We welcome Loon SC et al's article [1]. Earlier, we published our
finding of the SARS CoV in specimens collected by the novel technique of
conjunctiva upper respiratory tract irrigation (CURTI), but not in paired
nose and throat swabs, very early in the course of the disease [2]. In
designing CURTI, we considered safety to medical personnel but also, in
finding a method that samples all three portal...
We welcome Loon SC et al's article [1]. Earlier, we published our
finding of the SARS CoV in specimens collected by the novel technique of
conjunctiva upper respiratory tract irrigation (CURTI), but not in paired
nose and throat swabs, very early in the course of the disease [2]. In
designing CURTI, we considered safety to medical personnel but also, in
finding a method that samples all three portals of entry for upper
respiratory viral pathogens ¡V the eyes, nose and mouth. Loon et al's
finding now complements our study by showing that SARS CoV indeed can be
found in tears.
While we agree with their conclusion that the ability to isolate the
virus early in the course is important, we do not feel that the eyes are
important organs that propagate the virus, other than to ophthalmologists
and to unwary close contacts. For instance, the eyes cannot generate
infectious aerosol. Rather, we feel that the eyes are important portals of
entry and have not been given sufficient attention - witness medical
personnel in full personal protection gears and N95 masks but without
watertight goggles, and sometimes without splashguards at all.
We also feel that employing the services of ophthalmologists for the
purpose of collecting tear specimens for the diagnosis of SARS is
difficult to achieve in most medical environments. On the other hand, our
method of CURTI is entirely self-help, deployable to quarantine locations,
and avoids unnecessary contact between an infectious source and
susceptible individuals.
The finding of SARS CoV in tear raises several additional questions:
1. How does the virus end up in the tear? Was it due to direct
inoculation at the time of infection to permissive conjunctival epithelial
cells, either by hands or aerosols, or was it the result of secretion from
a lacrimal gland infected hematogenously? The lacrimal glands are not very
different anatomically from the salivary glands. Yet saliva has been shown
to be a poor specimen for the laboratory diagnosis of SARS.[3]
2. Was there any evidence of conjunctivitis, lacrimitis, or evidence
of infection of the globe or nasolacrimal sac?
3. Is there any means or advantage in sampling the nasolacrimal sac,
to which the tear drains, and could the nasolacrimal duct system be itself
a hideout for the SARS CoV during the incubation period?
References
(1) Loon SC, Teoh SC, Oon LL, Se-Thoe SY, Ling AE, Leo YS, Leong HN.
The severe acute respiratory syndrome coronavirus in tears. Br J
Ophthalmol. 2004 Jul;88(7):861-3.
(2) Tong TR, Lam BH, Ng TK, Lai ST, Tong MK, Chau TN. Conjunctiva-
upper respiratory tract irrigation for early diagnosis of severe acute
respiratory syndrome. J Clin Microbiol. 2003 Nov;41(11):5352.
(3) Drosten C, Chiu LL, Panning M, Leong HN, Preiser W, Tam JS,
Gunther S, Kramme S, Emmerich P, Ng WL, Schmitz H, Koay ES. Evaluation of
Advanced Reverse Transcription-PCR Assays and an Alternative PCR Target
Region for Detection of Severe Acute Respiratory Syndrome-Associated
Coronavirus. J Clin Microbiol. 2004 May;42(5):2043-7.
We read with interest the article by Aisenbrey et al [1] who have described the results of surgical treatment of peripapillary choroidal neovascularisation in eight patients.
As reported, peripapillary choroidal neovascularisation is a relatively uncommon entity that can be a variant of macular choroidal neovascularisation in elderly patients.
Accordingly to the MPSG[2], early small peripapilla...
We read with interest the article by Aisenbrey et al [1] who have described the results of surgical treatment of peripapillary choroidal neovascularisation in eight patients.
As reported, peripapillary choroidal neovascularisation is a relatively uncommon entity that can be a variant of macular choroidal neovascularisation in elderly patients.
Accordingly to the MPSG[2], early small peripapillary choroidal neovascularisation should be first treated with red thermal laser photocoagulation. If applied by an experienced specialist the risk of burning the interpapillomacular bundle is limited.
However, the therapeutical approach is more delicate for laser resistant, extended and/or very exsudative peripapillary choroidal neovascularisation.
In their study, Aisenbrey et al report good clinical outcome after surgical treatment. Nevertheless, as published by Rosenblatt et al [3], photodynamic therapy with Verteporfin can also be a good option because of its efficacy and very limited risk. This is also our clinical experience.
Figure 1 shows the left eye of a male patient in his early seventies with very exsudative peripapillary choroidal neovascularisation before and one year after one photodynamic therapy with Verteporfin. The current parameters for choroidal neovascularisation and a spot of 4200 µ covering a great part of the optic nerve were used. This case looks very similar to the illustrated case of Aisenbrey et al, except the fact that we first unsuccessfully tried to treat the lesion with thermal laser.
Figure 1: left eye of a male patient in his early seventies with very exsudative peripapillary choroidal neovascularisation before (a) and one year after one photodynamic therapy with Verteporfin (b).
Figure 1a
Figure 1b
In our experience with Verteporfin we have never noted any clinical damage to the optic nerve after partial exposition and it has been shown by Schmidt-Erfurth et al [4] that optic nerve can be exposed to a light dose twice as high as conventionally used without showing histopathological alterations.
Regarding the potential major risks of the surgical approach of peripapillary choroidal neovascularisation we suggest that PDT could be the first therapeutical choice in these cases.
References
1. Aisenbrey S, Gelisken F, Szurman P, et al. Surgical treatment of
peripapillary choroidal neovascularisation. Br J Ophthalmol 2007;91:1027- 1030.
2. The Macular Photocoagulation Study Group. Laser photocoagulation
for neovascular lesions nasal to the fovea. Results from clinical trials for lesions secondary to ocular histoplasmosis or idiopathic causes.
Macular Photocoagulation Study Group. Arch. Ophthalmol. 1995; 113:56-61.
3. Rosenblatt BJ, Shah GK, Blinder K. Photodynamic therapy with
verteporfin for peripapillary choroidal neovascularisation. Retina. 2005; 25:33-37.
4. Schmidt-Erfurth U, Laqua H, Schlotzer-Schrehard U, et al.
Histopathological changes following photodynamic therapy in human eyes.
Arch. Ophthalmol. 2002 Jun; 120(6):835-44.
In the recent article published in British Journal of Ophthalmology,
Agrawal et
al1
reported two cases of desegmentation of Ozurdex implant in vitreous
cavity.
In this report, the authors comment that Allergan confirmed that fractured
implants in the applicator have not been found to date during the quality
control
process.
We recently reported2
also two cases of implant fragmentation in response t...
In the recent article published in British Journal of Ophthalmology,
Agrawal et
al1
reported two cases of desegmentation of Ozurdex implant in vitreous
cavity.
In this report, the authors comment that Allergan confirmed that fractured
implants in the applicator have not been found to date during the quality
control
process.
We recently reported2
also two cases of implant fragmentation in response to a
Roy et al3
. These authors reported a broken implant at the end of the injection.
They postulate that the reason for breakage could be friction at the tip
of the
needle or some drug loading problem
Our first case showed similar fundus image, dexamethasone implant
fragments
within vitreous cavity one month after injection In the second case, the
implant
broken after the ejection during an instructional wet-lab, outside
surgical
conditions. This event was recorded in a video that is available with our
report.
Therefore, this video proves that for a break to happen during the
implantation
is utterly feasible and .taking into account the comment of Allergan,
reinforces
that the friction at the tip of the needle during de ejection must be the
reason for
breakage.
We agree with the authors that these patients with defragmented implants
should be followed up carefully to monitor for unexpected complications,
even
more in patients with zonular dehiscence.
REFERENCES:
1. Agrawal R, Fernandez-Sanz G, Bala S, et al. Desegmentation of
Ozurdex implant in vitreous cavity: report of two cases. Br J Ophthalmol.
2014;98:961-3
2. Cabrerizo J, Garay-Aramburu G. Re: intravitreal dexamethasone implant
fragmentation.Can J Ophthalmol. 2013;48:343.
3. Roy R,HegdeS. Split Ozurdex implant: a caution. Can JOphthalmol.
2013;48:e15-6
We read with great interest the clinical report by Pate et al. in which bacterial conifection in keratomycosis was reported by smear, culture or
both. We have seen in our own practice in a series of 110 cases of
infectious keratitis (unpublished data) between year 2001-2005, six
cases
of bacterial co infection in keratomycosis. Five of them were smear
positive and one case was only culture positive...
We read with great interest the clinical report by Pate et al. in which bacterial conifection in keratomycosis was reported by smear, culture or
both. We have seen in our own practice in a series of 110 cases of
infectious keratitis (unpublished data) between year 2001-2005, six
cases
of bacterial co infection in keratomycosis. Five of them were smear
positive and one case was only culture positive for bacteria. In
all
these cases, the mycotic element was septate fungus - Fusariunm sps
and
not yeast as reported by these authors. We had suspected polymicrobial
keratitis clinically in all these cases due to certain distinctive
features at presentation. The typical raised dry infiltrate with hyphate margins which is so characteristic of keratomycosis was modified into
wet
looking necrotic infiltate in some areas; epithelial defect overlying
the
infiltrate showed extension beyond the infiltrate in some areas.
Treatment in all these cases is incomplete if thorogh microbiological
work
up is not done. Clinical judgement does suffice to treat microbial
keratitis in many cases, rather we advocate laboratory support.
We thank Lenio S Alvarenga for his comment on our article about using
fibrin glue for pterygium surgery.
1. We write in the Material and Methods section that only the
thickened and keratinised portion of the conjunctiva was excised and the
graft was prepared to have the same size as the nasal conjunctival defect,
regardless which group the patient was randomized to. Thus the knowledge
of the...
We thank Lenio S Alvarenga for his comment on our article about using
fibrin glue for pterygium surgery.
1. We write in the Material and Methods section that only the
thickened and keratinised portion of the conjunctiva was excised and the
graft was prepared to have the same size as the nasal conjunctival defect,
regardless which group the patient was randomized to. Thus the knowledge
of the surgery method did not influence the results or conclusions of the
study. It is also impossible to randomize the patients without the
surgeon’s knowledge, because the grafts were handled somewhat differently
in the different methods described.
2. The fibrin adhesives in the references mentioned by Alvarenga are
clearly not Tisseel Duo Quick from Baxter: In the article by Hino et al,
the specific trade name of the fibrin sealant is not given, but the text
states that the sealant in question is treated by dry heat to inactivate
viruses - Tisseel is vapour-heated, so it cannot be Tisseel. In the
Kawamura et al article the product is Beriplast - Aventis Behring.
Nevertheless, we will pay attention to this matter in the future. We have
not been able to find any report of HPV B19 infection when fibrin glue was
used in minor surgery. To date we have used the fibrin glue in more than
700 eye procedures since 1999. Any clinical infection with HPV B19 has not
yet been detected in our patients.
I read with interest the article by Pedroza-Seres M and associates
who assessed the pathogenic roles of peripheral CD57+ natural killer T
(NKT) cell in pars planitis.[1] The authors compared the frequencies of
CD57+ NKT cell in peripheral blood between pars planitis patients and
healthy controls, and then evaluated the effector-related surface
molecules and functions of CD57+ NKT cells derived from pa...
I read with interest the article by Pedroza-Seres M and associates
who assessed the pathogenic roles of peripheral CD57+ natural killer T
(NKT) cell in pars planitis.[1] The authors compared the frequencies of
CD57+ NKT cell in peripheral blood between pars planitis patients and
healthy controls, and then evaluated the effector-related surface
molecules and functions of CD57+ NKT cells derived from patients. The
authors conclude that CD57+ NKT cell subsets may function as memory-effector T cells during pars planitis immunopathogenesis. My experience of
using similar methods to investigate the phenotypes and functions of
CD8brightCD56+ T cells in Behçet uveitis supports the notion that
NK-typed CD8+ T cells play an effector role in chronic uveitis.[2] I would
like to offer my opinion to their interpretation of experimental results.
I observed that CD8bright CD56+ cells in peripheral blood were composed of
more than 95% TCRαβ cells and that CD8dimCD56+ cells consisted of
natural killer cells and γδTCR+ cells.[2,3] Because the authors used the
different gate of CD8 expression in figure 1 and 3, it is possible to
overestimate the frequencies of peripheral CD8+CD57+ T cells including
CD8dim populations. Likewise CD56+ cells, CD8dimCD57+ cells may not be
TCRαβcells, which require confirmation of TCR expression.
As shown in Figure 4 and Table 3, the authors found that CD57+CD8+ T cells
significantly produced IL-4 after nonspecific stimulation. However, these
results are not compatible with the idea that terminally differentiated NK-typed CD8+ T cells are polarized to produce cytokines, like CD56+CD8+ T cells.[2] Apoptosis of ex vivo CD57+CD8+ T cells may contribute to these
findings because of smaller cell counts after stimulation (thick lines).
The authors described that stimulared or unstimulated immune cells were
used for intracellular staining of perforin. Because CD8+CD56+ T cells
shed the preformed intracellular
perforin after in vitro stimulation, the authors should measure the
amounts of intracellular perforin in unstimulated cells.
I agree with the authors that NK-typed CD8+ T cells exert potent effector
functions over conventional CD8+ T cells. CD56+ T cells are recruited into
eye, particularly in Behçet uveitis, which are different from other
etiologies of uveitis.[3] Moreover, these cells show phenotypical or
functional changes after immunosuppresive treatments.[4] However, I did not
observe upregulation of CD56+ T cells in aqueous or peripheral blood in
patients with intermediate uveitis.[3] The specific roles of CD57+CD8+ T
cells in pars planitis pathogenesis are not definite because the authors
did not evaluate phenotypical or functional differences of CD57+CD8+ T
cells according to the disease activity or compare their results with
other etiologies of uveitis. Therefore, further investigations are needed
to identify the pathogenic roles of CD57+CD8+ T cells in pars planitis.
References
1. Pedroza-Seres M, Linares M, Voorduin S, et al. Pars planitis is
associated with an increased frequency of effector-memory CD57+ T cells.
Br J Ophthalmol 2007;91:1393-8.
2. Ahn JK, Chung H, Lee DS, Yu YS, Yu HG. CD8brightCD56+ T cells are
cytotoxic effectors in patients with active Behçet's uveitis. J
Immunol 2005;175:6133-42.
3. Yu HG, Lee DS, Seo JM, et al. The number of CD8+ T cells and NKT cells
increases in the aqueous humor of patients with Behçet's uveitis.
Clin Exp Immunol 2004;137:437-43.
4. Ahn JK, Park YG, Park SW, et al. Combined low dose cyclosporine and
prednisone down-regulate natural killer cell-like effector functions of
CD8brightCD56+ T cells in patients with active Behçet's uveitis.
Ocul Immunol Inflamm 2006;14:267-275.
We were interested to read the paper by Huelle JO and colleagues
published in the May 2014 issue of BJO. The authors aimed to provide the
first clinical data in determining the feasibility, quality and precision
of intraoperative wavefront aberrometry (IWA)-based refraction in patients
with cataract. Precision (reproducibility) and measurement quality was
evaluated by the 'limits of agreement' approach, regression analysi...
We were interested to read the paper by Huelle JO and colleagues
published in the May 2014 issue of BJO. The authors aimed to provide the
first clinical data in determining the feasibility, quality and precision
of intraoperative wavefront aberrometry (IWA)-based refraction in patients
with cataract. Precision (reproducibility) and measurement quality was
evaluated by the 'limits of agreement' approach, regression analysis,
correlation analysis, Analysis of variance (ANOVA) and ORs for predicting
measurement failure. Wavefront map (WFM) quality was objectivised and
compared with the Pentacam Nuclear Staging analysis.1 They have reported
high consistency across repeated measures were found for mean spherical
equivalent (SE) differences in aphakia with -0.01D and pseudophakia with -
0.01D, but ranges were high (limits of agreement +0.69 D and -0.72 D;
+1.53 D and -1.54 D, respectively). With increasing WFM quality, higher
precision in measurements was observed.1 Why did the authors not use
(agreement and not consistency) Intra class correlation coefficient (ICC)
to assess the precision (reproducibility)? 2-4
Regarding inter-observer reliability or agreement, it is good to know that
statistics cannot provide a simple substitute for clinical judgment.
They also reported that IWA refraction in aphakia, for instance, appears
to be reliable once stable and pressurised anterior chamber conditions are
achieved. Such conclusion can be misleading due to inappropriate use and
interpretation of statistical tests to evaluate relaibility.2-4
Siamak Sabour, MD, PhD1
Fariba Ghassemi, MD2
1 Shahid Beheshti University of Medical Sciences, Tehran, Iran
2 Farabi Hospital, Eye Research Centre, Tehran University of Medical
Sciences, Tehran, Iran
References:
1- Huelle JO, Katz T, Druchkiv V, et al. First clinicial results on
the feasibility, quality and reproducibility of aberrometry-based
intraoperative refraction during cataract surgery. Br J Ophthalmol. 2014
May 30. pii: bjophthalmol-2013-304786. doi: 10.1136/bjophthalmol-2013-
304786. [Epub ahead of print]
2- Epidemiology, biostatistics and preventive medicine, Jeckel, 1st
edition, 2008
3- Modern Epidemiology, K. Rothman, 3 rd edition, 2010
4- Epidemiology beyond the basics, Moyses Szklo and F. Javier Nieto, 2nd
edition, 2007
The article by Bernauer et al. takes a new focus on the topic of
corneal calcification related to the phosphate content of
eye medications. This topic has been addressed previously by our group,
first with the observation in glaucoma patients published by Huige et
al. (1) then on the normal eye (2), and finally on patients with eye
burns receiving phosphate buffer treatment(3).
Other reports of non ph...
The article by Bernauer et al. takes a new focus on the topic of
corneal calcification related to the phosphate content of
eye medications. This topic has been addressed previously by our group,
first with the observation in glaucoma patients published by Huige et
al. (1) then on the normal eye (2), and finally on patients with eye
burns receiving phosphate buffer treatment(3).
Other reports of non physiologic elements being applied to the cornea,
from silver deposits after accidental high exposure with silver (4), to
particulate matter being observed from trauma and therapy on in eye
burns (5), to corneal calcification in the case of damaged epithelium,
have supported our recent study on phosphate-containing buffer therapy
following eye burns (6).
Severe changes of the cornea as observed by Bernauer et al. are
very likely due to high dosing. The application of Hylo Comod more than
100 times daily as reported in this paper might be sufficient to be
declared at least "off label use" or misuse of
artificial tears. Mostly astonishing is the fact that the
appearance of white plaques on the cornea did not lead to a change in
the
management in any of the 6 patients described. The combination of
norfloxacin (Floxal Edo), known to form precipitates itself as cited
above, dexamethasone phosphate (Dexa sine) and Hylo comod in patient 1
of the study might have caused the calcified plaques, with the
artificial tears being only contributory in this case. Case 3, 4, 5, and
6 received dexamytrex eye drops containing phosphate buffer with Hylo
Comod. This might be an additional factor causative for the
calcification.
The authors to warning that phosphate containing drugs may lead to
corneal epithelial damage is very important. The other important aspect
is that recommended dosing (10), must be taken into
account. The old wisdom that "the dose makes the poison" applies to the
need to advise our patients to use eye drops as
well as oral medications under recommended dosing.
References
(1) Huige WM, Beekhuis WH, Rijneveld WJ, Schrage N, Remeijer L. Deposits in the superficial corneal stroma after combined topical corticosteroid
and beta-blocking medication. Eur J Ophthalmol. 1991 Oct-Dec;1(4):198-9.
(2) Schrage NF, Flick S, Redbrake C, Reim M. Electrolytes in the
cornea: a therapeutic challenge.
Graefes Arch Clin Exp Ophthalmol. 1996 Dec;234(12):761-4. Erratum in:
Graefes Arch Clin Exp Ophthalmol 1997 Apr;235(4):262.
(3) Schrage NF, Schlossmacher B, Aschenbernner W, Langefeld S:
Phosphate buffer in alkali eye burns as an inducer of experimental
corneal
calcification. Burns. 2001 Aug;27(5):459-64.
(4) Schirner G, Schrage NF, Salla S, Teping C, Reim M, Burchard WG,
Schwab B. Corneal silver deposits following Crede's prophylaxis an
examination with electron dispersive x-ray analysis (EDX-analysis) and
scanning electron microscope (SEM). Lens Eye Toxic Res. 1990;7(3-4):445-
57.
(5) Schrage NF, Reim M, Burchard WG. Particulate matter
contamination
in the corneal stroma of severe eye burns in humans. Lens Eye Toxic Res.
1990;7(3-4):427-44.
(6) Schrage NF, Kompa S, Ballmann B, Reim M, Langefeld S.
Relationship of eye burns with calcifications of the cornea? Graefes
Arch
Clin Exp Ophthalmol. 2005 Aug;243(8):780-4. Epub 2005 Mar 9.
(7) Tanhehco TY, Chiavetta SV 3rd, Lee PP, Fowler AM, Afshari NA. "Cracked-mud" ciprofloxacin precipitates on a corneal graft. Ophthalmic
Surg Lasers Imaging. 2005 May-Jun;36(3):252-3.
(8) Castillo A, Benitez del Castillo JM, Toledano N, Diaz-Valle D,
Sayagues O, Garcia-Sanchez J. Deposits of topical norfloxacin in the
treatment of bacterial keratitis. Cornea. 1997 Jul;16(4):420-3.
(9) Lopez JD, del Castillo JM, Lopez CD, Sanchez JG. Confocal
microscopy in ocular chrysiasis. Cornea. 2003 Aug;22(6):573-5.
Financial statement: The Aachen Center of Technologytransfer in
Ophthalmology "ACTO.de" is involved in research on corneal trauma with
phosphate containing eye drops since 10 years and received several
research funds from pharmaceutical industry.
We appreciated the paper by Iriyama et al.[1] The authors have
investigated the role of anti vascular endothelial growth factor (VEGF)
antibodies on retinal ganglion cells in rats. It is an interesting and
relevant paper considering the clinical use of anti-VEGF antibodies in a
variety of ocular conditions.[2] However, there are a couple of issues
that require further clarification.
We appreciated the paper by Iriyama et al.[1] The authors have
investigated the role of anti vascular endothelial growth factor (VEGF)
antibodies on retinal ganglion cells in rats. It is an interesting and
relevant paper considering the clinical use of anti-VEGF antibodies in a
variety of ocular conditions.[2] However, there are a couple of issues
that require further clarification.
The authors demonstrate, in figure 1, that bevacizumab (AvastinTM;
Genentech Inc. San Francisco, CA) is unable to bind to murine VEGF and
they provide evidence by doing Western blot on rat ocular tissue (retina
and choroid) using anti-rat VEGF antibody (R&D systems, Minneapolis) and
bevacizumab. Membranes were developed using rabbit anti mouse IgG and
anti-goat IgG. Authors demonstrate that only anti rat VEGF antibody was
able to detect rat VEGF and not bevacizumab. Although the authors have
not mentioned it in their paper, the anti-rat VEGF antibody that the
authors used is raised in goat according to the information provided by
the source. It justifies the use of anti-goat secondary antibody. It is
not clear why and where they used anti-mouse IgG. On the other hand,
bevacizumab is a humanized antibody and it should be detected by
anti-human IgG 3, which was not used by the authors. This might explain
why they could not detect bevacizumab binding with rat VEGF. Consistent
with this argument, Bock et al. in a recent paper[4] have been able to
show that bevacizumab binds to murine VEGF. They used a similar
technique (Western blot), and by using anti-human IgG were able to
detect bevacizumab bound to the murine VEGF. They further confirmed
their results using additional techniques such as ELISA (again utilizing
anti-human IgG) and surface Plasmon resonance (BIAcore assay).
Also, the figure legend of Figure 2 does not match the figure, nor
does the legend for Figure 4. It seems figures have switched.
Rajesh K Sharma, MD, PhD
Kakarla V Chalam, MD, PhD, MBA, FACS
Department of Ophthalmology
University of Florida, College of Medicine
Jacksonville FL
References
1. Iriyama A, Chen YN, Tamaki Y et al. Effect of anti-VEGF antibody on retinal ganglion cells in rats. Br.J.Ophthalmol. 2007;91:1230-3.
2. Aggio FB, Farah ME, Silva WC et al. Intravitreal
bevacizumab for exudative age-related macular degeneration after multiple treatments.
Graefes Arch.Clin.Exp.Ophthalmol. 2006.
3. Heiduschka P, Fietz H, Hofmeister S et al. Penetration of bevacizumab through the retina after intravitreal injection in the monkey.
Invest Ophthalmol.Vis.Sci. 2007;48:2814-23.
4. Bock F, Onderka J, Dietrich T et al. Bevacizumab as a potent inhibitor of inflammatory corneal angiogenesis and lymphangiogenesis.
Invest Ophthalmol.Vis.Sci. 2007;48:2545-52.
It is interesting to read the attempt by Harun et [1] mounting a
robust defence of their purely theoretical modification of the Roper Hall
classification which has stood us well over the years but now takes its
proud place in history. In the penultimate paragraph of the recent eLetter
they contend that it is incorrect to state that their proposal is purely
theoretical as they "..have based it on a...
It is interesting to read the attempt by Harun et [1] mounting a
robust defence of their purely theoretical modification of the Roper Hall
classification which has stood us well over the years but now takes its
proud place in history. In the penultimate paragraph of the recent eLetter
they contend that it is incorrect to state that their proposal is purely
theoretical as they "..have based it on a widely accepted classification,
which has almost 40 years of clinical use." The point is that the Roper
Hall classification is widely accepted, their modification of it is purely
theoretical and not clinically tested. I do not see how they can justify
their modification by piggy backing on the very classification they are
trying to modify?
In their second eLetter they make the technical point that three
clock hours is 1/4 of limbal involvement and not 1/3rd. They miss the real
point however that any classification equating more than 1/3rd limbal
involvement with total (12 clock hours) limbal involvement and lumping
the entire range therein in one grade of III+, is inaccurate as a
prognostic indicator. They illustrate this flaw in paragraph four where
they claim that injuries involving more than 3 to 6 clock hours of the
limbus would be classified as Grade III (as would someone with 12 clock
hours of limbal involvement). To give an eye with just over 1/3rd limbal
damage and just over 1/3rd conjunctival damage the same "guarded"
prognosis (grade III+) as an eye with 12 clock hours of limbal damage and
total bulbar and forniceal conjunctival damage (also grade III+ in the
proposed modification [2])incorrect and unacceptable. The prognosis for
the latter is "very poor" not "guarded".
It is correct that The Roper Hall classification [3] did not take into
account conjunctival involvement in the same sense as is considered in the
Dua, King and Joseph classification [4] or indeed in the proposed
modification [2]. The Roper Hall classification refers to the limbus and
"contiguous conjunctiva" which implies the involvement of conjunctiva
adjacent to the limbus only. This is reflected in the table of the Roper
Hall classification where the word 'conjunctiva' only appears at the
heading of a column with no allowance made for including conjunctiva in
the actual grading of the burn. Harun et al, [1,2] make an important point
about the tarsal conjunctiva and clearly it is important to examine it in
every ocular burns patient. However, for the purpose of the classification
it does not make any material difference, as in my experience I have never
encountered a case of tarsal burn without associated bulblar and/or
foniceal conjunctival involvement. I would be interested to know if the
Harun et al have. They imply that the Dua, King and Joseph
classification [4] does not take into consideration forniceal involvement.
This is not correct. In the original paper [4] a whole paragraph is devoted
to his aspect. Harun et al in their original letter [2] distinguish
between bulbar forniceal and tarsal conjunctiva and the mucocutaneous
junction emphasising the importance of the latter two. Why then in their
proposed modification do they not take into account the latter two? In
paragraph six of the original letter [2] they account for one hundred
percent of the conjunctival surface by divvying up the bulbar and tarsal
conjunctiva. What about the forniceal conjunctiva, where the stem cells of
the conjunctival epithelium are believed to reside [5,6]. Why is this not
accounted for in the modification?
Harun et al [1] state that "Dua also misinterprets the quantification
of corneal damage. He admits that corneal haze is an indicator of severity
of injury and of the offending chemical..." They have clearly misquoted
me on this. Neither in the original paper nor in my response to their
first letter have I stated the above. On the contrary I have stated that
"Corneal haze can be an indicator of the offending chemical rather than
the severity of the insult." Corneal haze or lack thereof can be very
varying and misleading especially soon after a chemical insult.
In Harun et al's proposed modification [2] the confusion is confounded
because the table is not consistent with the text that supports it. In the
table grade III+ equates to Hazy cornea OR >1/3 limbal ischaemia OR
>1/3 conjunctival involvement. The text states "Grade III includes
either a hazy cornea....and/or greater than one third of limbal or
conjunctival damage." This begs the questions: What is the difference
between III+ and III? Is "or" the same as "and/or"? to most people it
isn't. Will greater than 1/3 conjunctival damage without limbal damage
carry the same prognosis (as implied in the proposed modification) as
greater than 1/3 conjunctival damage with more than 1/3 limbal damage? In
their arguments they make a case, for retaining the term "ischaemia" over
"involvement" yet use the terms "ischaemia", "involvement" and "damage"
interchangeably through the text for both limbus and conjunctiva. For
example "Grade II includes limbal or conjunctival involvement, but
involving less than one third of the area involved" [2]. Furthermore, what
is "... Involving less than one third of the area involved" supposed to
mean?
The authors allege that the Dua, King and Joseph classification [4] is
"..a complicated semi-analogue sub-classification." Here again it is
likely that they have misunderstood the classification. The table in the
paper [4], as has been adequately explained by the supporting text, refers
to a stepped graded classification, consistent with past and current
systems, in the left hand columns and to an analogue scale (which one may
prefer to call semi-analogue) in the right hand columns. On balance, in
the paper, the analogue scale is recommended.
What can be more simple than documenting the clock hours of limbus
involvement and percentage of conjunctival involvement (tarsal conjunctiva
included or not) as a true representation of the extent of damage
following a chemical burn? These two are the key indicators of the
eventual prognosis in terms of ocular surface reconstruction and visual
improvement thereof. Even an attempt to put these into grades I to III or
IV or VI would be superfluous as that is merely a 'lumping' exercise. For
the purpose of any study or comparison, the documentation of clock hours
of limbal involvement and extent of conjunctival involvement, whether in
proportions or percentages, as accurately as possible will allow
subsequent groupings tailored to address the question posed.
The authors end with a profound statement "Without good evidence to
the contrary, it would be irresponsible to disregard a widely accepted
grading system." Unfortunately it applies aptly to their proposed
modification.
References
(1) Harun S, Srinivasan S, Hollingworth K, Batterbury M, Kaye SB.
Classification of ocular chemical injuries, continued BJO second eLetter
(13 July 2004)
(2) Harun S et al. Modification of classifiaction of ocular chemical
injuries [electronic response to Dua et al. A new classification of ocular
surface burns] bjophthalmol.com 2004
http://bjo.bmjjournals.com/cgi/eletters/85/11/1379#219
(3) Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc UK
1965;85:631-53
(4) Dua HS, King AJ, Joseph A. New Classification of Ocular surface
burns. Br J Ophthalmol 2001; 85:1379-83
(5) Wei Z-G, Cotsarelis G, Sun T-T, Lavker RM. Label-retaining cells
are preferentially located in the forniceal epithelium: implications on
conjunctival epithelial homeostasis. Invest Ophthalmol Vis Sci 1995;36:
236-46.
(6) Pellegrini G, Golisano O, Paterna P et al. Location and clonal
analysis of stem cells and their differentiated progeny in the human
ocular surface. J Cell Biol 1999;145:769-82.
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