We read with interest the article by Wong T.Y. et al[1], which
studied a non-diabetic population consisting of 7992 people aged 49-73
years. Non-mydriatic retinal photographs of one eye were taken and graded
for retinopathy lesions using to standardised protocols. Surprisingly, the
presence of typical retinopathy lesions (microaneurysms or retinal
haemorrhages) in persons without diabetes did not signi...
We read with interest the article by Wong T.Y. et al[1], which
studied a non-diabetic population consisting of 7992 people aged 49-73
years. Non-mydriatic retinal photographs of one eye were taken and graded
for retinopathy lesions using to standardised protocols. Surprisingly, the
presence of typical retinopathy lesions (microaneurysms or retinal
haemorrhages) in persons without diabetes did not significantly predict
subsequent development of diabetes over a period of 3.5 years. Incident
diabetes developed in 4.7% and 3.6% of persons with and without
retinopathy lesions at baseline, respectively, with a multivariate
adjusted odds ratio, OR, 1.1, 95% confidence interval, CI, 0.7-1.9.
However, in persons with a family history of diabetes, presence of
retinopathy lesions at baseline predicted a doubling of the risk of
incident diabetes (OR 2.0, CI 1.1-3.8).
We previously reported findings from the Blue Mountains Eye Study
cohort (BMES, n=3654) that the 5-year risk of developing diabetes in
persons without diabetes but with retinopathy lesions at baseline was 3.5%
(7/202).[2] The BMES examined 3654 participants at baseline (1992-94) and
re-examined 2335 participants (75% of survivors) 5 years later (1997-99).
Dilated 6-field retinal photographs of all participants were taken at the
baseline and follow up examinations. Diabetes was diagnosed either from
medical history or fasting blood glucose >=7.0 mmol/L at examination.
Of the baseline participants without diabetes, 202 had retinopathy lesions
(haemorrhages, microaneurysms, soft and hard exudates). Our 3.5% diabetes
incidence over 5 years in this group is relatively similar to the 4.7%
diabetes incidence over 3.5 years reported by Wong T.Y. et al[1] in
persons with retinopathy lesions at baseline. These consistent findings
suggest that retinopathy lesions occurring in persons without diabetes are
likely to have multiple aetiologies. In persons with a family history of
diabetes, retinopathy lesions may indicate a pre-clinical stage of
diabetes. In the great majority of persons without diabetes, however,
retinopathy lesions are not necessarily linked to blood glucose. Reports
from the BMES[3] and Hoorn Study[4] showed that baseline impaired fasting
glucose or impaired glucose metabolism did not predict incident
retinopathy lesions in persons without diabetes. Older age and blood
pressure, however, were strongly related.[2,5] It is possible that the
same phenotype can result from different pathogenic conditions (such as
hypertension[6]) that damage the microvasculature. Given that retinopathy
lesions predict systemic vascular outcomes,[7] further research to clarify
the causes of these lesions is warranted.
References
1. Wong TY, Mohamed Q, Klein R, Couper DJ. Do retinopathy signs in
non-diabetic individuals predict the subsequent risk of diabetes? Br J
Ophthalmol 2006;90:301-3.
2. Cugati S, Cikamatana L, Wang JJ, Kifley A, Liew G, Mitchell P.
Five-year incidence and progression of vascular retinopathy in persons
without diabetes: the Blue Mountains Eye Study. Eye 2005 Sep 16; [Epub
ahead of print].
3. Babisch W, Beule B, Schust M, Kersten N, Ising H. Traffic noise
and risk of myocardial infarction. Epidemiology 2005;16:33-40.
4. van Leiden HA, Dekker JM, Moll AC, Nijpels G, Heine RJ, Bouter LM
et al. Risk factors for incident retinopathy in a diabetic and nondiabetic
population: the Hoorn study. Arch Ophthalmol 2003;121:245-51.
5. Yu T, Mitchell P, Berry G, Li W, Wang JJ. Retinopathy in older
persons without diabetes and its relationship to hypertension.
Arch.Ophthalmol. 1998;116:83-9.
6. Wong TY, Klein R, Sharrett AR, Manolio TA, Hubbard LD, Marino EK
et al. The prevalence and risk factors of retinal microvascular
abnormalities in older persons: The Cardiovascular Health Study.
Ophthalmology 2003;110:658-66.
7. Wong TY, Mitchell P. Hypertensive retinopathy. N.Engl.J.Med.
2004;351:2310-7.
We read with great interest, Singh et. al.’s[1] perspective on
impression cytology and its uses in diagnosing ocular surface pathology.
The known higher exposure to UV radiation in both Australia and New
Zealand, and the increased incidence of ocular surface squamous neoplasia
(OSSN) in Australia,[2][3] recently led us to audit the incidence of OSSN
in conjunctival biopsies in New Zealand over a 6...
We read with great interest, Singh et. al.’s[1] perspective on
impression cytology and its uses in diagnosing ocular surface pathology.
The known higher exposure to UV radiation in both Australia and New
Zealand, and the increased incidence of ocular surface squamous neoplasia
(OSSN) in Australia,[2][3] recently led us to audit the incidence of OSSN
in conjunctival biopsies in New Zealand over a 6 year period.
We identified 132 invasive conjunctival and/or corneal biopsies
performed on 115 patients at Auckland City Hospital. Among the many
histopathological diagnoses, 6% of patients had no histological
abnormality, questioning the need for an invasive diagnostic procedure.
However, 62 (47%) biopsies were diagnosed with OSSN and 84% of those
affected were men, with an average age of 72 years. Published recurrence
rates are generally higher for more severe grades of OSSN[4] and four
subjects in our audit eventually required an exenteration. Furthermore, of
all biopsies on patients with OSSN, 27 biopsies had involvement of the
margins and 12 patients required more than one surgical procedure. Two
patients had recurrences even after clear margins at excisional biopsy and
one patient had repeat biopsy, as there was clinical suspicion of
recurrence but there was no histological evidence of further OSSN.
Although this disease is often regarded as a low grade malignancy
affecting elderly men,[4] it is not without significant morbidity and
occasionally mortality. However, these patients may not always be
medically fit, have sufficiently healthy ocular surface for a large
excision biopsy, or wish/consent to a biopsy.[5] Impression cytology may
therefore offer an inexpensive, non-invasive tool that can be used in the
outpatient clinic setting to help provide an objective evaluation of
suspicious conjunctival/corneal lesions that enables patients to make more
informed decisions about the need for surgery. Results of impression
cytology may also help the ophthalmologist in forming the decision to
perform an incisional or excisional biopsy and the necessity for any other
associated procedures, such as freeze-thaw cryotherapy of the
sclera/limbus and/or ethanol application to the cornea. Of course, the
size of the lesion, macroscopic appearance and overall clinical opinion
may still guide clinical decisions but impression cytology offers an
additional confirmatory tool to aid the process. In addition, impression
cytology can be used to monitor for recurrences in patients with
previously treated OSSN in the outpatient setting.
Although impression cytology only allows sampling of the superficial
cell layers,[1] the sensitivity of this technique has been documented at
70% when the lesion is found to be invasive by histology.[2] Consequently,
some invasive lesions may still be missed. We anticipate that there are
likely to be further improvements to the technique of impression cytology
to make it more logistically simple and less time consuming, with perhaps
an increase in sensitivity. In the meantime we agree that is a useful,
often underused, complimentary investigation in the management of OSSN.
References
1 Singh R, Joseph A, Umapathy T, Tint NL, Dua HS. Impression cytology
of the ocular surface. Br J Ophthalmol 2005;89:1655-9.
2 Nolan GR, Hirst LW, Bancroft BJ. The cytomorphology of ocular
surface squamous neoplasia by using impression cytology. Cancer 2001;93:60-7.
3 Lee GA, Hirst LW. Retrospective study of ocular surface squamous
neoplasia. Aust N Z J Ophthalmol 1997;25:269-76.
4 McKelvie PA, Daniell M, McNab A, Loughnan M, Santamaria JD.
Squamous cell carcinoma of the conjunctiva: a series of 26 cases. Br J
Ophthalmol 2002;86:168-73.
5 Tole DM, McKelvie PA, Daniell M. Reliability of impression cytology
for the diagnosis of ocular surface squamous neoplasia employing the
Biopore membrane. Br J Ophthalmol 2001;85:154-8.
We congratulate Kogure et al,[1] on a well designed longitudinal
study, which confirms the suspicions of many earlier investigators, who
conjectured that Frequency Doubling Perimetry (FDP) may be able to detect
visual field loss earlier than Achromatic Automated Perimetry (AAP) based
on cross-sectional data. In their text they refer to our longitudinal
study[2] as a cross-sectional one and go on to s...
We congratulate Kogure et al,[1] on a well designed longitudinal
study, which confirms the suspicions of many earlier investigators, who
conjectured that Frequency Doubling Perimetry (FDP) may be able to detect
visual field loss earlier than Achromatic Automated Perimetry (AAP) based
on cross-sectional data. In their text they refer to our longitudinal
study[2] as a cross-sectional one and go on to say that there have only
been two other papers, which have demonstrated that FDP predicts future
AAP visual field loss in a longitudinal fashion. Our paper was conducted
over a four-year period, with the first-year data presented as a cross-
sectional study[3] and the final data showing the relationship between FDP
and AAP longitudinally.[2]
In addition, Kogure et al. have shown quantitatively that the
location of FDP field loss can predict the location of future AAP field
loss. We also noted qualitatively a topographical relationship between the
two perimeters, however our original methodology had not included this
premise. Their topographical analysis adds credence to the principle that
these early FDP changes are the same visual field loss seen several years
later on AAP.
References
1. Kogure S, Toda Y, Tsukahara S. Prediction of future scotoma on
conventional automated static perimetry using frequency doubling
technology perimetry. Br J Ophthalmol. 2006;90:347–52.
2. Landers J, Goldberg I, Graham S. Detection of Early Visual Field
Loss in Glaucoma Using Frequency Doubling Perimetry and Short Wavelength
Automated Perimetry. Arch. Ophthalmol. 2003;121:1705-10.
3. Landers J, Goldberg I, Graham S. A Comparison of Short Wavelength
Automated Perimetry with Frequency Doubling Perimetry for the Early
Detection of Visual Field Loss in Ocular Hypertension. Clin. Exp.
Ophthalmol. 2000;28:248-52.
RE: Non-arteritic anterior ischaemic optic neuropathy and the treatment of erectile dysfunction.
McGwin et al.[1] suggest that treatment of erectile dysfunction with sildenafil (Viagra®) or tadalafil (Cialis®), two phosphodiesterase
inhibitors (PDE5-I), may increase the odds of non-arteritic anterior
ischaemic optic neuropathy (NAION) in men with a history of myocardial
infarction (MI...
RE: Non-arteritic anterior ischaemic optic neuropathy and the treatment of erectile dysfunction.
McGwin et al.[1] suggest that treatment of erectile dysfunction with sildenafil (Viagra®) or tadalafil (Cialis®), two phosphodiesterase
inhibitors (PDE5-I), may increase the odds of non-arteritic anterior
ischaemic optic neuropathy (NAION) in men with a history of myocardial
infarction (MI) or hypertension (HTN). We believe, however, that this
study is fraught with significant limitations (as the authors acknowledge)
that preclude drawing any conclusions about this relationship.
Case-control studies are susceptible to several biases that must be
carefully considered and controlled for in the study design,
implementation, and analysis.[2] For example, accurate and complete
ascertainment of exposure is critical in a retrospective case-control
study because both disease and exposure occur prior to study initiation.
The authors note that the interviewers were not blinded to the case or
control status of the patient, making it possible that the interviewer
may, even unconsciously, probe cases differently from controls for
exposure to a PDE5-I (interviewer bias). Another obstacle is that
patients were not consistently interviewed at the time of NAION event (or
index date for controls) about their PDE5-I usage. Hence, NAION patients
may have been more likely to remember drug usage (recall bias).
Furthermore, exposure misclassification may have occurred as timing, dose,
and duration of drug use relative to event onset were not captured
(exposure bias). This information is crucial for drugs used as needed
such as PDE5-I and particularly for short half-life drugs like sildenafil.
Perhaps, the most troublesome weakness of the study was the limited
sample size and differential participation rates of cases and controls,
likely resulting in selection bias that distorts the conclusion. The
authors note that almost one-fifth of the cases and one-third of the
controls refused to participate. The baseline cardiovascular
characteristics, while not significantly different (with the exception of
MI) between cases and controls, were consistently more prevalent in the
NAION group. This finding is not surprising given that these
cardiovascular conditions, especially in combination, are also risk
factors for NAION.[3] Thus, the MI and HTN subgroup analyses presented in Table 3 should be interpreted with skepticism.
Exacerbating the inherent problems are subgroup analyses that had no
a priori hypothesis. The dangers of unplanned subgroup analyses in
research are well documented.[4] Compounding matters is the sparse number
of patients, reflected in the exceptionally wide confidence intervals
(Table 3). The robustness of such extremely small cell numbers must also
be questioned, as the observed statistical significance for patients with
MI can be eliminated if only one or two patients are switched to an
alternative category. The authors also did not provide individual
patient totals by exposure group with and without MI, rendering it
impossible to replicate their results. Furthermore, there appear to be
errors in the numbers/percentages and crude odds ratios presented in Table 2.
In summary, the methodological limitations call into serious question
the authors’ conclusions. For men with a history of MI or HTN, therefore,
this study does not provide any valid evidence that the use of Viagra or
Cialis may increase the risk of NAION.
Rachel E. Sobel, MPH,
Pfizer Inc,
150 E 42nd St., MS#150-3-72,
New York, NY 10017.
Rachel.Sobel@pfizer.com
Joseph C. Cappelleri, PhD, MPH,
Pfizer Inc,
Global Research and Development,
Groton, CT.
References
1 McGwin G, Vaphiades MS, Hall TA, Owsley C. Non-arteritic anterior
ischaemic optic neuropathy and the treatment of erectile dysfunction. Br
J Ophthalmol 2006; 90:154-157.
2 Rothman KJ, Greenland S. Modern Epidemiology. Philadelphia, PA:
Lippincott-Raven Publishers, 1998.
3 Hatzichristou, D. Phosphodiesterase 5 Inhibitors and Nonarteritic
Anterior Ischemic Optic Neuropathy (NAION): Coincidence or Causality? J
Sex Med 2005; 2:751–758.
4 Assman SF, Pocock SJ, Enos LE, Kasten LE. Subgroup analysis and
other (mis)uses of baseline data in clinical trials. Lancet 2000; 35:1064-
1069.
We congratulate the authors Ghazi-Nouri et al. to their recently
published study “Visual function and quality of life following vitrectomy
and epiretinal peel surgery”. It mainly confirms our results on a very
similar consecutive cohort of 20 patients followed for three months which
was published August 2005 in the Medline indexed German “Ophthalmologe”
[1] and therefore represents the first paper...
We congratulate the authors Ghazi-Nouri et al. to their recently
published study “Visual function and quality of life following vitrectomy
and epiretinal peel surgery”. It mainly confirms our results on a very
similar consecutive cohort of 20 patients followed for three months which
was published August 2005 in the Medline indexed German “Ophthalmologe”
[1] and therefore represents the first paper on this subject. The first
oral presentation was at the 2004 annual meeting of the German
Ophthalmological Society (DOG).
For assessing the benefit in visual quality of life after
vitreoretinal surgery for epiretinal membranes, we used the commonly
accepted Visual Function 14 (VF-14) test. A larger patient series using
the NEI-VFQ 25 is ongoing. Similarly as in the recent study of Ghazi-Nouri
et al., a significant increase in visual quality of life 3 months after
surgery was observed. The VF-14 values increased significantly from 72.8
preoperatively to 83.3 postoperatively (p<0.05) - although the fellow
eye had good visual acuity (visual acuity of –logMAR 0.2 or better was an
inclusion criteria), so that every patient underwent surgery on the worse
seeing eye. In contrast to Ghazi-Nouri et al., visual acuity increased
significantly from –logMAR 0.55 to 0.4 (p=0.018), which is approximately
1.5 Snellen lines and consistent with most previously reported results in
the literature (2, 3). However, all surgery had been performed by only one
experienced surgeon.
We performed statistic analyses on the data in order to isolate
predictive factors for surgery. When splitting our 20 patients in the two
halves with lowest and highest preoperative VF-14 values, it could be
shown that patients with preoperatively low VF-14 values benefited from
surgery in visual quality of life, while those with preoperatively high VF
-14 values did not. In an analysis of variance model it could be further
shown, that the increase in visual quality of life could better be
estimated than the increase of visual acuity. If in such modelling only
the preoperative VF-14 values and preoperative visual acuity were used to
assess the increase in visual quality of life, those two parameters had a
surprisingly high predictive value (R2=0.80). Cataract surgery did not
influence results significantly. Thus in addition to the later published
results of Ghazi-Nouri et al., we can give practical recommendations for
patient selection: a patient with preoperatively low VF-14 values (i.e.
the patient is highly bothered by the visual performance) and a
preoperatively low visual acuity is very likely to benefit from surgery.
Together with the information that the increase in visual acuity will
probably be not very high, this allows for best consulting and patient
selection for epiretinal membrane surgery.
C. Hirneiss, MD
A.S. Neubauer, MD
A. Kampik, MD
Dept. of Ophthalmology
Ludwig-Maximilians University
Mathildenstr. 8
80336 Muenchen
Germany
References
1. Hirneiss C, Rombold F, Kampik A, Neubauer AS. Visual quality of
life after vitreoretinal surgery for epiretinal membranes. Ophthalmologe
2005 Aug 3 [Epub ahead of print]
2. Michels RG. Vitrektomy for macular pucker. Ophthalmology
1984;91:1384-1388
3. Haritoglou C, Eibl K, Schaumberger M et al. Functional outcome
after trypan blue-assisted vitrectomy for macular pucker: a prospective,
randomized, comparative trial. Am J Ophthalmol 2004;138:1-5
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 read with great interest the article titled 'Characteristic
clinical features as an aid to the diagnosis of suppurative keratitis caused by filamentous fungi' by Thomas and associates1. We would like to congratulate the authors on this attempt to validate the signs of fungal keratitis, which would be helpful to the ophthalmologists of developing
nations. We would like to make following comments:...
We read with great interest the article titled 'Characteristic
clinical features as an aid to the diagnosis of suppurative keratitis caused by filamentous fungi' by Thomas and associates1. We would like to congratulate the authors on this attempt to validate the signs of fungal keratitis, which would be helpful to the ophthalmologists of developing
nations. We would like to make following comments:
In the light of the fact that in the tropics laboratory facilities
are
rare and the diagnosis and treatment of cases is based on clinical
characteristics, the authors conclusion that "the probability of fungal
etiology in a case of microbial keratitis is 63% if one of the 3
clinical
signs are present (serrated margin, raised slough and coloration other
than yellow) and at least 85% if all of three are present" becomes very
important. However, before applying this conclusion in clinical practice
we will have to take into account following facts of the study:
In this study the authors excluded cases with mixed infection (1.4%
and 5.5% in Ghana and India respectively), acanthamoeba keratitis (0.3%
& 0.9%), unconfirmed laboratory diagnosis (49.7% & 31.1%), and
small infiltrates (11.7% overall) 2. Since the score is designed for
application in community practice, it would have been better to apply
the scores to all cases (290) from Ghana rather than a subset of
patients.
Since this study aims at ophthalmologists at the primary health
care
level, including cases that had small infiltrate i.e. less than 4 mm
would
have been very useful because clinicians at the primary care level are
likely to see early cases.
The predictive value of a positive test depends on relative pretest probability or prevalence of the disease in the group of individuals
tested. Therefore, the "score" will be useful only in countries with a
high prevalence of fungal keratitis. At a prevalence of 30% the positive predictive value of even a high score will not allow a conclusive
diagnosis.
Therefore, the statement that the three signs described by the
authors allow the diagnosis of fungal keratitis with 85% confidence can
be
misleading. Rather, this study further highlights that there are no
exclusive clinical signs in microbial keratitis to diagnose the
etiological
agent.
To address this difficulty, addition of simple, cost effective
microbiology tests such as microscopic examination of smears using 10%
potassium hydroxide or lactophenol cotton blue will help ophthalmologist to be surer of diagnosis and to start initial treatment with more
certainty.
References
1 Thomas P A, Leck A K and Myatt M. Characteristic clinical
features
as an aid to the diagnosis of suppurative keratitis caused by
filamentous
fungi. Br. J. Ophthalmol 2005;89;1554-1558
2 Leck AK, Thomas PA, Hagan M, et al. Aetiology of suppurative
corneal ulcers
in Ghana and south India, and epidemiology of fungal keratitis.
Br J Ophthalmol 2002;86:1211-15.
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 read with interest the paper by Hamada et al 1, which draws a
number of conclusions from a five year follow up study of 69 periocular
BCCs treated by conventional surgery, and in particular suggests that
there is no place for Mohs micrographic surgery (MMS) in patients with
periocular BCCs. MMS is the serial saucerisation excision with mapped
horizontal tissue sections examining 100% of the surg...
We read with interest the paper by Hamada et al 1, which draws a
number of conclusions from a five year follow up study of 69 periocular
BCCs treated by conventional surgery, and in particular suggests that
there is no place for Mohs micrographic surgery (MMS) in patients with
periocular BCCs. MMS is the serial saucerisation excision with mapped
horizontal tissue sections examining 100% of the surgical margins to
produce histological evidence of tumour negative margins. Unfortunately,
the data included in the paper are incomplete and if such conclusions are
to be considered, then further clarification is required.
Risk of BCC recurrence relates directly to the nature of the tumours
treated2. The principle risk factors for recurrence include previous
treatment, large tumour size, and an infiltrative or micronodular
histological growth pattern. No information is given on the first 2
factors and the histological subtype was non-specified in approx 45% of
cases. We calculate from the data provided that the authors experienced a
19% 5 year recurrence rate in patients with a histologically infiltrative
BCC.
If most of the “non-specified” tumours in Hamada’s series were small
nodular tumours, as the paper implies, then Hamada’s series also differs
significantly from other larger series in that it represents a group of
patients with an inherently better prognosis. Other comments hint at this,
in that 76% of BCCs were on the lower eyelid and 72% were amenable to
direct closure. If the majority of the tumours in this series were not in
a high- risk group then only one recurrence would be anticipated. In
contrast, the Australian Mohs’ database series3 reported on a much higher
incidence of high-risk tumours (50% were infiltrative, morphoeic,
basosquamous or superficial), of which only 54% were on the lower eyelid
while 41% affected the medial canthus, a site with a proven higher risk of
recurrence. Despite this, they reported a 0% recurrence rate for primary
BCCs of all histological subtypes treated by MMS surgery.
Hamada also concludes that 4mm margins are justified for well-defined
nodular tumours, on the basis of the 5-year recurrence rates and the fact
that most eyelids can still be directly repaired after such excisions. It
is of interest however that 16% of the patients reported had incomplete
tumour excision at the first attempt, although we do not know what margins
were used for this group. As conventional pathological sectioning examines
less than 1% of the margins4, it is likely that the actual incomplete
excision rate was higher.
Hamada argues that MMS is not necessary for periocular tumours on the
basis that it is difficult to obtain true MMS sections. Unless either
periosteum or anterior orbital septum are breached by the tumour, then
there is no evidence for the former statement. What about cost benefit?
MMS histology costs are greater than routine sections. However, when the
other advantages of MMS are taken into account MMS is cost-effective in
comparison to traditional surgical excision5.
The current best evidence shows that recurrence rates are lower with
MMS than with any other technique, with MMS for recurrent or high-risk
tumours showing the greatest advantage over conventional surgery.
Furthermore, Hamada acknowledges that the tissue sparing quality of MMS is
an important issue in that 36% of patients will develop a second BCC
within 5 years.
Although we believe that MMS is the treatment of choice for optimal
cure rates in periocular BCC, we would agree with Hamada that is currently
impractical for all tumours because of the patchy availability of the
service in the UK. However we believe the current evidence shows that MMS
remains the optimal treatment for all high risk tumours based on treatment
status, site, size and histological subgroup and do not feel that the data
presented warrant a different conclusion.
2. Lawrence CM. Mohs surgery - A critical review. Br J Plast Surg
1993, 46, 599-606
3. Malhotra R, Huilgol SC, Huynh NT, Selva D. The Australian Mohs
Database, part II: Periocular basal cell carcinoma outcome at 5 year
follow up. Ophthalmol 2004, 111, 631-636.
4.Abide JM, Nahai F, Bennet RG. The meaning of surgical margins.
Plast Reconstr Surg 1984;73:492-6
5. Cook J, Zitelli JA. Mohs micrographic surgery: a cost analysis. J
Am Acad Dermatol. 1998; 39:698-703.
EA Barnes1, AJ Dickinson1, J AA Langtry2 and CM Lawrence2
1Department of Ophthalmology
Royal Victoria Infirmary
Newcastle-upon-Tyne, NE1 4LP
2Department of Dermatology
Royal Victoria Infirmary
Newcastle-upon-Tyne, NE1 4LP
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