published between 2000 and 2003
I commend Xie et al for their paper on the treatment of fungal keratitis by penetrating keratoplasty . Though the subject is increasingly brought to the notice of the ophthalmic community, it requires more emphasis. This is not a unique problem for China but a major problem for many developing and underdeveloped countries.
In response to this article, a number of questions are raised. Wheth...
In response to this article, a number of questions are raised. Whether all these cases are pure fungal keratitis or mixed fungal/bacterial infections were also included? No mention was made on this, and it is important to know as the treatment modalities differ on both types. It is also unclear from the report whether all eyes were KOH smear-proved or not. Further, was there any rationale to perform KOH staining for corneal ulcer unlike dermatological fungal infection? Presently, calcoflour white and acridine orange stain have become more popular and KOH wet mount preparation is replaced by saline wet mount preparation. What is the authors' opinion?
The authors have classified the ulcers into different categories according to size. But I wonder why they have given systemic antifungal medication to all the patients even when the ulcer's size was less than 6mm. Moreover, fungal corneal ulcers require repeated debridement and (if required) keratectomy for better drug penetration. No mention was made of this aspect. The rationale for fluconazole use in all eyes was not given; this drug is not effective for all fungi and the cultures from surgically removed corneal buttons demonstrate a variety of fungal isolates including Fusarium. Conjunctival flap in active ulcer is usually not advised because of the spread of the ulcer underneath the flap. Lamellar keratoplasty in fungal ulcer is also not indicated as the fungi have the tendency for deeper involvement, even in a vertical manner , which is very difficult to judge on the operating table.
Infective corneal tissue removal 0.5 mm larger than the exact dimension of the corneal lesion is a worthy point; this approach accounts for negligible re-infection rate [1,3]. While surgical procedures are very well described , for an eye with total corneal ulcer, a sclerokeratoplasty  would have been a better choice than a total PKP using a 14 mm penetrating graft.
Subconjunctival injections of fluconazole at the time of surgery and for another 3 consecutive days following surgery is again confusing as discussed earlier. Topical antifungals to a recently grafted cornea could be epitheliotoxic. I would like to know the experience of the authors on this.
I agree with the authors' view that earlier surgical intervention to remove the infected tissue may help in the final outcome. But it is also equally important to make the fungi nonviable prior to therapeutic keratoplasty. Furthermore, poor outcomes in such eyes are due to (i) surgery in an inflamed eye; (ii) presence of vascularization; (iii) deeper involvement of ocular tissue by the organism; (iv) the increased incidence of operative and post-operative complications; and (v) grater need of a larger recipient window .
The authors have very rightly pointed out the value of histopathological evaluation of surgically removed corneal tissue following keratoplasty . However, the characteristic features which may help for further management were not discussed.
Following therapeutic keratoplasty both anatomical and functional success need equal mention. Visual outcomes following therapeutic keratoplasty reported by the authors are really exciting1. Reports from various series, listed in the table below, reveal functional success between 13-60% of eyes with over 85% anatomical success [3,5-7]. Functional success of 54.7% was achieved in a previous series  where the graft size was less than 8.5 mm. The percentage of success receded as the size increased accounting for their excellent achievement.
Finally, I would like to know from the authors whether they had tried amniotic membrane graft prior to therapeutic keratoplasty in any eyes, as this is one of the current modes of management of recalcitrant ulcers.
Professor A Panda
Therapeutic Keratoplasty (Comparative Study)
Authors & Year
Anatomical Success: Anatomical integrity of the globe is maintained
Functional Success: Visual gain 6/60
In a recent "Perspective" article by Morlet et al titled "Astigmatism and the analysis of its surgical correction"  there are a number of omissions and fundamental errors of content that lead to erroneous conclusions. These significant inaccuracies overlooked in the review process compromise the article's broad contribution.
In Dr Morlet's attempt to detail "the use and limitations of vector...
In Dr Morlet's attempt to detail "the use and limitations of vectors. . . for the analysis of change in astigmatism" he displays an incomplete understanding of the subject. He has made a valiant attempt to assemble an abundance of historical and contemporary references on a subject of significant interest, but key material has been omitted or misquoted. This has resulted in leading statements of the article, in both the body of the text and even the conclusion that require re-evaluation and substantial revision.
The most obvious omission, is the paper's absence of any discussion of the difference vector, a precise absolute measure of surgical error described in reference 70 . When the difference vector is related to the treatment (ie: TIA or target induced astigmatism vector) one has an extremely useful relative value of success of astigmatism treatment. Dr Morlet has overlooked this key vectorial entity and struggles to find any useful alternative. In sharp contrast Dr Doug Koch, Editor of the Journal of Cataract and Refractive Surgery, in his editorial introduction to the Analyzing Astigmatism issue of January 2001  described the difference vector and the index of success as "remarkably useful and intuitive means of understanding the effects of the surgery".
The authors state more than once for their principle foundation of the article that "Vector analysis alone does not provide any indication of the relative value of the surgical procedure and that it (vector analysis) does not assign a value to the outcome". These statements are erroneous, and the author's failure to discuss or dispute the value of the difference vector and index of success leaves the assertion unsupported and lacking credibility. If the surgical induced astigmatism vector (SIA) (and its further translation) was the only product of vector analysis, indeed vector analysis would be a limited tool. This seems to be Dr Morlet's contention. This is far from the truth and as a result the restatement in the conclusion that "vector analysis does not give a measure of outcome" is factually inaccurate.
In addition, Dr Morlet's interpretation that the off-axis effects of treatment at 45 degrees to the surgical plane are deemed to be rotation, would more accurately be termed "torque" the component of the SIA that has been ineffective in reducing astigmatism. The relevant reference  describing flattening, steepening, torque and effect of off-axis treatments has been omitted from the attempt at a comprehensive list of relevant published material. The phenomena of rotation and torque are fundamentally different physical processes. The polar value at 45 degrees to the "surgical plane" quantifies the torque which causes an increase in the existing astigmatism associated with its change in orientation. It does not properly gauge the cylinder rotation where no concurrent change in the amount of existing astigmatism occurs. Rotation includes some associated flattening (or steepening) effect occurring as a result of the SIA.
The article's conclusion that "a better evaluation of the effect of astigmatism axis requires the use of the 'by the rule' or mirror equivalent axis notation, or by a manual scoring method to produce an outcome summary measure" is convoluted and unworkable. If implemented this would adversely affect the comprehension of astigmatism outcome analysis by the average general ophthalmic or refractive surgeon.
It is unfortunate the reviewers of this paper did not direct the author to other significant fallacies that merited revision. The statement "vector analysis is only valid in the early post-operative period" because "the healing response has modified the initial result of the surgery" shows the authors' failure to understand that the healing response cannot be divorced from the surgical process. It is part of it. The amount of astigmatism correction (SIA/TIA) achieved shows consistent trends over time when examining aggregate data, and this phenomenon requires surgeons to examine outcomes facilitating adjustment of nomograms based on longterm (at least 6 months) and not immediate outcomes. The later statement "the use of vector analysis over time is conceptually invalid, because unlike the initial surgical event, the wound healing process is continuous" is seriously flawed. Vector analysis is an essential component of this refinement process. In fact, vector analysis could be used to determine the astigmatic effect of the healing process itself by comparison of data at various stages in the post-operative period.
The recommendations promoted by Dr Morlet introduce greater complexity to an already complicated subject. For example, mixing negative and positive cylinder notation is unnecessary. The technique put forward does not address the changes that occur in corneal shape as measured by keratometry and topography, and cannot be readily applied when targeting non-zero goals associated with incomplete or off-axis refractive astigmatism treatments.
It is probable that the authors are careless in raising phantom "problems" for planning techniques based on incorrect quoting of information (such as reference 33).  The merits of this customized treatment technique are that refractive as well as keratometric data are employed (contrary to its misrepresentation that the technique "only uses keratometric data for the planning of refractive surgery").
Dr Morlet's unfortunate statement of opinion that "a lack of critical evaluation" has resulted in "the surgical vector's adoption as the de facto standard used in most reports concerning the surgical management of astigmatism" is not shared by many experienced investigative surgeons in the field. This has been shown by its admitted prevalence by the authors, and the usefulness of vectorial analysis in understanding the surgical process . Indeed, many of the erroneous statements and omissions in the Perspective article might lead one to ask where the "lack of critical evaluation" actually lies.
(1) Morlet N, Minassian D, Dart J. Astigmatism and the analysis of its surgical
correction. Br J Ophthalmol 2001; 85:1127-1138
(2) Alpins NA. A new method of analyzing vectors for changes in astigmatism.
J Cataract Refract Surg 1993;19:524-533
(3) Koch DD. How should we analyze astigmatic data? J Cataract Refract Surg
(4) Alpins NA. Vector Analysis of astigmatism changes by flattening, steepening
and torque. J Cataract Refract Surg 1997;23:1503-1514
(5) Alpins NA. Astigmatism analysis by the Alpins Method. J Cataract Refract
(6) Alpins NA. New method of targeting vectors to treat astigmatism. J Cataract
Refract Surg 1997;23:63-75
We would like to thank Dr Panda for the comments on our paper. We agree that amniotic membrane grafts yield excellent results in various ocular surface defects, without donor site morbidity.
We also agree that frozen section control of excised tissue might prevent incomplete removal of a malignant conjunctival melanoma. Although we were able to totally excise this tumour in our four reported cases, we wil...
We also agree that frozen section control of excised tissue might prevent incomplete removal of a malignant conjunctival melanoma. Although we were able to totally excise this tumour in our four reported cases, we will surely consider this option in relevant cases.
A point of criticism regards the use of a corneo-scleral graft to reconstruct a partial-thickness corneo-limbal defect in two of our cases, since the lack of transparency of such a graft might interfere with the detection of any deep melanoma recurrence. We agree that this might be possible - especially in the scleral part - but we believe that primary reconstruction is easier and leads to better functional results than corneo-scleral grafting at a later stage, when fibrosis and scarring may hamper surgery. In the event that the histopathologist indicates that there was incomplete excision of tumour, we prefer to remove the graft to facilitate further excision. We are looking forward to reports from other surgeons in these regards.
WA van den Bosch
We are grateful to Dr Anita Panda and colleagues for supporting our
work and comments made in the above article (Panda A eletter BJO 21st
A new classification to include all the variables expanded on by
ourselves and by Panda A et al in the eletter is indeed essential and has
been proposed by us and published in the British Journal of
Ophthalmology. It is very important t...
A new classification to include all the variables expanded on by
ourselves and by Panda A et al in the eletter is indeed essential and has
been proposed by us and published in the British Journal of
Ophthalmology. It is very important to take into consideration the
amount of surviving conjunctiva and the clock hours of viable limbus.
Inflammation is a crucial factor post burn. Hence the importance of
witholding any form of autologous or living related donor derived tissue
in the acute stages following burns. These tissues are a valuable resource
and can be destroyed in the inflammatory and cicatrizing processes that
accompany acute burns.
The new classification has been examined by other clinicians involved
in the treatment of such burns and is proving to be a useful alternative
to the existing classification.
Although amniotic membrane grafting is not very successful in acute
(total) burns (12/100% new classification), the role of ex-vivo expanded
limbus derived cells on amniotic membrane transplant, combined with
autologous serum (in the presence of an avascular bed) remains to be fully
Reference: (1) Dua HS, King AJ, Joseph A. A new classification of ocular surface
burns. Br J Ophthalmol 2001;85:1379-83
We read with interest the article titled "Amniotic membrane transplantation in the management of conjunctival malignant melanoma and primary acquired melanosis with atypia" by Paridaens D et al and compliment the authors for bringing the important upcoming issue of Amniotic membrane transplantation (AMT) to the limelight.
The authors described the favourable outcome of AMT for the reconstruction of su...
The authors described the favourable outcome of AMT for the reconstruction of surface defects resulting from surgical excision of conjunctival malignant melanoma and primary acquired melanosis (PAM) with atypia. They have further commented on its role in repairing larger defects involving the fornix or palpebral conjunctiva still needs to be established. As per our experience goes we feel the procedure should be followed after any type of ocular surface reconstruction as a primary procedure. Besides the advantages put forward by the authors that it helps in post operative monitoring of tumour recurrence and cosmesis, it provides the additional encouraging factor that unlike other grafting procedures, it does not hamper the recipient tissue integrity for which it can be repeated several times. Moreover, even if there is formation of some degree of symblepharon in due course of time the same can be tackled by local excision and repeat AMT without hampering the integrity of recipient's vital ocular tissues.
While we entirely agree with the technique the authors described, our only concern is about the frozen section. It is always better to perform the frozen section in suspected tumour as its exact malignant nature could not be predicted clinically. It is more so for the extensive tumour in guiding the surgeon for precise excision.
The second point, which bothers us about the corneo-scleral graft. No doubt, the corneo scleral grafting is desirable following the side partial thickness excision of cornea and sclera[3,4]. However, while the procedure is quite safe and effective for inflammatory and degenerative lesions, its use may raise questions in neoplastic lesions. Though very barely evident, the fear of masking the recurrent lesion in surgeon's mind always persists. Therefore, in an era of AMT, we do not advocate the corneo scleral grafting for neoplastic lesions for primary procedure. However, either tectonic sclero corneal graft or limbal cell transplantation can be performed at a later date depending on the situation/status of the recipient's eye.
Once again we congratulate the authors for bringing this valuable technique to the attention of ophthalmic surgeons.
(1) Paridaens D, Beekhuis H, Vanden Bosch W, Remeyer L, Melles G. Amniotic membrane transplantation in the management of conjunctival malignant melanoma and primary acquired melanosis with atypia. Br Jour Ophthalmol 2001; 85:658-61.
(2) Panda A, Sharma N. Frozen section guided excision and LK. Ophthalmic Surg. News International 1996;7:42.
(3) Panda A, Sharma N, Sen S, Ghose S, Tityal JS, Das GK. Lamello lamellar sclerokeratoplasty in squamous cell carcinoma of conjunctiva and cornea. Year Book. Proceedings A.I.O.S. 1996, pp278-9.
(4) Panda A, Sharma N, Sen S. Frozen section guided excision and lamellar sclerokeratoplasty for squamous cell carcinoma of conjunctiva and cornea. Advance cornea 1997, Plenium press, Boston pp 373-79.
Recently, Cahill et al. published a paper on pupillary autonomic denervation in diabetic patients. In our own recent study we can confirm the presence of a small dark-adapted pupil size (DAP) before cardiovascular autonomic dysfunction is detected in patients with type-1 diabetes mellitus. We believe that this is an important observation, since autonomic alterations may cause an increase in mortality as...
Recently, Cahill et al. published a paper on pupillary autonomic denervation in diabetic patients. In our own recent study we can confirm the presence of a small dark-adapted pupil size (DAP) before cardiovascular autonomic dysfunction is detected in patients with type-1 diabetes mellitus. We believe that this is an important observation, since autonomic alterations may cause an increase in mortality as repeatedly evidenced for cardiac autonomic neuropathy (CAN).
In particular, we found a significantly reduced DAP in patients with normal ranges in high frequency waves of heart spectral analysis as a marker for cardiac parasympathetic nerve lesions and in variation coefficient of heart rate variability. Like Cahill et al., we could also show significant reduced pupillary responses to cocaine 4% eye drops in patients with CAN as a test for sympathetic nerve alterations. The DAP of patients with CAN did not yield significant differences with the age-matched controls. Patients without any systemic diabetic long-term complication defined as CAN, peripheral sensomotor neuropathy, retinopathy and nephropathy had no significant differences in their DAP as compared to the probands.
Thus, it is of interest if in this study patients with CAN also significantly differ in their pupillary responses to cocaine, and if patients without CAN possibly have other diabetic long-term complications or increased gylcosylated hemoglobin levels, which may correlate with the small DAP.
Nevertheless, this study by Cahill et al. also clearly indicates that screening for pupillary dysfunction is mandatory as early as possible to prevent the sequelae of other autonomic neuropathic disorders.
(1) Cahill M, Eustace P, de Jesus V. Pupillary autonomic denervation with increasing duration of diabetes mellitus. Br J Ophthalmol 2001; 85: 1225-30.
(2) Pittasch D, Lobmann R, Behrens-Baumann W, Lehnert H. Autonomic sympathetic neuropathy of the pupil in patients with diabetes mellitus type 1. Exp Clin Endocrinol Diabetes 2000; suppl. 1: S37.
(3) McNally PG, Lawrence IG, Panerai RB, Weston PJ, Thurston H. Sudden death in type-1 diabetes. Diab Obes Metabol 1999; 1:151-8.
(4) Sharma S, Hoskin-Mott A, Benstead T, Maxner C. Correlation of the pilo-pupil ratio average, a new test for autonomic denervation, to the severity of diabetic retinopathy. Can J Ophthalmol 1997; 32.170-4.
Miyata and colleagues have elegantly described an interesting and rare complication of phototherapeutic keratectomy (PTK) in their recent report of an unusual case of keratectasia after PTK. The hypothesis that risk of ectasia is proportional to residual stromal base, or depth of ablation, fits with the assumed biomechanical aetiology of this recently reported complication of laser refractive surgery. The gene...
Miyata and colleagues have elegantly described an interesting and rare complication of phototherapeutic keratectomy (PTK) in their recent report of an unusual case of keratectasia after PTK. The hypothesis that risk of ectasia is proportional to residual stromal base, or depth of ablation, fits with the assumed biomechanical aetiology of this recently reported complication of laser refractive surgery. The generally accepted empirical minimum thickness of 250-300µm of corneal stroma, excluding flap thickness, remains speculative, as we do not understand the underlying pathophysiology. Indeed, although Holland et al highlighted the association of thin residual stromal thicknesses, post PRK and LASIK, with keratectasia, they also described this complication after surface based Hypermetropic-PRK ablation, where the centre was minimally ablated and residual stromal thickness was greater than 360µm.
The authors suggest, in the reported case, that Band Shaped Keratopathy (BSK) may have compromised the tensile strength of the cornea. This seems unlikely as this condition generally affects the superficial anterior cornea, and usually does not penetrate deeper than Bowman's, hence its suitability for treatment by PTK. However, further clinical detail which the authors have not provided might reveal underlying corneal pathology with secondary "rough" BSK, rather than "smooth" BSK.
However, there are a number of alternative reasons, other than simple biomechanical compromise, for keratectasia following PTK in this case.
A) Forme fruste keratoconus - as no pre-op topography or surface asymmetry values are presented to enable the reader to rule this out.
B) Clinical keratoconus - which seems less likely in respect to patients age and a pre-operative cylindrical error of only -1.5D.
C) Idiopathic keratectasia - possibly secondary to widespread de-regulated keratocyte apoptosis. The latter has been demonstrated after LASIK, with a considerable and longstanding decrease in keratocytes in the peri-ablation area. Also, Helena et al (1998) demonstrated apoptosis to a depth of at least 50µm following all the procedures: epithelial scrape, corneal scrape PTK, transepithelial PRK, and LASIK. Epithelial scrape and LASIK demonstrated keratocyte apoptosis to depths of up to 75µm and 100µm respectively. The authors have recently identified a keratocyte free zone 160µm into the stroma following LASIK, and theoretically more widespread apoptosis as a response to excimer laser photorefractive surgery, which may contribute to keratectasia.
Whilst it is difficult to ascertain why keratectasia occurs, in this case with a residual stromal thickness of over 500µm, from the data provided the most likely aetiologies would seem to be either undiagnosed forme fruste keratoconus or idiopathic keratectasia. Currently recent reviews illustrate the dearth of substantial information available regarding idiopathic keratectasia (iatrogenic keratoconus), with a little over 50 cases published. At this point in time, although some are likely to be due to over-ablation, for many cases such as this the exact aetiology remains unknown and is likely to be multifactorial, and one of these factors is residual corneal thickness. The fact that keratectasia can occur, after what would be considered minimal ablation, highlights the unpredictability of occurrence, but with over a million cases of LASIK or PRK occurring each year, the stimulus to identify contributing factors is significant.
Dr Simon J Dean MB ChB
Professor Charles N J McGhee
Discipline of Ophthalmology, Faculty of Medicine and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand
(1) Miyata K. Takahashi T. Tomidokoro A. Ono K. Oshika T. Iatrogenic keratectasia after phototherapeutic keratectomy. Br J Ophthalmol 2001; 85: 247-8
(2) Holland SP. Srivannaboon S. Reinstein DZ. Avoiding serious corneal complications of laser assisted in situ keratomileusis and photorefractive keratectomy. Ophthalmology 2000; 107(4):640-52
(3)Vesaluoma M. Perez-Santonja J. Petroll WM. Linna T. Alio J. Tervo T. Corneal stromal changes induced by myopic LASIK Investigative Ophthalmology & Visual Science 2000; 41(2):369-76
(4)Helena MC. Baerveldt F. Kim WJ. Wilson SE. Keratocyte apoptosis after corneal surgery. Investigative Ophthalmology & Visual Science 1998; 39(2):276-83,
(5)Edwards M. Kent D. McGhee CNJ. Idiopathic keratectasia (Iatrogenic keratoconus). J CME Ophthalmol (in press)
This series is certainly the largest ever reported in west Africa . However, it is worth noting that Xeroderma Pigmentosum (XP) has already been described in two Mauritanian half cousins in France . Two isolated cases have been reported in Senegal and Cameroon, respectively [3,4]. The skin of black people, rich in melanin provides some protection from the oncogenic effects of ultraviolet rays. It is possib...
This series is certainly the largest ever reported in west Africa . However, it is worth noting that Xeroderma Pigmentosum (XP) has already been described in two Mauritanian half cousins in France . Two isolated cases have been reported in Senegal and Cameroon, respectively [3,4]. The skin of black people, rich in melanin provides some protection from the oncogenic effects of ultraviolet rays. It is possible, in my opinion, that it prevents the occurrence of skin lesions in subclinical forms and reduces the frequency of XP. This hypothesis raises the question of the protection of mucosae.
In south Cameroon where the sickle cell trait affects up to 40% of the population, it is well known among the Bantu tribes that marriages within the same clan is not allowed. The people still consider themselves brothers and sisters in the same clan even after an exponential number of generations. Consequently, there is a low coefficient of consanguinity concerning all hereditary disorders with an autosomal recessive transmission mode.
(1) Ahmed H, Hassan R, Pindiga U. Xeroderma pigmentosum in three
consecutive siblings of a Nigerian family: observations on oculocutaneous manifestations in black African children. Br J Ophthalmol 2001; 85: 110.
(2) Bouzamel F, Sarasin A, Fohlen M, Blanchet-Gardon C. Xeroderma
pigmentosum associé à un syndrome de Cockayne. Ann Dermatol Veneorol (Paris) 1992; 119: 823-825.
(3) Ndiaye B, Ball MD, Strobel M, Niang I. Xeroderma pigmentosum. Première observation sénégalaise. Dakar Médical 1983; 28: 167-172.
(4) Moussala M, Behar-Cohen F, D'Hermies F, Bisseck AC, Renard G. Le
xeroderma pigmentosum et ses manifestations oculaires. A propos du premier cas camerounais. J Fr Ophtalmol 2000; 23(4): 369-374.
We read with interest the article titled "Failure of amniotic membrane transplantation (AMT) in the treatment of acute ocular burns" by Joseph et al. It is to be appreciated that they have come forward to report the negative results of their study along with the need of an upgraded classification for the chemical burn. The authors must be congratulated for highlighting the pitfalls of the AMT in acute cases w...
We read with interest the article titled "Failure of amniotic membrane transplantation (AMT) in the treatment of acute ocular burns" by Joseph et al. It is to be appreciated that they have come forward to report the negative results of their study along with the need of an upgraded classification for the chemical burn. The authors must be congratulated for highlighting the pitfalls of the AMT in acute cases with sufficient scientific explanation.
Whenever a new technique is described, it is aggressively followed without realizing the consequences. The authors have very rightly suggested that the most important strategy for the management of thermal and chemical burns in the acute stage is to reduce inflammation, promote vascularization of the ischaemic ocular surface and epithelialisation of the cornea. It is reported in the literature that AMT does help in all these 3 conditions at acute stage of burn for which the procedure is advocated. but when and to what stage? It is essential to have some amount of healthy conjunctival tissue for graft to take up. Further, rather than performing the AMT at an acute stage, some gap should be given between burn and surgery. This may help to reduce inflammation, thus, allowing the surgeons to perform an elective surgery. As regards to the stage of the chemical burn, the author has very rightly pointed out that there is a remarkable limitation in modified Roper Halls classification at grade IV. Do the eyes with 100% limbal ischaemia behave the same as those with 55% ischaemia1.
Dating back to 1984 it was thought of and a modified classification was suggested in these eyes prior to keratoplasty as a prognostic factor. However, the same was restricted to healed lesions and now the time has come the modification is needed for acute lesions.
Once again we would like to commend the authors for their boldness and wonder how many of the corneal surgeons would have felt the same.
(1) Joseph A, Dua HS, King AJ. Failure of amniotic membrane transplantation (AMT) in the treatment of acute ocular burns. Br. Jour Ophthalmol 2001;85:1065-9.
(2) Mellor D, Renato TF, Pires et al. AMT for acute chemical or thermal burns. Ophthalmology 2001;107:980-90.
(3) Roper Hall MJ. Thermal and chemical burns. Trans ophthalmol soc UK 1965;85-631-40.
(4) Panda A, Mohan M, Gupta AK, Chowdhary S. Keratoplasty in alkali burned corneas. Indian J. Ophthalmol 1984;32:441-6
I read with interest the article by Ekatomatis  on latanoprost treatment for primary open angle glaucoma causing herpes simplex dendritic keratitis. He should be applauded for reporting a serious side effect of latanoprost. His assertion however that latanoprost has been known to have almost no serious side effects is not entirely accurate. In fact, Wand et al  reported three patients who developed herp...
I read with interest the article by Ekatomatis  on latanoprost treatment for primary open angle glaucoma causing herpes simplex dendritic keratitis. He should be applauded for reporting a serious side effect of latanoprost. His assertion however that latanoprost has been known to have almost no serious side effects is not entirely accurate. In fact, Wand et al  reported three patients who developed herpes simplex dendritic keratitis after therapy with latanoprost for primary open angel glaucoma. One patient with a previous history of herpes simplex keratitis had a recurrence while taking latanoprost, and resolved when latanoprost was discontinued. When rechallenged with latanoprost the patient again developed herpes simplex dendritic keratitis. A second patient with a history of bilateral herpes simplex dendritic keratitis had recurrence in both eyes on latanoprost treatment, confirmed on viral cultures, which only resolved on discontinuation of latanoprost and the start of antiviral treatment. When rechallenged with latanoprost therapy with concurrent prophylactic antiviral medication, the cornea remained clear. With discontinuation of antiviral suppression, herpes simplex dendritic keratitis recurred.
Using a rabbit model, Kaufman et al  have confirmed a relationship between latanoprost therapy and the recurrence and severity of herpes simplex keratitis. Latanoprost is a potent prostaglandin F2a analogue. Ekatomatis proposed biochemical disturbance of the surface of the cornea as a mechanism through which latanoprost causes recurrence of keratitis. It is more likely that prostaglandins, known to enhance the multiplication of herpes viruses , may be a common final pathway in herpes simplex keratitis recurrence. A multi-centre double blind case controlled study is required to clarify the side effect profile of this commonly used drug.
(1) Ekatomatis P. Herpes simplex dendritic keratitis after treatment with latanoprost for primary open angle glaucoma. Br J Ophthalmol 2001;85;1008-9.
(2) Wand M, Gilbert CM, Liesegang TJ. Latanoprost and herpes simplex keratitis. Am J Ophthalmol 1999;127:602-4.
(3) Kaufman HE, Varnell ED, Thompson HW. Latanoprost increases the severity and recurrence of herpetic keratitis in the rabbit (comment). Am J Ophthalmol 1999;127;531-6.
(4) Harbour DA, Blyth WA, Hill TJ. Prostaglandins enhance spread of herpes simplex virus in cell structures. J Gen Virol 1978;41:87-95.