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,
I was interested to read the case report of branch retinal artery
occlusion (BRAO) in a 69 year old male that was presumed to have been
caused by sildenafil.
In addition to transient cardiac arrhythmia, the authors speculate
that the underlying mechanism of arterial occlusion may have been a sudden
rise in intra-ocular pressure caused by Viagra. They do not mention
whether the arteri...
Editor,
I was interested to read the case report of branch retinal artery
occlusion (BRAO) in a 69 year old male that was presumed to have been
caused by sildenafil.
In addition to transient cardiac arrhythmia, the authors speculate
that the underlying mechanism of arterial occlusion may have been a sudden
rise in intra-ocular pressure caused by Viagra. They do not mention
whether the arterial occlusion had any relationship to coitus. If the
speculation that Viagra did elevate IOP is correct, the physical activity
of coitus would tend to reduce intraocular pressure (1) possibly
normalising the IOP. On the other hand, sexual arousal has been found to
precipitate angle closure glaucoma in anatomically predisposed eyes (2, 3)
in which case the elevated IOP, if indeed it was ever present, possibly
may not have been caused by Viagra.
The absence of risk factors in the reported patient should not
automatically implicate Viagra as the cause of BRAO, since the underlying
aetiology is unclear in a sizeable minority of patients with retinal
arterial occlusive disease (4). Coitus has previously been associated with
amarosis fugax (5), and Tripathi and O'Donnell acknowledge that many
patients using Viagra would be at a high risk of vascular occlusions
anyway.
The authors recommend that branch retinal artery occlusion "should
be…discussed with all patients started on sildenafil". It would place an
unacceptable burden on both doctors and their patients if they had to
discuss every side effect of prescribed drugs, especially if the possible
side effect has only ever been reported once in many tens of millions
prescriptions. In many instances, even if the time was available for such
discussion, this would probably generate unnecessary anxiety and cause
further harm to the patient by reducing patient compliance.
I would avoid alarming patients with speculation that Viagra may
cause blindness until more compelling evidence is available to justify
this warning.
1) Harris A, Arend O, Bohnke K, et al. Retinal
blood flow during dynamic exercise. Graefes Arch Clin Exp Ophthalmol. 1996;234:440-4.
2) Friedberg DN, Fox LE. Blurred vision during sexual arousal
associated with narrow-angle glaucoma. Am J Ophthalmol 1999;128:647-648.
3) Markovits A. Ophthalmodynia hypertonica copulationis: a new
syndrome? Can J Ophthalmol 1974:9:484-485.
4) Haase CG, Buchner T. Microemboli are not a prerequisite in retinal
artery occlusive diseases. Eye 1998;12:659-662.
5) Teman A, Winterkorn J, Weiner D. Transient monocular blindness
associated with sexual intercourse. N Engl J Med 1995;333:393
Editor,
Could you please provide a reference for Bell's phenomenon and the occurrence of optical zone intrusion as well as the ability to control spontaneous eye movements during the procedure?
Editor,
I am a 76-year-old suffering from myopic degeneration (is this ARMD?).I have been operated for cataract on my left eye with no significant improvement. I am strongly convinced that the usual measurement of visual acuity is almost
meaningless. The major problem I find in practical life is the lack of adequate sensitivity to contrast. For example, in my bank they print their copy report with a gray ink...
Editor,
I am a 76-year-old suffering from myopic degeneration (is this ARMD?).I have been operated for cataract on my left eye with no significant improvement. I am strongly convinced that the usual measurement of visual acuity is almost
meaningless. The major problem I find in practical life is the lack of adequate sensitivity to contrast. For example, in my bank they print their copy report with a gray ink (for reasons of elegance, I suppose). These are not readable to me, but if I use a scanner copy they become immediately
readable. In the seventy years that I have undergone eye tests I do not remember one single time that somebody would care about contrast sensitivity. Is there at least a standard procedure to measure contrast sensitivity about which I could inquire and possibly use to check my progress?
Thank you.
Editor,
I read the paper by Liao et al with interest. It is indeed one of the biggest studies of mitomycin C in external DCR. I have few queries about how mitomycin C was
applied. Firstly, where should the pledget of mitomycin C be placed if the posterior flaps of the nasal mucosa and the sac are not sutured? My practice is to take a U-shaped flap of both the nasal mucosa and the lacrimal sac. Second...
Editor,
I read the paper by Liao et al with interest. It is indeed one of the biggest studies of mitomycin C in external DCR. I have few queries about how mitomycin C was
applied. Firstly, where should the pledget of mitomycin C be placed if the posterior flaps of the nasal mucosa and the sac are not sutured? My practice is to take a U-shaped flap of both the nasal mucosa and the lacrimal sac. Secondly, how is the cotton pledget removed after the 30 mins? Is it removed endoscopically?
Editor,
We read with interest the article by Culliance and Cleary on the method of prevention of visual field defects after macular hole surgery. In their series, one group of 82 eyes received conventional pars plana vitrectomy surgery with mechanical induction of posterior vitreous detachment (PVD) around the optic disc followed by complete posterior cortical vitreous removal. Twenty-two percent of these...
Editor,
We read with interest the article by Culliance and Cleary on the method of prevention of visual field defects after macular hole surgery. In their series, one group of 82 eyes received conventional pars plana vitrectomy surgery with mechanical induction of posterior vitreous detachment (PVD) around the optic disc followed by complete posterior cortical vitreous removal. Twenty-two percent of these eyes had certain postoperative visual field defect. On the contrary, another group of 20 eyes received pars plana vitrectomy with peeling of the posterior hyaloid
confined to the macular area with sparing of the peripapillary region. None of them had any postoperative visual field loss. The authors proposed that vitreopapillary traction around the optic nerve head during the mechanical separation of the posterior hyaloid is responsible for the
formation of the observed postoperative inferotemporal visual field defects. The microcirculation at the optic nerve head may be damaged during the induction of PVD as the posterior cortical vitreous is most adherent at the superonasal aspect of the optic disc.[1] However, we are
concerned about the standardisation of the method of removing the remaining peripheral cortical vitreous in these two groups of eyes, as peripheral vitreous may act as a protective cushion from dehydration during fluid/air exchange. Yan et al[2] had shown that no significant
correlation was found between iatrogenic detachment of vitreous cortex and postoperative visual field defect, but all patients who had postoperative visual field defect had undergone fluid/air exchange in their series.
Similarly, Ohji et al[3] had demonstrated that using humidified air for fluid/air exchange in macular hole surgery could prevent postoperative visual field defect. Others had demonstrated that the visual field defect
was dependent upon the site of the air infusion port.[4] [5] All these reports suggest that air dehydration of the peripheral retina may be a very important factor in causing postoperative visual field defect after macular hole surgery.
In conclusion, we congratulate Culliance and Cleary on their study describing the prevention of visual field defects after macular hole surgery by limited posterior hyaloid peeling. However, the exact mechanism behind this success needs further evaluation.
1. Katz B, Hoyt WF. Intrapapillar and peripapillary hemorrhage in young patients with incomplete posterior vitreous detachment. Signs of vitreopapillary traction. Ophthalmology 1995;102:349-54.
2. Yan H, Dhurjon L, Chow DR, et al. Visual field defect after pars plana vitrectomy. Ophthalmology 1998;105:1612-6.
3. Ohji M, Nao-IN, Saito Y, et al. Prevention of visual field defect after macular hole surgery by passing air used for fluid-air exchange through water. Am J Ophthalmol 1999;127:62.
4. Takenaka H, Maeno T, Mano T, et al. Causes of visual field defects after vitrectomy. Nippon Ganka Gakkai Zasshi 1999;103(5):399-403.
5. Welcj 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.
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...
Editor,
I was interested to read the case report of branch retinal artery occlusion (BRAO) in a 69 year old male that was presumed to have been caused by sildenafil.
In addition to transient cardiac arrhythmia, the authors speculate that the underlying mechanism of arterial occlusion may have been a sudden rise in intra-ocular pressure caused by Viagra. They do not mention whether the arteri...
Editor,
Could you please provide a reference for Bell's phenomenon and the occurrence of optical zone intrusion as well as the ability to control spontaneous eye movements during the procedure?
Editor,
I am a 76-year-old suffering from myopic degeneration (is this ARMD?).I have been operated for cataract on my left eye with no significant improvement. I am strongly convinced that the usual measurement of visual acuity is almost meaningless. The major problem I find in practical life is the lack of adequate sensitivity to contrast. For example, in my bank they print their copy report with a gray ink...
Editor,
I read the paper by Liao et al with interest. It is indeed one of the biggest studies of mitomycin C in external DCR. I have few queries about how mitomycin C was applied. Firstly, where should the pledget of mitomycin C be placed if the posterior flaps of the nasal mucosa and the sac are not sutured? My practice is to take a U-shaped flap of both the nasal mucosa and the lacrimal sac. Second...
Editor,
We read with interest the article by Culliance and Cleary on the method of prevention of visual field defects after macular hole surgery. In their series, one group of 82 eyes received conventional pars plana vitrectomy surgery with mechanical induction of posterior vitreous detachment (PVD) around the optic disc followed by complete posterior cortical vitreous removal. Twenty-two percent of these...
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