Editor,
With great interest we read the case report by Dr. Alwitry on "Vitamin A
deficiency in coeliac disease", which raises the question whether a
deficiency of vitamin A with subsequent keratomalacia may be caused by
this disorder. However, although coeliac disease cannot be excluded as a
cause of reduced vitamin A absorption,[1] Alwitry's report does not
convincingly show that the vitamin A deficie...
Editor,
With great interest we read the case report by Dr. Alwitry on "Vitamin A
deficiency in coeliac disease", which raises the question whether a
deficiency of vitamin A with subsequent keratomalacia may be caused by
this disorder. However, although coeliac disease cannot be excluded as a
cause of reduced vitamin A absorption,[1] Alwitry's report does not
convincingly show that the vitamin A deficiency in his patient was indeed
due to this disease. If, as was stated in the letter, the patient really
had been on a gluten-free diet, his diarrhoea - and probably related
vitamin A malabsorption - may well have had other causes; e.g., fat
maldigestion, mostly resulting from hepatic and/or pancreatic disorders.
In addition, it is not known whether Alwitry's patient received enough
dietary fat and (with it) vitamin A. Furthermore, Alwitry refers to the
report by Sommer et al[2] for the statement "supplementation via the oral
or intramuscular route, each of which have been demonstrated to be equally
efficacious." Sommer's article, however, deals with Indonesian children
with xerophthalmia, and not with patients with coeliac disease. This
should be considered, if different administration regimens of vitamin A
are compared. In agreement with Sommer's work, additional determination
of serum retinol-binding protein (RBP) would result in a more
comprehensive view of the patient's vitamin A status. In this context a
further criticism of Alwitry's contribution is that only a single serum
vitamin A value is presented and that the corresponding concentration unit
as well as sufficient information on the time of sampling in relation to
vitamin A administration are not given.
References
1. Johnson EJ, Krasinski SD, Howard LJ, et al. Evaluation of vitamin A
absorption by using oil-soluble and water-miscible vitamin A preparations
in normal adults and in patients with gastrointestinal disease. Am J Clin
Nutr 1992;55:857-64.
2. Sommer A, Muhilal, Tarwotjo I, et al. Oral versus intramuscular
vitamin A in the treatment of xerophthalmia. Lancet 1980;1:557-9.
Editor, I read the article by Bechmann et al with interest, and I
congratulate the authors on their work. In the discussion, they cover the
entire subject of tonometry on the basis of the central corneal thickness
(CCT). With the increasing number of corneal refractive procedures
performed every year, this point will be associated with much uncertainty
for diagnosing glaucoma in the near future. Appare...
Editor, I read the article by Bechmann et al with interest, and I
congratulate the authors on their work. In the discussion, they cover the
entire subject of tonometry on the basis of the central corneal thickness
(CCT). With the increasing number of corneal refractive procedures
performed every year, this point will be associated with much uncertainty
for diagnosing glaucoma in the near future. Apparently, ophthalmologists
are slowly becoming aware of this problem.[1]
In their conclusion, the authors emphasize the "need for a combined
measurement of IOP and CCT in order to be able to classify the different
types of glaucoma." There is, as we perceive it, a slight
misunderstanding of the problem. The Goldmann tonometer[2] measures the
force required for flattening the cornea. From this, it concludes the
pressure in the eye. From the original article of Goldmann, it is well
known that this relationship is only valid for a corneal thickness of
roughly 520 micrometers. However, the problem is not the thickness itself
of the cornea, but rather the cornea's biomechanical properties (e.g.,
elasticity), which are somehow related to its thickness. Thus, a better
solution for this problem would be a measurement of the eye pressure that
was independent of the thickness. In this case, each eye could be
measured correctly irrespective of the biomechanical properties of the
cornea. With the contact lens tonometer, now called SmartLens®, we have
been able to demonstrate that after LASIK the true IOP can be measured,[3]
thereby excluding any possible false negative glaucoma cases. The
SmartLens® tonometer directly measures the pressure in the middle of the
applanated area and, therefore, is independent of any corneal property,
including its thickness.[4] To the best of our knowledge, this is the only
way to prevent the ophthalmologist from possible incorrect diagnosis and
follow-up of glaucoma patients in the future.
1. Lewis, RA. Refractive surgery and the glaucoma patient (customized
corneas under pressure). Ophthalmology 2000;107(9):1621-1622.
2. Goldmann, H, Schmidt TH. Über Applanationstonometrie Ophthalmologica.
1957;134:221-241.
3. Kaufmann C, Schipper I, Robert YCA. SmartLens® Tonometry compared to
Goldmann Tonometry before and after Refractive Surgery. Invest Ophthalmol
Vis Sci 2000;41(4):S598. Abstract #2475.
4. Dekker PW, Robert YCA, Kanngiesser H, Pirani P, Entenmann B.
Principles of contact lens tonometry. International Ophthalmol
1999;22:105-111.
Dear Sir,
In India, we very commonly see mature cataracts. Doing capsulorhexis with
injection of dye is done very routinely by many of us. Forunately no
untoward reaction has been reported so far. This helps us to carry out the
phaco procedure with ease.
Dear Sir,
I was fascinated by Cheng and colleagues' article on Mooren's ulcer
in China. During the past 6 years I have worked for 3 years as an
ophthalmologist in rural Cameroun. I submit to you my experiences of
Mooren's ulcer there :
Patients: 5 (4 male, 1 female). Age: 1 patient aged 48 years, the rest all late teens and twenties.
Dear Sir,
I was fascinated by Cheng and colleagues' article on Mooren's ulcer
in China. During the past 6 years I have worked for 3 years as an
ophthalmologist in rural Cameroun. I submit to you my experiences of
Mooren's ulcer there :
Patients: 5 (4 male, 1 female). Age: 1 patient aged 48 years, the rest all late teens and twenties.
Out of 3 patients we tested (following a histology report on excised
conjunctiva), 2 had positive skin-snips for Onchocerca volvulus. None of
the predisposing factors referred to in Cheng's article applied to any of
these patients.
All ulcers were unilateral, and totally resistant to any medical
treatment that was available (topical prednisolone sodium phosphate 1%,
oral cyclophosphamide). I tried various surgical treatments and found that
the only one that gave satisfactory results was excision of a 3 mm-wide
band of conjunctiva next to the ulcer, and covering the ulcer and bared
sclera with a free conjunctival graft (conjunctival flaps simply retracted
and separated), followed by chloramphenicol and prednisolone drops for a
month. This became my first-line treatment. Corneal grafting was not
a possibility. One ulcer recurred by circumferential extension from the
original site.
Editor,
We read with interest the paper by Minasian et al. They quote that pain experienced during an injection is related to the temperature of the injection and the speed of delivery of the solution.[1] [2]
In their article, they have used all anaesthetics at room temperature. We have been pre-warming our anaesthetic solutions routinely for cataract surgery. We use a heat pad (Dreamland appliance...
Editor,
We read with interest the paper by Minasian et al. They quote that pain experienced during an injection is related to the temperature of the injection and the speed of delivery of the solution.[1] [2]
In their article, they have used all anaesthetics at room temperature. We have been pre-warming our anaesthetic solutions routinely for cataract surgery. We use a heat pad (Dreamland appliance services model HP3, 240V,52-60W) to warm solutions to 40ºC prior to subtenon's injection. We have noted that patients found this less painful than non pre-warmed solutions.
There are reports to support that pre-warming anaesthetic solution is less painful than using solutions at room temperature.[3] [4] Increasing
temperature or pH (alkalinising the anaesthetic solution) works in the
same fashion, that is, by increasing the concentration of non-ionised form
which is more lipid soluble and results in almost immediate sensory
blockade.[2] [5] [6] Though altering the pH and pre-warming the anaesthetic
solution have been tried separately, we have not encountered any study
that combines both these variables. We believe that such a study would be
worthwhile and needs to be looked at. Even if the pH of the solution
changes after warming, we do not believe that pH is a factor in reducing
pain, as confirmed by their study.
References
1. Gillart T, Bazin JE, Montetagaud M, et al. The effects of volume and
speed of injection in peribulbar anaesthesia. Anaesthesia 1998;53:486-91.
2. Christoph R, Buchanan L, Schwatz S. Pain reduction in local
anaesthetic administration through pH buffering. Ann Emerg Med
1998;17:117-20.
3. Ursell PG, Spalton DJ. The effect of solution temperature on the pain
of peribulbar anaesthesia. Ophthalmology 1996;103:839-41.
4. Hamilton RC. Does warming of anaesthetic solutions improve analgesia
and akinesia in retrobulbar anaesthesia? Ophthalmology 1997;104:429-32.
5. Ritchie JM, Ritchie B, Greenford B. The active structure of local
anaesthetics. J Pharmacol Exp Ther 1965;150:152-9.
6. Kamaya H, Hayes JJ, Ueda I. Dissociation constants of local
anaesthetics and their temperature dependence. Anaesth Analg 1983;62:1025-30.
Editor,
The paper by Cullinane and Cleary presents an excellent
prospective study of peripheral visual field loss in patients undergoing macular hole surgery. The authors compared vitrectomy with complete posterior cortical vitreous peeling to limited vitrectomy with removal of
cortical vitreous off the macula, but not off the optic nerve head or the peripheral retina. The authors showed a statistically...
Editor,
The paper by Cullinane and Cleary presents an excellent
prospective study of peripheral visual field loss in patients undergoing macular hole surgery. The authors compared vitrectomy with complete posterior cortical vitreous peeling to limited vitrectomy with removal of
cortical vitreous off the macula, but not off the optic nerve head or the peripheral retina. The authors showed a statistically significant decrease in peripheral visual field defects with the limited vitrectomy
technique (0% - 0/22 patients) compared to the complete vitrectomy group (22% - 18/82 patients). The authors postulated that this difference is due to the avoidance of
traction on the optic nerve head during peeling of the posterior hyaloid, thus limiting damage to the peripapillary nerve fiber layer, which they believed would be most severe nasally due to firmer vitreopapillary
attachments nasally.
However, this explanation does not take into account the
variable position of visual field defects found in other studies based on the position of the infusion cannula. If the infusion cannula is superiorly located, visual field defects occur superiorly, implicating inferior retinal damage.[1] If the infusion cannula is inferonasal, visual
field defects occur inferonasally, and not inferotemporally.[2] The inferotemporal location of field defects noted in most studies is based on the conventional placement of the infusion cannula inferotemporally in
three-port vitrectomy, which results in infused air directed towards the superonasal mid-peripheral retina.
Animal studies show damage to the inner limiting membrane, nerve fiber layer and ganglion cells of the retina in the path of the pressurized air flow from the infusion cannula.[3] [4] This inner retinal damage could be
caused by desiccation of the retina[1] or by direct mechanical damage by the pressurized air flow.[3] [4] However, humidification of air did not prevent inner retinal damage in animal models,[3] [4] and the sharp demarcation
between damaged and undamaged retina on electron microscopic studies supports the theory of direct mechanical damage to the inner retina.[4] In addition, decreasing the infusion air pressure also decreased the risk of inner retinal damage.[4]
I think this work by Cullinane and Cleary shows that leaving the peripheral vitreous in place is another way of
protecting the peripheral retina from mechanical damage by pressurized air flow. I would be concerned about the potential risk of increased postoperative retinal detachment, which was 10% in the limited vitrectomy
group and 4% in the complete vitrectomy group, but was not statistically significant due to small sample size. However, this increased risk of retinal detachment was also a concern in a previous study utilizing similar surgical techniques (Brian Conway, Western Association for Vitreoretinal Education Meeting, Maui, Hawaii, 1996).Because of the studies on retinal damage by pressurized air infusion and the significance of high infusion air pressure, it would be important to know the usual infusion air pressure utilized during fluid-air exchange by the authors, and if the infusion air pressure varied at any point during
the period of the study or between the two vitrectomy groups. Currently, in order to minimize retinal damage induced by pressurized air infusion during vitrectomy for any surgical indication requiring fluid-air exchange, I would recommend simply using a low infusion air pressure.
References
1. Welch JC. Dehydration injury as a possible cause of visual field defect after pars plana vitrectomy for macular hole. Am J Ophthalmol 1997;124:698-9.
2. Takenaka H, Maeno T, Mano T, et al. Causes of visual field defect after vitrectomy. J Jpn Ophthalmol Soc 1999;103:399-403.
3. Hasamura T, Yonemura N, Nirata A, et al. Retinal damage by fluid-air exchange during vitreous surgery in rabbits. Invest Ophthalmol Vis Sci 1999;40:S943.
4. Ishigooka H, Mawatari Y, Ogawa K, et al. Prophylactic trials for prevention of visual field defect after vitrectomy for macular hole. Invest Ophthal Vis Sci 2000;41:S343.
Editor,
We read with interest the article by Ishioka and coworkers, in which the authors studied the effect of trabeculectomy with and without mitomycin C in post-keratoplasty glaucoma. The authors conclude that trabeculectomy with mitomycin C showed better results for glaucoma following penetrating keratoplasty. We congratulate the authors for an excellent study. We have published similar observations on...
Editor,
We read with interest the article by Ishioka and coworkers, in which the authors studied the effect of trabeculectomy with and without mitomycin C in post-keratoplasty glaucoma. The authors conclude that trabeculectomy with mitomycin C showed better results for glaucoma following penetrating keratoplasty. We congratulate the authors for an excellent study. We have published similar observations on trabeculectomy with mitomycin C for post-
keratoplasty in 1997.[1] The salient features of this
study are worth mentioning as literature on mitomycin C augmented trabeculectomy in post-keratoplasty glaucoma is limited.
In the study by Sharma and coworkers trabeculectomy with mitomycin C (0.2 mg/ml for 2.5 minutes) was performed in 16 eyes of 16 patients for medically uncontrolled glaucoma following penetrating keratoplasty. The mean pre-trabeculectomy IOP with maximal medical therapy was 34.6 mm Hg (range 24 to 45 mm Hg). The mean IOP following trabeculectomy with mitomycin C was 14.2 mm Hg (range 8 to 36 mm Hg) by the end of follow-up of 14.2 months (range 8 to 32 months). Fourteen eyes (87.5%) had complete success, one eye (6.25%) had qualified success and one eye (6.25%) had
failure. All the patients had either better than or maintained pre-operative visual acuity. None of the patients developed postoperative complications such as shallow anterior chamber, epithelial defect of
hypotony. Earlier Khatana et al[2] presented in ARVO showed reduction of IOP following trabeculectomy with mitomycin C in most of their patients. In addition to the efficacy, safety of trabeculectomy with mitomycin C for
post-keratoplasty glaucoma reported is a major concern. Mitomycin C as an adjunct to trabeculectomy has been safe for corneal endothelium.[3] In an experimental study on rabbit eyes, the peak aqueous level of mitomycin C
after topical application (0.4 mg/ml) was 0.03 ± 0.02 mg/ml.[4] This aqueous concentration was considered above the therapeutic level for inhibition of subconjunctival fibroblast proliferation but below the level known to cause endothelial toxicity.[4] In studies by Sharma et al[1] and
Khatana et al,[2] mitomycin augmented trabeculectomy caused no damage to the clear penetrating grafts.
Our observations were in accordance with those by Ishioka, et al that in medically uncontrolled glaucoma following penetrating keratoplasty, trabeculectomy with mitomycin C may be considered unless there is a
contraindication to the use of adjuvant. However, the authors may have inadvertently missed our earlier report.
References
1. Sharma A, Kumar S, Ram J, et al. Trabeculectomy with mitomycin C for post-keratoplasty glaucoma: A preliminary study. Ophthal Surg Lasers 1997;28:891-5.
2. Khatana AK, Olivier M, Shin DH, et al. Safety and efficacy of adjunctive mitomycin-C in filtration surgery in eyes with corneal grafts. Invest Ophthalmol Vis Sci 1993;34(Suppl):1099.
3. Anglade E and Dreyer E. The effect of mitomycin-C and 5-fluorouracil on corneal endothelium in trabeculectomy surgery. Invest Ophthalmol Vis Sci 1993;34(Suppl):730A.
4. Eezuduemboi RD, Sarraf D, Wilson MR, et al. Aqueous and vitreous concentration of mitomycin following topical administration. Invest Ophthalmol Vis Sci 1993;34(Suppl):726.
Editor,
The commentary by Waldock and Cook on the survival rates of
corneal grafts highlights a number of issues. In particular, they focus on the lack of long-term follow-up data in the UK. The value of such data is clearly evident from the Australian Corneal Graft Register.[1] Moreover,
in the present climate of clinical audit and evidence-based medicine, the collection of such data has surely become a...
Editor,
The commentary by Waldock and Cook on the survival rates of
corneal grafts highlights a number of issues. In particular, they focus on the lack of long-term follow-up data in the UK. The value of such data is clearly evident from the Australian Corneal Graft Register.[1] Moreover,
in the present climate of clinical audit and evidence-based medicine, the collection of such data has surely become a necessity.[2] Many of the questions raised, whether simply comparing graft survival rates of individual units with national data or investigating more fundamental
issues such as HLA matching, visual outcome or surgeon experience, require large amounts of data, properly designed studies and appropriate statistical analysis-capabilities beyond most individual centres, but readily achievable within the NHS. The way forward as shown by the organ
transplant community, and to a certain extent by corneal graft surgeons, is through well-organized, centralized data collection and analysis. e.g.[1] [3] [4]
The good news is that just such a system is now in place for all corneal graft surgeons in the UK. The Royal College of Ophthalmologists and the UK Transplant (UKT) have initiated an Ocular Tissue Transplant Audit, which will provide the data for answering the sorts of questions posed by Waldock and Cook. Indeed, the Audit is already being used for data capture for the Corneal Transplant Follow-up Study II, which aims to resolve the uncertainty surrounding HLA-DR matching and corneal graft rejection. Instead of just one-year follow-up as in the original CTFS,[4]
follow-up for these patients will continue in the long-term through the Audit.
As important, however, is the opportunity for all ocular tissue transplants to be recorded and the outcome audited. Indeed one can foresee the day when this will be obligatory, as is the case with solid organs. To record such data with UKT will not only provide surgeons with details of their own activity, but an independent confidential analysis of
clinical outcomes, which they will increasingly be expected to have available.
References
1. Williams KA, Muehlberg SM, Lewis RF, et al. The Australian corneal graft registry 1996 report. Adelaide: Mercury Press, 1997.
2. Coster DJ. Evaluation of corneal transplantation [editorial]. Br J Ophthalmol 1997;81:618-619.
3. United Kingdom Transplant Support Service Authority Renal Transplant Audit 1984-1993. Bristol: UKTSSA, 1995.
4. Vail A, Gore SM, Bradley BA, et al. Conclusions of the corneal transplant follow-up study. Br J Ophthalmol
1997;81:631-6.
Editor,
The work of West and Gregor again points out the importance of sclerotomy complications following pars plana vitrectomy. They demonstrate that, even in the hands of a skillful and experienced surgeon, vitreous hemorrhage after vitrectomy for diabetic retinopathy is common and requires vitreous cavity washout (VCWO) in 12% of cases. In their series,
over half of the eyes had detectable fibrovascular...
Editor,
The work of West and Gregor again points out the importance of sclerotomy complications following pars plana vitrectomy. They demonstrate that, even in the hands of a skillful and experienced surgeon, vitreous hemorrhage after vitrectomy for diabetic retinopathy is common and requires vitreous cavity washout (VCWO) in 12% of cases. In their series,
over half of the eyes had detectable fibrovascular ingrowth (FVI) as the cause of the hemorrhage. Interestingly, in this case series of 159 eyes, no occurrences of anterior hyaloidal fibrovascular proliferation (AHPV)
were noted.
Definition of the relationship between these two entities has been controversial, to say the least.
Part of the controversy is due to a misunderstanding of the nature and pathogenesis of FVI. As McLeod points out in his editorial, FVI is a term that has been used inadvisedly, suggesting the episcleral tissue grows into the eye through the sclerotomy incision [1]. While episcleral tissue,
scleral fibroblasts, and ciliary epithelium all contribute, the majority of the fibroproliferative healing of a sclerotomy originates from the uvea of the ciliary body [2].
In normal wound healing, early fibrovascular proliferation in the incision is followed by its involution and contraction, with the result being the small scar seen at the internal aspect of a healed sclerotomy [2].
Inevitably, because of the proximity of the vitreous base and anterior hyaloid, vitreous strands are adherent to the wound and fibrous tissue extends a short way into the vitreous body. This tissue may contain blood
vessels, even with normal healing. From this perspective, all sclerotomy wounds heal with fibrovascular ingrowth. That is, ingrowth of tissue from the eye wall extends into the vitreous cavity. Fortunately, only in unusual circumstances does this process become exaggerated and result in what clinicians have termed FVI with its concomitant intraocular mischief [3].
McLeod pointed out that ischemia is an important factor in inducing FVI and that it is seen mainly following vitrectomy for ischemic retinopathies. I agree that this is the case if one includes anterior proliferative vitreoretinopathy (APVR) in this group. Patients with APVR
who have had previous vitrectomy frequently have an excessive amount of fibrovascular scarring from their sclerotomies that significantly affects the pathologic anatomy of the basal vitreous and its environs. These
patients, however, often have had extensive scleral buckling and cryopexy, processes which undoubtedly induce some anterior ischemia in themselves [2].
In the series of West and Gregor, no patient was found to have a retinal detachment utlrasonographically or at the time of VCWO. In the original description of AHFP, most of the patients had retinal detachments that had required scleral buckling [4]. Since retinal detachment and scleral buckling exacerbate anterior ischemia, it is likely that AHFP, which is fibrovascular proliferation into the vitreous base from the retina and ciliary body, is induced by an ischemic drive similar to that casing FVI. The two entities exist on a continuum. When there is a surgical injury
such as a sclerotomy, with disruption of tissue and inoculation of blood into the surrounding vitreous, excessive proliferation may occur with less
induction than that which causes AHFP. Personally, although I have observed cases of AHFP without having previous vitrectomy, I have never seen a case of post-vitrectomy AHFP without some concurrent FVI.
Finally, I'd like to make two other points. The first is that West and Gregor used clinical criteria to determine whether or not FVI existed and caused the recurrent vitreous hemorrhage. I have observed vitreous hemorrhage in an autopsy eye from what grossly appeared to be a normally
healed sclerotomy wound [5]. Microscopically, that white scar contained numerous capillaries that were the source of the hemorrhage. Therefore, it may be that some of their non-FVI patients might actually have had vitreous hemorrhage from a sub-clinical FVI. Furthermore, FVI can involute with time, becoming less vascular in its appearance. So, the
frequency of FVI may be even higher than reported.
Lastly, I agree that episcleral sentinel vessels, externally entering the wound site, sometimes, but now always, indicate a possible FVI. These vessels are the result of a high degree of metabolic activity during the healing of sclerotomy wounds and may persist even though wound fibroplasia becomes involutional and clinically unimportant. Similar vessels are seen microscopically in the ciliary body [2]. When present, sentinel[2] vessels
should raise our suspicions of FVI; but they do not rule it in, nor does their absence rule it out.
References
1. McLeod D. Entry site neovascularisation after diabetic vitrectomy. Br J Ophthalmol 2000;84:810-811.
2. Kreiger A. The pars plana incision: experimental studies, pathologic observations, and clinical experience. Trans Amer Ophthalmol Soc 1991;89:549-621.
3. Kreiger A, Straatsma B, Foos R. Incisional complications in pars plana vitrectomy. Mod Prob Ophthalmol 1977;18:210-233.
4. Lewis H, Abrams G, Williams G. Anterior hyaloidal fibrovascular proliferation after diabetic vitrectomy. Am J Ophthalmol 1987;104:607-613.
5. Foos R, Kreiger A, Nofsinger K. Pathologic study following vitrectomy for proliferative diabetic retinopathy. Retina 1985;5:101-106.
Editor
We read with interest the study that compared intraoperative mitomycin C to beta irradiation in primary pterygium surgery.
The authors rightly commented that long term complications of beta-irradiation, such as scleral necrosis, may arise more than 10 years after the irradiation. Longer follow-ups are necessary to reveal such
complications.
Editor
We read with interest the study that compared intraoperative mitomycin C to beta irradiation in primary pterygium surgery.
The authors rightly commented that long term complications of beta-irradiation, such as scleral necrosis, may arise more than 10 years after the irradiation. Longer follow-ups are necessary to reveal such
complications.
We performed primary pterygium excision with intraoperative beta-irradiation in one eye of 6 patients between 1988 and 1990. 1000 rads of
beta-irradiation was applied to the scleral bed intraoperatively and one week
later. They were recently reviewed in our clinic for recurrence and
complications.(1) We also performed ultrasound biomicroscopic examination
(UBM) for both eyes in each patient, looking for corneal and scleral
thinning. Corneal thickness was arbitrarily measured 0.5 mm anterior to
the scleral spur at the 12, 3, 6, and 9 o'clock positions of each eye,
while the scleral thickness was measured 2 mm posterior to the scleral
spur at the same positions.
Mean follow-up was 138.0 months. Mean age at time of surgery was
37.5 years (range, 32 to 45 years). All 6 eyes were right eyes with nasal
pterygia in male patients. No recurrence was found, using the same
definition. There was neither significant deterioration in visual acuity
nor increase in intraocular pressure in any eye. There were no signs of
inflammation.
There were no significant differences in the scleral and corneal
thickness between the treated nasal position of the operated eye (mean
scleral, 0.617 +/- 0.112 mm; mean corneal, 0.656 +/- 0.076 mm) and the
control nasal position of the fellow eye (mean scleral, 0.611 +/- 0.030
mm; mean corneal, 0.645 +/- 0.044 mm).
Furthermore, there were no significant differences in the mean
scleral and corneal thickness between the operated eye (scleral, 0.590 +/-
0.077 mm; corneal, 0.635 +/- 0.067 mm) and the fellow eye (scleral, 0.590
+/- 0.059 mm; corneal, 0.624 +/- 0.054 mm). The mean scleral and corneal
thickness were calculated by averaging the scleral or corneal thickness at
the 4 measured positions in each eye.
It appears that beta-irradiation is safe, even in the long term. We
believe these additional data could supplement the findings by Amano et
al.
1. Moriarty AP, Crawford GH, McAllister IL, et al. Severe corneoscleral
infection. A complication of beta scleral necrosis following pterygium
excision. Arch Ophthalmol 1993;111(7):947-51.
Editor,
With great interest we read the case report by Dr. Alwitry on "Vitamin A deficiency in coeliac disease", which raises the question whether a deficiency of vitamin A with subsequent keratomalacia may be caused by this disorder. However, although coeliac disease cannot be excluded as a cause of reduced vitamin A absorption,[1] Alwitry's report does not convincingly show that the vitamin A deficie...
Editor,
I read the article by Bechmann et al with interest, and I congratulate the authors on their work. In the discussion, they cover the entire subject of tonometry on the basis of the central corneal thickness (CCT). With the increasing number of corneal refractive procedures performed every year, this point will be associated with much uncertainty for diagnosing glaucoma in the near future. Appare...
Dear Sir,
In India, we very commonly see mature cataracts. Doing capsulorhexis with injection of dye is done very routinely by many of us. Forunately no untoward reaction has been reported so far. This helps us to carry out the phaco procedure with ease.
Dear Sir,
I was fascinated by Cheng and colleagues' article on Mooren's ulcer in China. During the past 6 years I have worked for 3 years as an ophthalmologist in rural Cameroun. I submit to you my experiences of Mooren's ulcer there :
Patients: 5 (4 male, 1 female).
Age: 1 patient aged 48 years, the rest all late teens and twenties.
Out of 3 patients we tested (foll...
Editor,
We read with interest the paper by Minasian et al. They quote that pain experienced during an injection is related to the temperature of the injection and the speed of delivery of the solution.[1] [2]
In their article, they have used all anaesthetics at room temperature. We have been pre-warming our anaesthetic solutions routinely for cataract surgery. We use a heat pad (Dreamland appliance...
Editor,
The paper by Cullinane and Cleary presents an excellent prospective study of peripheral visual field loss in patients undergoing macular hole surgery. The authors compared vitrectomy with complete posterior cortical vitreous peeling to limited vitrectomy with removal of cortical vitreous off the macula, but not off the optic nerve head or the peripheral retina. The authors showed a statistically...
Editor,
We read with interest the article by Ishioka and coworkers, in which the authors studied the effect of trabeculectomy with and without mitomycin C in post-keratoplasty glaucoma. The authors conclude that trabeculectomy with mitomycin C showed better results for glaucoma following penetrating keratoplasty. We congratulate the authors for an excellent study. We have published similar observations on...
Editor,
The commentary by Waldock and Cook on the survival rates of corneal grafts highlights a number of issues. In particular, they focus on the lack of long-term follow-up data in the UK. The value of such data is clearly evident from the Australian Corneal Graft Register.[1] Moreover, in the present climate of clinical audit and evidence-based medicine, the collection of such data has surely become a...
Editor,
The work of West and Gregor again points out the importance of sclerotomy complications following pars plana vitrectomy. They demonstrate that, even in the hands of a skillful and experienced surgeon, vitreous hemorrhage after vitrectomy for diabetic retinopathy is common and requires vitreous cavity washout (VCWO) in 12% of cases. In their series, over half of the eyes had detectable fibrovascular...
Editor
We read with interest the study that compared intraoperative mitomycin C to beta irradiation in primary pterygium surgery.
The authors rightly commented that long term complications of beta-irradiation, such as scleral necrosis, may arise more than 10 years after the irradiation. Longer follow-ups are necessary to reveal such complications.
We performed primary pterygium excision...
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