We read with interest the extended report by Hassell and colleagues
[1] demonstrating the adverse effect of quality of life in mild visual
impairment (<6/12) and worse. Their demonstration of the impact of
Age Related Macular Degeneration (AMD) on quality of life indices is an
important illustration of the difficulties experienced by the visually
impaired.
We read with interest the extended report by Hassell and colleagues
[1] demonstrating the adverse effect of quality of life in mild visual
impairment (<6/12) and worse. Their demonstration of the impact of
Age Related Macular Degeneration (AMD) on quality of life indices is an
important illustration of the difficulties experienced by the visually
impaired.
We have reported a similar experience in West Glamorgan (Wales,
United Kingdom) [2]. Our study comprised of 66 patients registered as
blind/partially sighted (59.1% because of AMD). The demographic
characteristics mirrored this study (mean age 81.33 (SD 9.87); 69.7%
female). We utilised an alternative index to the Impact of Vision
Impairment (IVI) questionnaire, the National Eye Institute Visual
Function
Questionnaire (NEI-VFQ 25) [3]. This has similar categories including
general health, general vision, ocular pain, near activities, distance
activities, social functioning, mental health, role difficulties,
dependency, colour vision, peripheral vision.
Hassell et al demonstrated a statistically significant restriction
in leisure and work, social and consumer interaction and household and
personal care difficulties between those with a mild/moderate compared
to the severely impaired group. This was our experience in the analogous
categories of social functioning (NEI-VFQ score 36.49% for the blind vs.
50% for the partially sighted; p = 0.0005) and dependency (NEI-VFQ score
30.07% for the blind vs. 46.98% for the partially sighted; p = 0.0003).
Furthermore, percentage scores in our study were less than 50% for all
categories except general health, ocular pain and peripheral vision for
the blind and partially sighted. Of the studies that have utilised the
NEI-VFQ in order to determine the extent of visual function, none have
previously demonstrated mean scores as low as our study (Brody et al
2001[4]; Klein et al 2001[5]). Hassell et al have therefore not only
demonstrated a worse quality of life in the severely visually impaired
(<6/60), but reinforce the important fact that all those with visual
impairment experience difficulties.
A second interesting finding in their paper was the absence of
correlation between duration of visual impairment and adaptation. We
found that the NEI-VFQ scores for those living alone were better than
for individuals living with someone for numerous categories including near
vision activities (20.9% vs. 15.3%, p=0.03), distant vision activities
(27.9% vs. 20.1%, p=0.056) and dependency (46.3 vs. 31.4%, p=0.004)
(Williams GP, Pathak-Ray V and Austin MW 2001, Unpublished Data).
This may imply that living alone forces people to adapt. We
interpreted this finding with caution however as a number of the people
'living with someone' resided in a nursing/residential home. This may
have occurred as a result living alone causing difficulties with coping in
the first instance.
Finally, their paper was undertaken before people had received low
vision services. Depressingly, our study found that there was incomplete
delivery of formal low visual aid assessment (n=44, 66%); of these 70%
found them to be of use. We therefore agree with the authors that not
only should there be consideration of referral to low visual services, but
adequate delivery and support is required in order to for it to be
effective.
Mr Geraint P Williams BSc, MRCOphth
Mrs Vanita Pathak-Ray FRCS (Ed)
Mr Michael W Austin FRCS, FRCOPhth
References
[1] Hassell JB, Lamoureux EL and Keefe JE. Impact of age related
macular degeneration on quality of life. British Journal of
Ophthalmology
2006;90:593-596
[2] Williams GP, Pathak-Ray V, Austin MW, Lloyd AP, Millngton IM
and
Bennett A. Quality of life and visual rehabilitation: an observational
study of low vision in West Glamorgan. Eye 2006 Feb 3 [Epub ahead of
print]
[3] Mangione CM, Lee PP, Gutierrez PR, Spritzer K, Berry S and
Hays
RD. Development of the 25-item National Eye Institute Visual Function
Questionnaire. Archives of Ophthalmology, 2001. 119(7):1050-8.
[4] Brody BL, Gamst AC, Williams RA, Smith AR, Lau PW, Dolnak D et
al. Depression, Visual Acuity, Comorbidity, and Disability Associated
with Age-related Macular Degeneration. Ophthalmology 2001;108(10)1893-
1900
[5] Klein R, Moss SE, Klein BEK, Gutierrez P and Mangione CM. The
NEI-VFQ-25 in People With Long Term Type-1 Diabetes Mellitus. Archives
of
Ophthalmology 2001;119:733-740.
We read with great interest the article published by Pate JC (1) in
your journal and the editorial (2), regarding polymicrobial infection of
cornea. Our centre is a tertiary level eye care centre in northern India
and also the apex centre for eye care of the country. We, in our
country come across a large number of fungal keratitis cases compared to
that
reported in western studies. Though the author...
We read with great interest the article published by Pate JC (1) in
your journal and the editorial (2), regarding polymicrobial infection of
cornea. Our centre is a tertiary level eye care centre in northern India
and also the apex centre for eye care of the country. We, in our
country come across a large number of fungal keratitis cases compared to
that
reported in western studies. Though the authors rightly state that the
findings
reported by them may not be generalized to populations like ours, we
would like to share our view. As a part of a recent project on fungal
keratitis, we
studied 76 eyes of presumed fungal keratitis in the last 1 year duration
prospectively. The pattern of polymicrobial infection was analyzed as
well.
The criteria mentioned for diagnosing the co-infection by Pate JC
(1)
were similar in our study. Of a total 76 eyes only 20 (26%) were proven
to have fungal keratitis by culture. Of these 20, pure fungal
infection was detected only in 5 (25%) and the remaining 15 had
bacterial co-infection (75%). The isolation of yeast is much
less in our country in contrast to that of western literature. Also
there
is intracountry variation in geographical distribution of filamentous
fungi such as Aspergillus and Fusarium. At our center, in northern
India,
the isolation of Aspergillus heads the list.
While the authors reported bacterial co-infection in 10% and 20% of
Moniliaceous and Dematiaceous filamentous fungi respectively, we found
66% and 100%. However, we feel that high percentages of co-
infection in our study could be attributed to small sample size.
The authors have also commented that the prevalence
may be due to a number of factors such as nonconformity in microbial co-
isolation, climatic effect, history of trauma, ocular
surface integrity, and prior therapy. The first factor was ruled
out in our study as the microbial co-isolation was carefully evaluated
in
our microbiology lab. The climatic effect did not show any correlation.
It
is not possible to comment on ocular surface as a negligible number of
eyes
with ulcer had associated ocular surface abnormalities. Though, 60%
&
86.6% of eyes with polymicrobial co-infection revealed a history of
trauma
and prior drug therapy respectively the same could not be compared with
that of growth without co-infection as the number of eyes was only 5. We
are in concurrence with our earlier reports (3,4) and that of the
authors
(1,2) that coexistence of Staphylococcal infection is most commonly
found
along with fungal infection . The authors have expressed their view that
there may be a mutual alliance for the co-pathogens. Tuft (2) has
commented about the super infection with a second organism which is
attributed to the inhibition of the local immune response by the topical
corticosteroid. This is an important aspect to note as the patients with
keratitis when referred to the tertiary center with extensive and non
responsive infection are found to be on topical corticosteroid sometime
or
other during course of the disease.
At the end, we congratulate the authors for bringing this important
issue to light so that clinicians may effectively manage polymicrobial
co-infection.
Table 1.
Isolate
Proven fungal case
Bacterial co-infection
Moniliaceous filamentous fungi
15
10 (66%)
Dematiaceous filamentous fungi
5
5 (100%)
Total
20
15
References
1. Pate J C, Jones DB, Wilhelmus KR. Prevalence and spectrum of
bacterial co-infection during fungal keratitis. Br J Ophthalmol 2006;
90:289-92.
2. Tuft S. Polymicrobial infection and the eye- Has important
management implications. Br J Ophthalmol 2006; 90:57-58.
3. Satpathy G, Vishalakshi P. Ulcerative keratitis: microbial
keratitis and sensitivity pattern-a five year study. Ann Ophthalmol 1995;
27:301-6.
4. Khanal B, Deb M, Panda A, et al. Laboratory diagnosis in
ulcerative keratitis. Ophthalmic Res 2005; 37:123-7
I have just finished reading the interesting paper by Daniell et al
and, being one of the first authors (Secchi AG et al, AJO, 1990, 110,
137-
42) to become interested in the topical use of Cyclosporine A in
"allergic" conditions concerning the ocular surface, I would like to
make
a few comments - based above all on a 20-year experience in the
treatment
of vernal keratoconjunctivitis (VKC) with topi...
I have just finished reading the interesting paper by Daniell et al
and, being one of the first authors (Secchi AG et al, AJO, 1990, 110,
137-
42) to become interested in the topical use of Cyclosporine A in
"allergic" conditions concerning the ocular surface, I would like to
make
a few comments - based above all on a 20-year experience in the
treatment
of vernal keratoconjunctivitis (VKC) with topical Cyclosporine A as my
first line prescription in over 1,000 patients.
I am certainly not the only one to use this
approach. Colleagues throughout the world use
topical Cyclosporine A in the treatment of VKC and, particularly in the
limbal forms. The tarsal forms usually
improve in as little as ten days of treatment as far as symptoms are
concerned, the mucus disappears, the giant papillae remain on the
contrary more or less unchanged, as the corneal sterile ulcers do. No
side
effects have been noticed even after years of treatment, beside some
corneal mild epitheliopathy and a frequent burning sensation upon
instillation, which often disappears within a few weeks. My personal
experience is that topical Cyclosporine A, on the overall, really
changes
the life in most cases of VKC patients.
Allergic keratoconjunctivitis (AKC) seems to be a rather different
story. The effect of topical CsA
is minimal, well below that of topical steroids, and in many cases good
results are obtained only with systemic use of the drug.
The results presented by our Australian colleagues seems to be, in
VKC cases, opposite to our observations. No statistical difference has
been found between Restasis and the placebo, neither for symptoms nor
for
signs. The reason, in my opinion, is that a 0.05 % concentration of
Cyclosporine A such as that present in Restasis is far too low for being
active in VKC patients. We use with full satisfaction, as do our
colleagues, a 1 to 2 % concentration
in either olive or maize oil. In maintenance regimens even a 0.5% may be
active. Lower concentrations, on the contrary, are not effective at
all.
Restasis, as a major fact, is intended neither for VKC nor for AKC.
Its off-label use in these clinical conditions is substantially
ineffective, as our Australian colleagues have clearly confirmed.
I quite agree on the Authors' last sentence "not to recommend
Restasis
eye drops in steroid dependent allergic conjunctivits", but I strongly
disagree on "tempering our enthusiasm": It is not topical CyclosporineA
which has been shown not to be useful in VKC, it is Restasis! Will
Allergan eventually provide a stronger topical preparation of
Cyclosporine A? There
are millions of patients suffering for VKC in the world, and steroids
are not the answer while even last-
generation antiallergic multivalent drugs are most often not effective
enough!
Antonio G. Secchi MD
Professor of Ophthalmology and Director
Department of Ophthalmology
University of Padua, Italy
School of Medicine
ag.secchi@unipd.it
Reference:
AG Secchi, MS Tognon, A Leonardi
Topical Use of Cyclosporine in the Treatment of Vernal
Keratoconjunctivitis
Am J Ophthal 1990, 110, 137-142.
We are deeply concerned by the conclusion made
by Vu et al that “there was a harmful effect of higher LZ intake on AMD
among those with high level of linoleic acid intake. Based on these data LZ
supplementation could not be recommended”.1 It is
counterintuitive, and goes against the evidence currently available in the
literature.2,3 The most likely explanation is that their results
reflect the success of the public health messages put out to patients with AMD
about eating foods high in antioxidants, such as green leafy vegetables and
spinach. This important message is in danger of being undermined by such
pronouncements.
It is our opinion that the letters section
of a medical journal is not the place to publish contentious nutritional
epidemiological data. It is too complex, and the limitation on the number of
words does not allow an adequate disclosure of methods and results, or an appropriate
depth of discussion. The readers, therefore, are not able to properly interpret
the data. This type of article cannot be properly peer reviewed without the
submission of much more data than was given in this case.
There are a number of problems with this
study.The possibility of selection
bias is a particular concern where the study is evaluating only 65 % of the
original target population and is only examining crossectional data. The
statistical method used to calculate the odds ratios was not given, although it
could be assumed that a logistic regression model would have been applied. A close
examination of the results indicates that there were only 4 cases of late AMD
in the higher than median linoleic acid group (table 1). The odds ratio of 4.72
at a significance level of 0.005 for the effects of adjusted daily LZ intake on
the prevalence of late AMD was based on these four cases. Regardless of the
validity of the statistical methods, it needs to be borne in mind that a
conclusion with major public health implications was based on such few cases. The
food frequency questionnaire used in this study was not validated for the key
variables, linoleic acid and LZ intake.4 The use of a single self-reported
instrument for the estimation of lutein intake is subject to large biases and
error, and has the lowest validity for lutein as opposed to the other
carotenoids.5 These possible confounders are present in addition to
the possibility of a dietary change towards higher LZ intake after the
diagnosis of AMD.
Table1. The estimated numbers of subjects
based on reported Odds Ratios
.
Group
Low
linoleic
High
linoleic
OR
Late
AMD
32
4
0.11
Early
AMD
102
45
0.44
Any
AMD
134
49
0.35
Non
AMD
852
937
total
986
986
Table legend: These estimates were based on
the odds ratios (OR) reported for all participants graded using Wisconsin definitions. The median daily linoleic acid
intake of 7.17 g divides the population into equal numbers of 986 cases. The OR
is calculated as the ratio between high and low linolieic acid intake groups,
of the odds of disease occurring in each group. The odds itself is the ratio
between the number of cases with and without disease. Due to the large number
of cases without disease, compared to the number with disease, the OR can be
approximated by the simple ratio of the number of cases with disease between
high and low linoleic acid groups.
Notwithstanding this, in order to better
understand the significance of the results, we need to know (a) more details on
how linoleic acid and LZ intake were calculated, and in particular, the chief
food sources of these variables; (b) whether the separate food items confirm
the trend; (c) what the demographics of the subset of patients with an above
median linoleic acid and high LZ intake were; (d) how many of this subset were
aware of their diagnosis; (e) whether more patients with AMD returned the food
frequency questionnaire than those without; (f) and how the ophthalmologic
diagnosis of AMD was validated.
Strong conclusions made in this article are
not justified by the provided data. Their publication creates confusion and
undermines professional, government and public confidence in the validity of other
data with great potential public health benefits. It takes enormous time,
effort and resources to educate the public on preventative lifestyle changes.
We must ensure that the messages to the public remain clear and consistent, and
that new findings are put through a process of rigorous examination to confirm
their validity. It appears that, in this case, the process may have failed.
References
1.Vu,
H. T.Robman, L.McCarty, C. A.Taylor, H. R.Hodge, A. Does dietary lutein and
zeaxanthin increase the risk of age related macular degeneration? The Melbourne
Visual Impairment Project. Br J Ophthalmol 2006:90:389-390
2.Seddon
JM, Ajani AU, Sperduto RD, et al. Dietary carotenoids,
vitamins A, C, and E, and advanced age-related macular degeneration. Eye
Disease Case-Control Study Group. JAMA 1994;272:1413–1420.
3.Cho
E, Seddon JM, Rosner B, et al. Prospective study of intake of fruits,
vegetables, vitamins, and carotenoids and risk of age-related maculopathy. Arch
Ophthalmol 2004;122:883–892.
4.Hodge
A, Patterson AJ, Brown WJ, et al. The AntiCancer Council of Victoria FFQ: relative validity of nutrient
intakes compared with weighed food records in young to middle-aged women in a
study of iron supplementation. Aust N Z J Public Health 2000;24:576–583.
5.Natarajan
L,Flatt WF,Xlaoying S, et al Validity and systematic error in measuring
carotenoids consumption with dietary self reported instruments Am J EpidemiolMarch 2006 (in print)
We would like to commend authors for describing a modification to
surgical technique for insertion of Molteno tube implant that eliminates
the need for a donor patch scleral graft.1 The purpose of this
modification is laudable however we do envisage few surgical difficulties
with this modification. Firstly the creation of scleral tunnel using a
curved 20 gauge microvitreoretinal (MVR) blade creat...
We would like to commend authors for describing a modification to
surgical technique for insertion of Molteno tube implant that eliminates
the need for a donor patch scleral graft.1 The purpose of this
modification is laudable however we do envisage few surgical difficulties
with this modification. Firstly the creation of scleral tunnel using a
curved 20 gauge microvitreoretinal (MVR) blade creates risk of mismatch
between the curve of the globe and that of MVR blade and thus a risk of
inadvertent intraocular entry and damage to ciliary body or lens.
Secondly the entry created by 20 gauge MVR blade is likely to be
significantly larger than the outer diameter of the anterior chamber tube
leading to aqueous leak around the tube entry into AC. This may increase
the risk of shallow AC and hypotony in early post-operative period. This
may have contributed to the frequent occurrence of corneal decompensation
(20.6%) in this case series.
We believe that the traditional partial thickness scleral flap has
some benefits over the scleral tunnel technique. There is no need for the
scleral patch graft with partial thickness scleral flap. All glaucoma
surgeons and most general ophthalmologists are familiar with this
technique. Furthermore it allows the creation of AC entry under direct
supervision using 22 gauge bent needle, ensuring the accurate placement of
the tube in the AC and snug fit between the tube and entry site. Ability
to visualize the entry site is important particularly for Ophthalmologists
in their early years of Glaucoma surgery training.
Dr S P Deokule, MS, FRCSEd, FRANZCO
Prof ACB Molteno, FRCSEd
Refrences
1. J K Leong, P McCluskey, S Lightman, H MA Towler. Outcome of graft
free Molteno Tube Insertion. Br J Ophthalmol 2006;90:501-505
2. ACB Molteno, MMB Van Rooyen, R Bartholomew. Implants for draining
neovascular glaucoma. Br J Ophthalmol 1977;61:120-125.
We read with great interest the report by Singh et al,1 describing the management of
subretinal macular haemorrhage by vitrectomy, subretinal injection of tissue
plasminogen activator (tPA) and pneumatic tamponade. Our experience with this
techinque has also been positive, and this approa...
We read with great interest the report by Singh et al,1 describing the management of
subretinal macular haemorrhage by vitrectomy, subretinal injection of tissue
plasminogen activator (tPA) and pneumatic tamponade. Our experience with this
techinque has also been positive, and this approach has replaced intravitreal tPA injection after vitrectomy and partial fluid-gas
exchange, or pneumatic displacement without vitrectomy, as the preferred
management of submacular haemorrhage in our unit. In most cases, the
haemorrhage is sufficiently displaced by two weeks to allow angiographic
studies and definitive treatment decisions to be made.
There are some notable differences between our approach and
the methods described by the authors. The concentration of 12 µg per 0.1
ml is significantly lower than the concentration we have used, which is 50
µg per 0.1 ml. We are not aware of any study that showed an optimal
concentration of tPA for subretinal injection, but this concentration has been
shown to be safe in experimental in vivo studies.2-4The authors
would have needed to inject 0.4 ml to reach the target dosage of 48 µg,
which is a large volume for a subretinal injection. There could be an argument
for a smaller injection volume to minimise distortion of the retinal
architecture. We aim to inject at the edge of the haemorrhage, rather than
directly into the body of the clot, in order to avoid detaching the fovea
further. The injection is performed under direct vision, with the end point
being an encirclement of the haemorrhage by the newly introduced subretinal
fluid.
We have not found it necessary to create a separate retinotomy
before the injection of tPA. We have most commonly used
a 32-gauge needle (Glaser Subretinal Injector, BD Ophthalmic Systems, Warks, United
Kingdom), which enables a direct injection
into the subretinal space with minimal trauma. However, we have found that the
needle allowed a significant amount of reflux of tPA
into the vitreous cavity. More recently, we have used a 41-gauge subretinal
needle (Storz Retinal Cannula 20G/41G, Bausch & Lomb, Rochester, United States) with great success,
which allows a precise placement of the bleb with minimal reflux.
We prefer SF6 20 % tamponade as it is our
impression that the haemorrhage takes at least one week to be displaced. A
comparative study with air would be useful. We have used SF6 10 % for
smaller haemorrhages.
Without treatment, the prognosis for submacular haemorrhage
is poor. Pneumatic displacement offers the means for an effective displacement of
submacular haemorrhage. With intravitreous tPA injection 5, and non-vitrectomy pneumatic
displacements reporting high success rates,6 we agree with the
authors’ conclusion that further studies will be needed to elucidate the
best approach of managing this difficult problem.
References
1.Singh
RP, Patel C, Sears JE. Management of subretinal macular
haemorrhage by direct administration of tissue plasminogen activator.Br J Ophthalmol 2006;90(4):429-431.
2.Benner
JD, Morse LS, Toth CA, Landers MB, 3rd, Hjelmeland LM. Evaluation
of a commercial recombinant tissue-type plasminogen activator preparation in
the subretinal space of the cat.Arch
Ophthalmol 1991;109(12):1731-1736.
3.Irvine
WD, Johnson MW, Hernandez E, Olsen KR. Retinal toxicity of human tissue
plasminogen activator in vitrectomized rabbit eyes. Arch Ophthalmol 1991;109(5):718-722.
4.Johnson
MW, Olsen KR, Hernandez E, Irvine WD, Johnson RN. Retinal
toxicity of recombinant tissue plasminogen activator in the rabbit.Arch Ophthalmol 1990;108(2):259-263.
5.Hassan
AS, Johnson MW, Schneiderman TE, et al. Management of submacular hemorrhage
with intravitreous tissue plasminogen activator injection and pneumatic
displacement. Ophthalmology 1999;106(10):1900-6; discussion 1906-1907.
6.Hattenbach
LO, Klais C, Koch FH, Gumbel HO. Intravitreous injection of tissue plasminogen
activator and gas in the treatment of submacular hemorrhage under various conditions.
Ophthalmology 2001;108(8):1485-1492.
I applaud the authors for attempting to address the issue of
microbial contamination of preservative free (PF) eye drops in multiple
application containers but wish to highlight a few points.
Although informed consent have been obtained from patients prior to
analysing their eye drops, it is surprising that ethical committee
approval was not sought before starting the study.
I applaud the authors for attempting to address the issue of
microbial contamination of preservative free (PF) eye drops in multiple
application containers but wish to highlight a few points.
Although informed consent have been obtained from patients prior to
analysing their eye drops, it is surprising that ethical committee
approval was not sought before starting the study.
The authors have stated that the ‘safety period for multidose
containers is arbitrary … not evidence based’. However, Oldham et al1
tested 21 different unpreserved multidose eyedrop formulations to
establish their inherent efficacy in antimicrobial preservation and
concluded that once opened by individual patients in a domiciliary
situation, a 7 day in use storage life is confirmed for unpreserved eye
drops containing alkaloids or antibiotics, if they are stored in the
refrigerator after opening.
There has been no mention of any exclusion criterion in the selection
of patients. Previous studies evaluating the issue of contamination of eye
drops have either excluded patients with infected ocular surface
disorders2,3 or have taken a conjunctival / corneal swab4 to evaluate
whether the same microorganism was recovered from the conjunctiva and from
the contaminated medication. Also, as rightly pointed out by Sher A Aslam
et al5, it has been assumed in the study that the multidose containers
were sterile at the time of dispensation. These two factors may invalidate
the actual incidence of contamination of the eye drops in the study. Also,
it does not throw any light as to whether all the contaminants isolated
were truly exogenous or not.
Apparently elderly patients and those with reduced visual acuity or
coordination are the ones who are most likely to inadvertently touch the
tip of the dropper to the external suface. Also, the incidence of
contamination of an eye drop which is being used hourly is more likely
than one which is being used two or three times a day. Hence it would be
interesting to know whether there is a correlation between age, visual
acuity and frequency of administration of drops and incidence of
contamination. Ultimately the onus remains on the medical practitioner to
ensure that the unpreserved multidose eyedrops are only used in
appropriate circumstances to ensure safe and effective therapy. Therefore,
any significant finding in this regard may raise a question as to whether
it is good practice to prescribe unpreserved multidose eyedrops to these
vulnerable group of patients.
REFERENCES
----------
1. Oldham GB, Andrews V. Control of microbial contamination in
unpreserved eyedrops. Br J Ophthalmol. 1996 Jul;80(7):588-91
2. Livingstone DJ, Hanlon GW, Dyke S. Evaluation of an extended
period of use for preserved eye drops in hospital practice. Br J
Ophthalmol. 1998 May;82(5):467.
We read with interest the article by Rahman and coauthors but wish to
highlight a number of points.
With regards to the aim of the study which was to evaluate and
compare microbial contamination arising after 3 days and 7 days use of
preservative free eye drops, this was not apparent from the study design.
There was no stratification of data according to these two time periods;
it would be i...
We read with interest the article by Rahman and coauthors but wish to
highlight a number of points.
With regards to the aim of the study which was to evaluate and
compare microbial contamination arising after 3 days and 7 days use of
preservative free eye drops, this was not apparent from the study design.
There was no stratification of data according to these two time periods;
it would be interesting to learn how contamination changes per unit time,
thus it may have been better to evaluate samples from bottles serially
form day 1 to day 7.
The authors identified a number of contaminating micro-organisms. It
would be helpful to express the relative frequency with which these
organisms were found in the inpatient and outpatient setting. Furthermore,
no evaluation was made of the rate of contamination inherent in
preservative free bottles at the time these bottles were dispensed.
Rather, an assumption was made that all unpreserved bottles were
uncontaminated.
The identity of micro-organism per agent in each bottle was not shown
which would otherwise strengthen the discussion point about which drops
should be prescribed with greater caution. Inclusion of coagulase negative
staphylococcus in the results to show a contamination rate of 8.4% is
misleading since, as the authors correctly point out, this is a normal
conjunctival commensal.
Finally, Rahman et al. point out the pathogenic potential in
instilling contaminated eye drops onto the ocular surface. It would have
been of interest to take conjunctival swabs from all patients applying the
drops in order to determine whether there was any cross contamination
between bottle and ocular surface.
We were interested to see the letter by Mitchell et al, written in
response to our earlier publication [1].
Mitchell and co-workers raise several points, the first of which is
the
way one handles missing data. AMD can be assessed either clinically or
photographically. Rather than throw away data and run the potential of
bias by excluding patients who did not have a retinal photograph, we
c...
We were interested to see the letter by Mitchell et al, written in
response to our earlier publication [1].
Mitchell and co-workers raise several points, the first of which is
the
way one handles missing data. AMD can be assessed either clinically or
photographically. Rather than throw away data and run the potential of
bias by excluding patients who did not have a retinal photograph, we
chose
to include in our analysis those people for whom we did not have a
retinal
photograph for one reason or another but for whom we had clinical
macular
grading. In separate analyses the data were not materially different if
the analysis was confined to only those with photograding. In the data
Mitchell et al report they excluded 15% of their sample as they lacked
data and
there is no evidence of what bias this may have induced.
We were very pleased to see the data from the Blue Mountains Study
and recognise the advantage of incidence data over cross-sectional data.
However, both cross sectional and longitudinal studies are susceptible
to
recall bias in the ascertainment of historical dietary intake. In
nutritionally non-deficient populations people do alter their diets in
response to the available commercial information. However, the bias
caused
by public awareness of hypothesized protective associations applies
equally to both cross-sectional and longitudinal observational studies,
as
many know about either their disease or family predisposition to AMD
before participation. However, our data were collected before the recent
upsurge in publicity given to the use of nutritional supplement for
macular degeneration.
The most striking thing from the data presented by Mitchell et al
is
that they show no evidence of a protective effect of dietary or
supplement
intake of Lutein and Zeaxanthin. The consistent finding of these two
population-based studies must seriously challenge the association
reported
by previous case control studies. Case control studies are always
strongly
influenced by the possibility of bias in selection of controls and may
frequently be influenced by the bias in the selection of. The fact that
the dietary intakes in the two population-based studies is so much lower
than the volunteer case control studies clearly indicates "healthy
volunteer bias" as we point out in our paper (Vu et al).
The lack of effect modification by linoleic acid found in the BMES
data is interesting and possibly not surprising. We found a complex U-
shaped interaction between dietary intake and the risk of AMD and the
decision as to where cut points are taken will strongly influence the
outcome (Fig 1). It would be more informative if Mitchell et al
presented
their data either with the same cut points that we had used, or
presented
their data in a continuous form.
Nevertheless, these two studies confirm the lack of evidence to
support recommendations for a specific increase in dietary intake of
Lutein and Zeaxanthin to protect against macular degeneration. At the
same
time of course no one would encourage people to deviate from a normal
healthy diet including fresh fruit and vegetables.
(Vu et al, Br. J. Ophthalmol, Mar 2006; 90: 389 - 390)
Luba Robman
Allison Hodge
Catherine A McCarty
Hugh R Taylor
References
1. Vu HTV, Robman L, McCarty CA, Taylor HR, and Hodge A. Does dietary
lutein and zeaxanthin increase the risk of age related macular
degeneration? The Melbourne Visual Impairment Project. Brit. J.
Ophthalmol, 2006; 90: 389-390.
There appear to be a number of questions with the regard to the
findings reported by Hrisos et al:[1]
1. The study could not distinguish between amblyopia and other forms
of “unilateral visual impairment,” but groups all cases together. This
limits the study’s utility in demonstrating the functional effects of
amblyopia.
2. The paper describes its acuity testing only as a "Snell...
There appear to be a number of questions with the regard to the
findings reported by Hrisos et al:[1]
1. The study could not distinguish between amblyopia and other forms
of “unilateral visual impairment,” but groups all cases together. This
limits the study’s utility in demonstrating the functional effects of
amblyopia.
2. The paper describes its acuity testing only as a "Snellen based
vision test." The citation given is Sheridan's STYCAR test (reference #
11). If that test was in fact used by Hrisos et al., the accuracy of the
study's acuity measurements in amblyopes is open to question, in view of
that test’s lack of crowding, which is critical to accurate acuity
measurement in amblyopes.[2]
3. My major concern with this paper, however, is the question of
whether its sample of nominally visually impaired children in fact had
visual acuity significantly worse than that of the normal sample. Thus:
(a) The Results section states that four children with normal acuity
in both eyes were included in the impaired vision sample. The abstract
and Results section state that the unilaterally impaired children had
acuity as good as 6/6 in their worse eye. (The Methods section states that
their acuity was as good as 6/9, but if visually normal children were
included in the impaired vision sample, the 6/6 figure would appear
correct.)
(b) Only straight-eyed patients were used, which means that, to the
extent amblyopes were included in the sample, they were anisometropic
amblyopes. Of the 30 children in the “unilaterally impaired” group, 10
had been in glasses for up to 6 weeks, and 5 for more than 12 weeks, at
the time of the study. In other words, half the sample had been so
treated. Since glasses alone will improve acuity in some anisometropic
amblyopes, [3, 4] if any of these refractively corrected “impaired”
children had been amblyopic, the amblyopia may have been mitigated.
(c) The median acuity of the unilaterally impaired sample’s worse
eyes, uncorrected, was 6/12, which would be considered normal acuity for
the younger children in the sample by some standards.[5]
(d) The authors report that poorer amblyopic eye acuities were
significantly under-represented in their sample.
(e) Interpretation is complicated by the fact that the children
wearing glasses were classified on the basis of acuity testing done
without correction which, as the authors themselves note, may have
produced a treatment effect.
4. Another difficulty with this study lies in the stereotest used,
the Randot 2 Circles test.
(a) Stereo tests such as the Randot 2, with visible contours (i.e.
with notable low spatial frequency content and of parafoveal or larger
diameter), are able in many cases to be passed by anisometropic
amblyopes.[2, 6] Here again, as in the case of the visual acuity
measure, to the extent this occurred it would reduce the apparent
difference between the nominally visually impaired and normal subjects.
(b) Further complicating the matter is the finding of anomalous
responses to the Randot test in some subjects in both the impaired and
normal study groups (see Table 2[1]). Similar anomalies have been
reported in a previous study.[7] Three of the five such subjects had 6/6
to 6/12 acuity but failed the stereotest and so were assigned a 600 arc-
second “notional” threshold, which would, again, tend to reduce the
apparent difference between the impaired and normal groups.
(c) Anisometropic amblyopia is a condition apparently more benign
than strabismic amblyopia,[3] and thus more likely to achieve normal or
near-normal stereopsis than would strabismic amblyopes. If the patients in
the "visually impaired" sample were such amblyopes, those fit with glasses
may have had their stereoacuity improved as well as their visual
acuity.[3, 4]
In summary, the Hrisos et al.[1] study’s failure to find a “visuo-
motor integration” function difference between its nominally visually
impaired and normal samples may have been due to the two samples’ acuities
not in fact being significantly different. On the other hand, the
association that was found between stereoacuity and “visuo-motor
integration” functions may have underestimated what would have been a
stronger association if the stereoacuity difference between the two groups
had not been reduced by the artifacts noted.
Kurt Simons, Ph.D.
Krieger Children’s Eye Center
The Wilmer Institute
Johns Hopkins Hospital
Baltimore, MD 21287
References
1. Hrisos S, Clarke MP, Kelly T, Henderson J, Wright CM. Unilateral
visual impairment and neuro-developmental performance in pre-school
children. Br J Ophthalmol, 2006.
2. Simons K. Major review. Preschool vision screening: rationale,
methodology and outcome. Surv Ophthalmol 1996;41: 3-30.
3. Simons K. Amblyopia characterization, treatment, and prophylaxis.
Surv Ophthalmol 2005;50: 123-66.
4. Steele AL, Bradfield YS, Kushner BJ, France TD, Struck MC, Gangnon
RE. Successful treatment of anisometropic amblyopia with spectacles alone.
J AAPOS 2006;10: 37-43.
5. Williams C, Harrad, RA, Harvey, I, et al. Screening for amblyopia
in preschool children: Results of a population-based, randomised control
trial. Ophthal Epidemiol 2001;8: 279-295.
6. Fawcett SL. An evaluation of the agreement between contour-based
circles and random dot-based near stereoacuity tests. J AAPOS 2005;9: 572-8.
7. Lam SR, LaRoche R, DeBecker I, Macpherson H. The range and
variability of ophthalmological parameters in normal children aged 4 1/2
to 5 1/2 years. J Ped Ophthalmol Strab 1996;33: 251-56.
Dear Editor
We read with interest the extended report by Hassell and colleagues [1] demonstrating the adverse effect of quality of life in mild visual impairment (<6/12) and worse. Their demonstration of the impact of Age Related Macular Degeneration (AMD) on quality of life indices is an important illustration of the difficulties experienced by the visually impaired.
We have reported a similar exper...
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We read with interest the article by Rahman and coauthors but wish to highlight a number of points.
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Dear Editor,
We were interested to see the letter by Mitchell et al, written in response to our earlier publication [1].
Mitchell and co-workers raise several points, the first of which is the way one handles missing data. AMD can be assessed either clinically or photographically. Rather than throw away data and run the potential of bias by excluding patients who did not have a retinal photograph, we c...
Dear Editor,
There appear to be a number of questions with the regard to the findings reported by Hrisos et al:[1]
1. The study could not distinguish between amblyopia and other forms of “unilateral visual impairment,” but groups all cases together. This limits the study’s utility in demonstrating the functional effects of amblyopia.
2. The paper describes its acuity testing only as a "Snell...
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