159:3109-12.
Castellarin and colleagues [1] recount their recent experience of
infusing silicone oil in a small series of patients with advanced diabetic
eye disease, either during primary vitrectomy (12 eyes) or after earlier
surgery had failed (11 eyes). They compare their results with previous
reports and conclude that silicone oil remains a useful adjunct in
diabetic vitrectomy. However, their conclusions and h...
Castellarin and colleagues [1] recount their recent experience of
infusing silicone oil in a small series of patients with advanced diabetic
eye disease, either during primary vitrectomy (12 eyes) or after earlier
surgery had failed (11 eyes). They compare their results with previous
reports and conclude that silicone oil remains a useful adjunct in
diabetic vitrectomy. However, their conclusions and historical
comparisons are open to question.
Silicone oil was first used in primary diabetic vitrectomy in an era (1979-84) before the introduction of endolaser and the Landers' double concave lens for phakic fluid: air exchange.[2-4] Dealing with large or
multiple posteriorly-located breaks (whether pre-existing or iatrogenic)
was problematic, and direct fluid:silicone oil exchange (by virtue of the
optical advantages of oil over air in the phakic eye) provided a surgical
escape route, obviating the need for lensectomy. Furthermore, the clarity
of the media immediately postoperatively facilitated the slit-lamp
delivery of focal laser in order to seal retinal breaks that had been
closed by the internal tamponade, and in addition the application of
scatter laser to re-attached, untreated, ischaemic retina that had
undergone deturgescence, in part through the 'waterproofing' effect of
silicone oil.[3,4] All being well, the silicone oil could then be
removed shortly thereafter, and some eyes that would undoubtedly have been lost were saved by the intervention of silicone oil in this
way. Often, however, there were considerable associated problems, not
least the rapid development of reparative epiretinal fibrosis whereby the
retina re-detached under tangential traction and/or from re-opening of
retinal breaks.[2-6] Sometimes huge areas of retinal disintegration
eventually developed.[5,7] The fibroglial epiretinal proliferation
appeared (both clinically and pathologically) to be particularly induced
by clotted blood trapped between the silicone oil and the retinal surface
or, ironically, by fibrin released as a result of the extensive scatter
laser that was often needed to prevent highly vascularised membranes from
re-proliferating behind the silicone oil.[4,5,8,9]
It was hoped that the so-called 'compartmentalisation' of the eye by
silicone oil (to which the retro-silicone oil neovascularisation was
attributed) might in turn result in prevention or reversal of rubeosis
iridis through its putative barrier effect against anterior diffusion of
angiogenic substances derived from the ischaemic retina.[3-8]
Paradoxically, eyes with successful retinal reattachment (albeit with
unabated ischaemia) often underwent rapid development or progression of
iris neovascularisation,[3,8] while those with failed surgery from
postoperative rhegmatogenous recurrence of retinal detachment (and
therefore eyes with an exaggerated angiogenic drive) had evidence of
protection from rubeotic phthisis, at least in the short term.[3]
Perhaps naively it was postulated that rhegmatogenous confinement of the
re-detachment by intravitreal silicone oil (and the consequent 100% oil
filling of the shrinking vitreous cavity) might allow an effective
obstruction to anterior molecular diffusion to be established in these failed cases.[3] Others had planned from the outset to employ silicone oil in their
surgical protocol, not least for those diabetic eyes wherein earlier
vitrectomy had been unsuccessful as a consequence of retinal re-detachment [4,10,11] or recurrent vitreous cavity haemorrhages.[4] However, whether
used during primary diabetic vitrectomy or secondarily, whether
unpremeditated or planned, and whether infused by direct fluid:oil
exchange or sequential fluid:air and air:oil exchanges, the possibility
of silicone oil limiting rubeosis and maintaining macular attachment
despite peripheral retinal re-detachment was always welcome, even if
surgical 'success' (that is, retinal attachment through 360 degrees) had
strictly been denied.[2-4,8,12]
Nowadays, posterior retinal breaks and retinectomies can generally be
managed successfully by employing wide-angle viewing systems, heavy
liquids, endolaser, and long-acting gases. However, silicone oil continues
to be infused during diabetic vitrectomy despite the attendant posterior
segment and anterior segment complications that have only been partially
mitigated by the improved quality of the silicone oil. The important
question that thus arises is: what is the appropriate use of silicone oil
in the diabetic eye in the modern era? Where retinal breaks might be
closed just as readily using gas tamponade, or where rubeosis iridis might
be reversed or prevented by retinal reattachment and/or a sufficiency of
scatter laser photocoagulation, the use of silicone oil might be described
fairly as 'gratuitous'. Exceptions might include anticipated posturing
difficulties [3] or the need for early visual rehabilitation in one-eyed
patients.[4] However, recent reports documenting the use of silicone oil in diabetic vitrectomy have failed to
provide clear criteria or explanations regarding case selection.[1,12,13]
Only 7 of the 23 eyes in Castellarin and colleagues' series, for example,
had retinal breaks (2 pre-existing, 4 iatrogenic and 1 retinectomy), so
the need for prolonged internal break tamponade was presumably not an
issue in the majority of their eyes. More information is needed on the
rationale for silicone oil infusion (not just the overall indications for
surgery) in the remaining eyes in order to enable the potential benefits
of this surgical adjunct to be assessed at this time. Furthemore,
surgical success can really only be judged after a minimum of six months
from the last vitreoretinal procedure,[3,4,8,10-12] and that judgement
should preferably include consideration of whether the silicone oil has
been removed and the status of the fellow eye.[14] The fact that 10 of
the 23 eyes in Castellarins series were followed for only one or two months was thus a further serious limitation of their
study.[1]
Infusion of silicone oil can be a most beguiling option during the
closed microsurgical management of the stricken diabetic eye but, as
mentioned, complications are prone to accumulate with time.
Distinguishing the gratuitous from the virtuous use of silicone oil can be
problematic, and equally it may be difficult to define the line between a
surgeon's infusing silicone oil in anticipation of eventual surgical
failure and such infusion representing his/her unstated admission that
surgical failure has occurred already. All these issues need to born in
mind when making historical comparisons between case series and in
defining the place in history for silicone oil in diabetic vitrectomy.
References
(1) Castellarin A, Grigorian R, Bhagat N, et al. Vitrectomy with
silicone oil infusion in severe diabetic retinopathy. Br J Ophthalmol
2003; 87: 318-21.
(2) Lean JS, Leaver PK, Cooling RJ, McLeod D. Management of complex
retinal detachments by vitrectomy and fluid/silicone exchange. Trans
Ophthalmol Soc UK 1982;102: 203-5.
(3) McLeod D. Silicone-oil injection during closed microsurgery for
diabetic traction retinal detachment. Graefe's Arch Clin Exp Ophthalmol
1986; 224:55-9.
(4) Lucke KH, Foerster MH, Laqua H. Long-term results of vitrectomy
and silicone oil in 500 cases of complicated retinal detachment. Am J
Ophthalmol 1987; 104: 624-33.
(5) Barry PJ, Hiscott PS, Grierson I, et al. Reparative epiretinal
fibrosis after diabetic vitrectomy. Trans Ophthal Soc UK 1985; 104: 285-
96.
(6) Charles S. Vitreous surgery, 2nd edition Baltimore: Williams and Wilkins, 1987. Pp 115-31.
(7) Wilson-Holt N, Gregor Z. Spontaneous relieving retinotomies in
diabetic silicone filled eyes. Eye 1992; 6: 461-4.
(8) Yeo JH, Glaser BM, Michels RG. Silicone oil in the treatment of
complicated retinal detachments. Ophthalmology 1987; 94: 1109-113.
(9) McLeod D, James CR. Viscodelamination at the vitreoretinal
juncture in severe diabetic eye disease. Br J Ophthalmol 1988; 72: 413-9.
(10) Rinkoff JS, de Juan E, McCuen BW II. Silicone oil for retinal
detachment with advanced proliferative vitreoretinopathy following failed
vitrectomy for proliferative diabetic retinopathy. Am J Ophthalmol 1986;
101: 181-6.
(11) Brourman ND, Blumenkranz MS, Cox MS, Trese MT. Silicone oil for
the treatment of severe proliferative diabetic retinopathy. Ophthalmology
1989; 96
: 759-64.
(12) Azen SP, Scott IU, Flynn HW Jnr, et al. Silicone oil in the
repair of complex retinal detachments. A prospective observational
multicenter study. Ophthalmology 1998;105: 1587-97.
(13) Scott IU, Flynn HW Jnr, Lai M-Y, Chang S, Azen SP. First
operation anatomic success and other predictors of postoperative vision
after complex retinal detachment repair with vitrectomy and silicone oil
tamponade. Am J Ophthalmol 2000; 130: 745-50.
(14) McLeod D. Microsurgical management of neovascularisation
secondary to posterior segment ischaemia. Eye 1991; 5: 252-9.
Developmental mosaicism in the eye may follow the “lines of
Blaschko”
Ruggieri M et al. nicely described the ophthalmological manifestations in
segmental neurofibromatosis type 1 [1]. They postulated that segmental NF1
is a somatic mosaicism for the NF1-gene expressing two different
embryological tissues in the eye.
Previously we described a patient with unilateral sectorial
hyperpigmented ski...
Developmental mosaicism in the eye may follow the “lines of
Blaschko”
Ruggieri M et al. nicely described the ophthalmological manifestations in
segmental neurofibromatosis type 1 [1]. They postulated that segmental NF1
is a somatic mosaicism for the NF1-gene expressing two different
embryological tissues in the eye.
Previously we described a patient with unilateral sectorial
hyperpigmented skin lesions on his left shoulder and additional grouped
CHRPE in the left eye. These sectorial pigmentations were also noticed
during the first months of life and did not correspond to the distribution
of cutaneous nerves (dermatomes) [2]. Pigmentary mosaicism of the human
skin follow well-established segmental archetypes and were published by
the dermatologist Alfred Blaschko in 1901. He emphasized that these
“nevus lines” could neither be related to the
distribution of the nerves nor to vascular or lymphatic structures of the
skin [3].
These “lines of Blaschko” therefore reflect the dorso-
ventral outgrowth of precursor of the skin and may manifest the stream,
distribution, migration and proliferation of embryonic tissue. They
possibly originate during early embryogenesis by various genetic
mechanisms including postzygotic mutations, functional X-chromosomal
mosaicism, gametic halfchromatid mutations or loss of a heterozygosity
(LOH). If one of these events occurs, both homozygosity or heterozygosity
may predispose to sectorial pigmentation of these somatic cells. The
distinct stem-cell clones may give rise to the observed sectorial
mosaicism [4-5].
The precise pattern of the cutaneous lines of Blaschko
on the face, neck and trunk of the body were reported by Happle et al.
after observing numerous clinical examples of segmental skin disorders
[6].
Analogous patterns for the “lines of Blaschko” in the
eye [7] were described for heterozygous women with one randomly
inactivated X-chromosome (Lyonization) for X-linked Lowe-Syndrome
exhibiting segmental cataracts [8] or X-linked ocular albinism with stria-
like patchy fundus hypopigmentations with orientation toward the optic
nerve [9]. Recently we reviewed the literature over a period of 130 years
and identidied 41 publications with grouped congenital hypertrophy of the
retinal pigment epithelium (CHRPE). The sectorial pigmentations radiated
in a crescent shape from the optic nerve towards the periphery, providing
evidence, that there was no causal relationship to the retinal nerve fiber
system. We suggested that these lesions may follow developmental lines in
the eye analogous to the cutaneous lines of Blaschko. The sectorial
pattern of the neuroepithelial pigment epithelial in grouped CHRPE may
therefore reflect the outgrowth and migration of RPE-cells during
embryogenesis [10].
The important findings by Ruggieri M et al. give
further evidence, that two different embryological cellular clones may
present sectorial mosaicism in the eye following the lines of Blaschko.
References
(1) Ruggieri M, Pavone P, Polizzi A, Di Pietro M, Scuderi A, Gabriele A,
Spalice A, Iannetti P. Ophthalmological manifestations in segmental
neurofibromatosis type 1. Br J Ophthalmol 2004;88:1429-1433
(2) Meyer CH, Freyschmidt-Paul P, Happle R, Kroll P. Unilateral linear
hyperpigmentation of the skin with ipsilateral sectorial hyperpigmentation
of the retina. Am J Med Gen 2004;126A:89-92.
(3) Blaschko A. Die Nervenverteilung in der Haut in ihrer Beziehung zu den
Erkrankungen der Haut. 1901; Wien-Leipzig, W. Braumüller
(4) Happle R. Transposable elements and the lines of Blaschko: A new
perspective. Dermatology 2002;204;4-7.
(5) Happle R. Loss of heterozygosity in human skin. J Am Acad Dermantol
1999;41:143-61.
(6) Happle R, Assim A. The lines of Blaschko on the head and neck. J Am
Acad Dermatol 2001;44:612-5.
(7) Rott HD. Extracutaneous analogies of Blaschko lines. Am J Med Gen
1999;85:338-341.
(8) Happle R, Küchle HJ. Sectorial cataract: a possible explanation
Lyonisation. Lancet 1983;2:919-20.
(9) Rott HD, Rix R. Fundus changes in a carrier women for X-linked ocular
albinism: a proof of Lyon’s hypothesis in man. Klin Monatsbl
Augenheilkd 1984;184:128-9.
(10) Meyer CH, Rodrigues EB, Mennel S, Schmidt JC, Kroll P. Grouped
congenital hypertrophy of the retinal pigment epithelium follows
developmental patterns of pigmentary mosaicism. Ophthalmology (accepted)
The authors wish to thank Gandorfer and colleagues for their interest
in our paper [1] and for the kind comments and encouragement with regard
to our work. Certainly, these correspondents are compiling evidence
concerning the effect of indocyanine green (ICG) on the retina in both
their published and unpublished studies.[2,3]
In our report, we restricted our comments regarding retinal damage
and...
The authors wish to thank Gandorfer and colleagues for their interest
in our paper [1] and for the kind comments and encouragement with regard
to our work. Certainly, these correspondents are compiling evidence
concerning the effect of indocyanine green (ICG) on the retina in both
their published and unpublished studies.[2,3]
In our report, we restricted our comments regarding retinal damage
and dye usage to the specimens wherein an epiretinal membrane (ERM) was
present.[1] Evidence of retinal damage was observed in four of these five
specimens, mostly in the form of neural and glial elements adherent to
the retinal side of the inner limiting membrane (ILM). The apparent lack
of such elements in some ERM specimens may reflect partial separation of
the ILM due to traction from the membrane prior to surgery. [4]
Nevertheless, in one of our specimens a substantial fragment of
neuroretina was also present.[1] We have, indeed, long considered such
fragments as potential confounding factors in immunohistochemical studies
of surgically-excised ERMs.[5,6] Since they are present in ERMs removed
without the use of any dye at all, we cannot blame their presence on these
surgical aids. Perhaps these fragments are avulsed as a result of enhanced
adhesion between the ERM and retina via glial anchorage sites running
through dehiscences in the ILM.[5] It is clear that our investigation does not
exclude an effect of ICG on the retina [2,3] and we wholeheartedly agree
with Gandorfer and coworkers that agents such as trypan blue warrant
further evaluation as aids to ERM and ILM peeling.
References
(1) Li K, Wong D, Hiscott P, Stanga P, Groenewald C, McGalliard J. Trypan
blue staining of internal limiting membrane and epiretinal membrane during
vitrectomy: visual results and histopathological findings. Br J Ophthalmol
2003;87:216-9.
(2) Gandorfer A, Haritoglou C, Gass CA, Ulbig MW, Kampik A.
Indocyanine green-assisted peeling of the internal limiting membrane may
cause retinal damage. Am J Ophthalmol 2001;132:431-3.
(3) Gandorfer A, Haritoglou C, Gandorfer A, Kampik A. Retinal damage
from indocyanine green in experimental macular surgery. Invest Ophthalmol
Vis Sci 2003;44:316-23.
(4) Michels RG. A clinical and histopathologic study of epiretinal
membranes affecting the macula and removed by vitreous surgery. Trans Am
Ophthalmol Soc 1982;80:580-656.
(5) Hiscott PS, Grierson I, Trombetta C, Rahi AHS, Marshall J, McLeod
D. Retinal and epiretinal glia an immunohistochemical study. Br J
Ophthalmol 1984;68:698 707.
(6) Morino I, Hiscott P, McKechnie N, Grierson, I. Variation in
epiretinal membrane components with clinical duration of the proliferative
tissue. Br J Ophthalmol 1990;74:393 9.
Editor,
I read the paper by Liao et al with interest. It is indeed one of the biggest studies of mitomycin C in external DCR. I have few queries about how mitomycin C was
applied. Firstly, where should the pledget of mitomycin C be placed if the posterior flaps of the nasal mucosa and the sac are not sutured? My practice is to take a U-shaped flap of both the nasal mucosa and the lacrimal sac. Second...
Editor,
I read the paper by Liao et al with interest. It is indeed one of the biggest studies of mitomycin C in external DCR. I have few queries about how mitomycin C was
applied. Firstly, where should the pledget of mitomycin C be placed if the posterior flaps of the nasal mucosa and the sac are not sutured? My practice is to take a U-shaped flap of both the nasal mucosa and the lacrimal sac. Secondly, how is the cotton pledget removed after the 30 mins? Is it removed endoscopically?
Dear Editor
We have been conducting high volume cataract surgery (hospital-based with full fledged ophthalmic facilities) in rural parts of Maharastra state in India, conducting about 4000 to 5000 thousand sutureless cataract extractions with lens implantations in last 5 years.
Patients with mature cataract with vision not more than finger counting at 5 feet are selected. They all undergo routine eye exams and...
Dear Editor,
We appreciate the comments of Sridhar et al. regarding our letter: “The role of corticosteroids in fungal keratitis: a different view” published in your journal [1]. The authors comment on our recommendation for a gradual tapering of corticosteroids in cases where steroids were used for the treatment of initially misdiagnosed fungal corneal infections.
As mentioned in our cases rep...
Editor,
We read with interest the article by Culliance and Cleary on the method of prevention of visual field defects after macular hole surgery. In their series, one group of 82 eyes received conventional pars plana vitrectomy surgery with mechanical induction of posterior vitreous detachment (PVD) around the optic disc followed by complete posterior cortical vitreous removal. Twenty-two percent of these...
Dear Editor
I read with interest the World View article by Ezegwui et al.[1] entitled: "The Causes of Childhood blindness: results from schools for the blind in South Eastern Nigeria". Childhood blindness has profound consequences not only for the individual but for the family and community. Approximating the average life span at 60 years, the man-year loss caused by childhood blindness is roughly six-fold, which...
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We read with interest the article by Ebner et al [1] investigating the efficacy of periocular triamcinolone for the treatment of Thyroid Associated Ophthalmopathy (TAO) and the presence of ocular or systemic adverse effects also previously published in 2001 [2]. The study used patients with TAO of less than 6 months duration previously untre...
Editor,
We read with interest the Newsdesk piece in the March 2000 issue of the journal, commenting on recent studies indicating a conceptual shift in the understanding of the molecular basis of differential susceptibility to organ-specific autoimmune diseases. However, we were disappointed that the Newsdesk piece was restricted to studies of the animal model of multiple sclerosis and not that of uveitis....
Dear Editor
Castellarin and colleagues [1] recount their recent experience of infusing silicone oil in a small series of patients with advanced diabetic eye disease, either during primary vitrectomy (12 eyes) or after earlier surgery had failed (11 eyes). They compare their results with previous reports and conclude that silicone oil remains a useful adjunct in diabetic vitrectomy. However, their conclusions and h...
Dear Editor
Developmental mosaicism in the eye may follow the “lines of Blaschko” Ruggieri M et al. nicely described the ophthalmological manifestations in segmental neurofibromatosis type 1 [1]. They postulated that segmental NF1 is a somatic mosaicism for the NF1-gene expressing two different embryological tissues in the eye.
Previously we described a patient with unilateral sectorial hyperpigmented ski...
Dear Editor
The authors wish to thank Gandorfer and colleagues for their interest in our paper [1] and for the kind comments and encouragement with regard to our work. Certainly, these correspondents are compiling evidence concerning the effect of indocyanine green (ICG) on the retina in both their published and unpublished studies.[2,3]
In our report, we restricted our comments regarding retinal damage and...
Editor,
I read the paper by Liao et al with interest. It is indeed one of the biggest studies of mitomycin C in external DCR. I have few queries about how mitomycin C was applied. Firstly, where should the pledget of mitomycin C be placed if the posterior flaps of the nasal mucosa and the sac are not sutured? My practice is to take a U-shaped flap of both the nasal mucosa and the lacrimal sac. Second...
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