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.
We read with interest the paper by Tan et al. [1] on Charles Bonnet
Syndrome (CBS) in Asian patients. Their finding of a lower CBS prevalence
than European or North American surveys demands further investigation,
although this may reflect the stringent criteria of hallucination
complexity they used in making the diagnosis (thus excluding the commonest
CBS hallucinations of coloured blobs and gri...
We read with interest the paper by Tan et al. [1] on Charles Bonnet
Syndrome (CBS) in Asian patients. Their finding of a lower CBS prevalence
than European or North American surveys demands further investigation,
although this may reflect the stringent criteria of hallucination
complexity they used in making the diagnosis (thus excluding the commonest
CBS hallucinations of coloured blobs and grid-like ‘tesselloptic’
patterns [2,3]) and, as pointed out in the accompanying editorial comment,
the relatively low prevalence of macular disease in their cohort.
However, it is not this aspect of the report we found most intriguing - it
was the observation that CBS occurred with good acuity. In fact, 3 of the
4 CBS patients described had a degree of impairment which placed them at
risk for CBS (best eye acuity 0.3 or worse [4]). It is the remaining
patient (patient three, a 72 year old male) who is of particular
importance as his relative preservation of acuity bilaterally (20/30 RE,
20/40 LE) challenges the view that significant acuity loss is a
prerequisite for ‘ophthalmological’ visual hallucinations. This case
mirrors 4 patients we have recently studied with Charles Bonnet Syndrome
secondary to glaucoma and bilaterally good acuity. We describe the cases
below and offer a pathophysiological mechanism for the association.
In one sense, the finding that CBS occurs with preserved acuity is
hardly novel. As cited by Tan et al.[1], several previous reports have
found such an association. However, all is not as it seems, the term
Charles Bonnet Syndrome (CBS) being used in different ways by different
authors. Some use the term to describe visual hallucinations with insight,
irrespective of the presence of eye disease, age or clinical context [5,6].
Others use the term to describe the association of visual hallucinations
with age and intact cognition, without reference to eye disease or
hallucination phenomenology [7,8]. Under these definitions it is hardly
surprising that a patient with ‘CBS’ has preserved acuity, the patients in
these studies having a diverse range of conditions from delirium to
Parkinson’s disease and beyond. In contrast, ophthalmologists and
neurologists have used CBS to emphasise eye or visual pathway disease,
with the phenomenology of the hallucinations and age being of secondary
importance [9,10]. Although each definition of CBS has its merits, the ophthalmological definition reminds us best of Bonnet’s original
description and helps characterise a distinctive subgroup of visually
hallucinating patients with predicable prognosis and specific
pathophysiology [2,11]. However, even CBS as defined ophthalmologically
carries with it an inherent ambiguity: is it eye disease itself or the
loss of acuity that is the important factor? The consistent finding of
acuity loss as a risk factor [4,12,13] suggests the latter, or at least
that the central retina plays a key role in the underlying pathophysiological mechanism.
As part of a larger study into the visual phenomenology of CBS, we
have recruited 4 patients with advanced glaucoma (3 POAG and 1 chronic
narrow angle) but preserved visual acuity. The age range of the patients
was 81 to 91, 3 men and 1 woman. Their visual acuities ranged from 6/6 to
6/12 monocularly with all patients having 6/9 or better in their better
eye. All had extensive field defects bilaterally and cup to disc ratios of
0.8 or greater in both eyes. 2 patients had bilateral trabeculectomies now
off treatment, one was on g.bimatoprost and g.trusopt to both eyes and one
on g.timolol 0.25% to both eyes. 2 patients were bilaterally pseudophakic.
The patient with chronic narrow angle glaucoma had previous surgical
iridectomies. The duration of their hallucinations ranged from 6 months to
6 years. 3 patients hallucinated in colour and one in black and white. The
most common hallucination was of tessellopsia [2] experienced by all the
patients, with 2 patients seeing, in addition, formed buildings and 2
patients, letter-like shapes. There were also single reports of
hallucinations of groups of people, animals, branching shapes
(dendropsia [2]) and one patient described visual allesthesia [14]. In three
of the patients the hallucinations encompassed the entire visual field, in
the fourth they were restricted to the visual field defect. None had
hallucinations in other sensory modalities and all had insight into the
nature of the experiences. The phenomenology of the hallucinations and the
relative frequency of the different hallucination categories are
consistent with previous descriptions of ophthalmologically-defined
CBS [2,3]. Non-ophthalmological causes of visual hallucinations [2,3] were
excluded. As far as we are aware this is the largest case series of
patients with visual hallucinations secondary to eye disease and
bilaterally preserved visual acuity yet to be reported.
Current aetiological theories of CBS emphasise the importance of
deafferentation [15] (both ‘physiological’ through ganglion cell loss and
‘functional’, e.g. related to blindfolding or cataract), the loss of
visual input resulting in a change in cortical excitability [2]. Although
it has been assumed that deafferentation of sufficient severity to
precipitate CBS implies a consequent loss of acuity, our cases and that of
Tan et al.[1] suggest otherwise. Patients with advanced glaucoma can have
a significant degree of ganglion cell loss and consequent physiological deafferentation without a loss of acuity, placing them at risk for CBS.
This contrasts with age related macular disease where the loss of central
retinal ganglion cells leads, indirectly, to an association of CBS with
acuity loss. We conclude that reduced acuity is not a necessary
prerequisite for ophthalmologically-defined CBS and that ophthalmologists
should be aware that patients with preserved acuity but significant
deafferenting ocular disease are at risk of the syndrome.
References
(1) Tan CSH, Lim VSY, Ho DYM, Yeo E, Ng BY, Au Eong KG. Charles Bonnet
syndrome in Asian patients in a tertiary ophthalmic centre. Br J
Ophthalmol 2004; 88: 1325-1329.
(2) ffytche DH, Howard RJ. The perceptual consequences of visual loss:
positive pathologies of vision. Brain 1999; 122: 1247-1260.
(3) Santhouse AM, Howard RJ, ffytche DH. Visual hallucinatory syndromes
and the anatomy of the visual brain. Brain 2000; 123: 2055-2064.
(4) Teunisse RJ, Cruysberg JR, Verbeek AL, Zitman FG. The Charles
Bonnet syndrome: a large prospective study in the Netherlands. Br J
Psychiatry 1995; 166: 254-257.
(5) Damas-Mora J, Skelton-Robinson M, Jenner FA. The Charles Bonnet
Syndrome in perspective. Psychol Med 1982; 12: 251-261.
(6) Gold K, Rabins PV. Isolated visual hallucinations and the Charles
Bonnet syndrome: a review of the literature and presentation of six cases.
Compr Psychiatry 1989; 30: 90-98.
(7) Podoll K, Osterheider M, Noth J. Das Charles Bonnet-Syndrom.
Fortschr. Neurol. Psychiat. 1989; 57: 43-60.
(8) de Morsier G. Le syndrome de Charles Bonnet: hallucinations
visuelles des vieillards sans deficience mentale. Annales Medico-
Psychologiques 1967; 125: 677-702.
(9) Manford M, Andermann F. Complex visual hallucinations. Clinical and
neurobiological insights. Brain 1998; 121: 1819-1840.
(10) Menon GJ, Rahman I, Menon SJ, Dutton GN. Complex visual
hallucinations in the visually impaired: the Charles Bonnet Syndrome. Surv
Ophthalmol 2003; 48: 58-72.
(11) ffytche DH. Visual hallucination and illusion disorders: a
clinical guide. Advances Clin Neurosci Rehab 2004; 4: 16-18.
(12) Holroyd S, Rabins PV, Finkelstein D, Nicholson MC, Chase GA,
Wisniewski SC. Visual hallucinations in patients with macular
degeneration. Am J Psychiatry 1992; 149: 1701-1706.
(13) Scott IU, Schein OD, Feuer WJ, Folstein MF. Visual hallucinations
in patients with retinal disease. Am J Ophthalmology 2001; 131: 590-598.
(14) Girkin CA, Miller NR. Central disorders of vision in humans. Surv
Ophthalmol 2001; 45: 379-405.
(15) Burke W. The neural basis of Charles Bonnet hallucinations: a
hypothesis. J Neurol Neurosurg Psychiatry 2002; 73: 535-541.
I would like to congratulate Abugreen et al.[1] for publishing an
interesting article on the relationship between choroidal
neovascularisation (CNV) in one eye and age related maculopathy (ARM) in
the opposite eye. However, the required data to support some of the
authors’ conclusions were not given in the paper.
The authors stated in the abstracts that ‘the area occupied by the
CNV in t...
I would like to congratulate Abugreen et al.[1] for publishing an
interesting article on the relationship between choroidal
neovascularisation (CNV) in one eye and age related maculopathy (ARM) in
the opposite eye. However, the required data to support some of the
authors’ conclusions were not given in the paper.
The authors stated in the abstracts that ‘the area occupied by the
CNV in the first eye also influenced severity of ARM changes in the fellow
eye.’ In the results section it was stated that ‘age, sex, cardiovascular
disorder and smoking status were not significant predictors for ARM
severity in this model’. In the statistical analysis section of ‘Methods’,
as well as in the footnotes to table 5 of ‘Results’, it was mentioned that
the ‘CNV subtype’ was the dependent variable and not the ‘ARM severity in
the fellow eye’. Therefore, the model was attempting to predict the ‘type
of CNV in the same eye’, and not the ‘ARM severity in the fellow eye’
using the independent variables: age, sex, cardiovascular disorder, etc.
In addition, there appears to be typographical errors in the p values on
the right of table 5, 0.57 should read 0.057, 0.19 should read 0.019.
In table 5, the odds ratio of stage 3 ARM (soft indistinct drusen or
reticular drusen with pigmentary irregularities) being 9.48 times more
than no ARM predicting an occult CNV over a classic CNV was also
misleading. This is because the individual coefficients of the independent
variables reflect the contribution of these factors (including area of the
CNV lesion) to the variance of the dependent variable (the CNV subtype)!
In order to examine the effect of CNV subtype in one eye on the severity
of ARM in the other eye, perhaps the authors should collapse the five
possible values for the severity of ARM into two and designate this the
dependent variable in the logistic regression model. Since the logistic
regression model predicts the log odds that an observation will have an
indicator equal to 1, to facilitate interpretation of odd ratios, it is
crucial to specify which of the response condition (‘occult CNV’ or
classic CNV’) is designated as ‘1’ (the counterpart being ‘0’).
Alternatively, they could perform ‘multiple linear regression’ and
designate ‘severity of ARM’ as the dependent variable with five possible
values. In either of these two alternatives, area of lesion (in the eye
with CNV), age etc could be additional independent variables.
If the authors were to compare only ‘severity of ARM’ with ‘CNV
subtype’ (4 possible values), Kendall’s rank correlation is also a
reasonable approach.
Reference
(1) Abugreen S, Muldrew, KA, Stevenson MR et al. CNV subtype in the first eyes predicts severity of ARM in fellow eyes. Br J Ophthalmol 2003;87:307-311.
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.
In his second eLetter (1), Dua continues his criticism of our
proposed modification of the classification of ocular surface burns(2)
but
once again fails to understand our motivation, which is to simplify the
grading of such injuries in the light of recent advances in the
management
of ocular surface disease (3-6). The result is a modification of a well
established classification, which is easily reme...
In his second eLetter (1), Dua continues his criticism of our
proposed modification of the classification of ocular surface burns(2)
but
once again fails to understand our motivation, which is to simplify the
grading of such injuries in the light of recent advances in the
management
of ocular surface disease (3-6). The result is a modification of a well
established classification, which is easily remembered and can be used
by
all ophthalmologists and not just by corneal specialists. The Dua, King
and Joseph classification (7) allows quantification of the injury, which
is useful in a research environment but is trapped in its detail for
routine clinical use.
We would reiterate that our modifications are based on
recent advances in the management of ocular surface injuries, which have
meant that even severe injuries can have good outcomes (3-6). This is
the
rationale for having Grade III as the most severe injury grade and for
uniformly assigning to it a guarded prognosis. Within that grade,
different injury patterns will have different management protocols and
different rates of recovery. The work by Roper Hall (8) elegantly showed
that a good and doubtful prognosis correlated respectively to less or
more
than one third of conjunctival ischaemia at the limbus. Hence we
retained
this element of his classification to separate Grade II and Grade III in
our modification. It serves to identify a serious ocular surface injury
to
the non-corneal specialist who can then arrange an appropriate referral.
Dua's confusion about the role of 'OR' in our table in order to define
the
Grade of injury is actually dealt with in the text of the original
article
(2): the Grade of the injury is assigned simply on the basis of the most
severe sign, rather than on the complex analysis of a combination of
signs.
Dua is supportive of our inclusion of conjunctival injury in our
proposed modification (1) but disagrees with the inclusion of tarsal
conjunctival assessment, on the basis that it does not influence
prognosis. This is clearly wrong. Contiguous tarsal and bulbar injury
can
lead to symblepharon formation and shortening of the conjunctival
fornices, which is detrimental to the ocular surface and therefore
deserves inclusion in any assessment of ocular surface injury. The
bulbar
and tarsal conjunctiva extends into the fornices and forniceal
conjunctival involvement is therefore included in the measured area of
involvement - important for possible stem cell sites (9).
We would leave it to readers of the Journal and those involved in
this field to judge the value of the different grading systems.
References
1. Dua HS. Classification of ocular surface burns. Br J Ophthalmol
eLetter ( 11 August 2004)
2. Harun S, Srinivasan S, Hollingworth K, Batterbury M, Kaye SB.
Modification of the classification of ocular chemical injuries. Br J
Ophthalmol 2003;88:1353-1354
3. Kobayashi A, Shirao Y, Yoshita T, et al.Temporory amniotic
membrane patching for acute chemical burns. Eye 2003; 17: 149-158
4. Stoiber J, Muss WH, Pohla-Gubo G, Ruckhofer J, Grabner G.
Histopathology of human corneas after amniotic membrane and limbal stem
cell transplantation for severe chemical burn. Cornea
2002;21(5):482-489.
5.Nishiwaki-Dantas MC, Dantas PE, Reggi JR. Ipsilateral limbal
translocation for treatment of partial limbal deficiency secondary to
ocular alkali burn. Br J Ophthalmol 2001;85(9):1031-1033
6.Ozdemir O, Tekeli O, Ornek K, Arslanpence A, Yalcindag NF. Limbal
autograft and allograft transplantations in patients with corneal burns.
Eye 2004;18(3):241-248
7.Dua HS, King AJ, Joseph A. A new classification of ocular surface
burns. Br J Ophthalmol 2001;85:1379-1383
8.Roper-Hall MJ. Themal and chemical burns.Trans Ophthalmol Soc UK
1965;85:631-53
9.Wei Z-G, Cotsarelis G, Sun T-T, Lavker RM. Label-retaining cells
are preferentially located in the forniceal epithelium:implications on
conjunctival epithelial haemostasis. Invest Ophthal Vis Sci
1995;36:236-46
I read the article by Pun et al.[1] with interest. My experience with
ketamine is (thankfully) limited to operating in Bosnia after the war.
Out of the six patients one vomited on the field. Difficulty is
encountered in re-ops due to lack of muscle paralysis. Ketamine also
has well known after
effects. In my opinion it is neither safe nor effective. Learning and
using safe anesthesia techniques...
I read the article by Pun et al.[1] with interest. My experience with
ketamine is (thankfully) limited to operating in Bosnia after the war.
Out of the six patients one vomited on the field. Difficulty is
encountered in re-ops due to lack of muscle paralysis. Ketamine also
has well known after
effects. In my opinion it is neither safe nor effective. Learning and
using safe anesthesia techniques would be the best in any country.
Reference
(1) M S Pun, J Thakur, G Poudyal, R Gurung, S Rana, G Tabin, W V Good, and S Ruit. Ketamine anaesthesia for paediatric ophthalmology surgery. Br J Ophthalmol 2003;87:535-537.
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.
We read with interest the report by Henderson et al.[1] The title of the paper includes the word "early" and the
median time to leak is 3.5 days, but the range of time taken for bleb
leakage to develop extends to 408 days postoperatively. We do not think
this is early nor a postoperative complication.
Wound leakage complicates the management of trabeculectomy: some eyes
develop anter...
We read with interest the report by Henderson et al.[1] The title of the paper includes the word "early" and the
median time to leak is 3.5 days, but the range of time taken for bleb
leakage to develop extends to 408 days postoperatively. We do not think
this is early nor a postoperative complication.
Wound leakage complicates the management of trabeculectomy: some eyes
develop anterior chamber shallowing, choroidal detachment and even
hypotony, causing the clinician to intervene by a variety of methods.
Whilst leakage is occurring subconjunctival fibrosis may proceed
unchecked, but standard interventions, such as needling with injection of
5-fluorouracil, may be contraindicated in the presence of a wound leak.
It would be helpful for the reader to know whether any interventions were
needed or were delayed, since not only may these affect the long term
outcome but also will help to guide the surgeon managing a wound leak.
1. H W A Henderson, E Ezra, and I E Murdoch
Early postoperative trabeculectomy leakage: incidence, time course, severity, and impact on surgical outcome
Br J Ophthalmol 2004; 88: 626-629.
First of all let me congratulate the authors for their work on
exudative ARMD. But there are still some issues which need to be
brought into account:
1. Some published studies show that even 4.0 mg of intravitreal
triamcinolone has significant side effects in terms of increased IOP and
more so for eyes which needed the second dose of the triamcinolone, with
a few of them even needing a filtratio...
First of all let me congratulate the authors for their work on
exudative ARMD. But there are still some issues which need to be
brought into account:
1. Some published studies show that even 4.0 mg of intravitreal
triamcinolone has significant side effects in terms of increased IOP and
more so for eyes which needed the second dose of the triamcinolone, with
a few of them even needing a filtration surgery. In this particular
study however 25mg of Triamcinolone has been used which may cause even
more increased elevation of IOP. This issue is an important one as many
of our ARMD patients have co-existing chronic open angle glaucoma with a
compromised blood supply of the optic nerve head. With the intravitreal
steroids induced rise in IOP, we may tilt the balance on the wrong side
thereby taking their peripheral vision along-with the central loss due
to the ARMD. [1,2,5]
2. The effect of intravitreal steroids in the progression of
cataract is
not very much emphasized in various studies. If earlier cataract surgery
in treated ARMD patients is required, this has theoretical implications
in terms of ultraviolet light exposure, one of the environmental factors
implicated in ARMD. If there is no long term benefit for preventing the
progression of ARMD with the steroids then why should we increase the
chances of cataract in these patients thereby rendering their retinas
more vulnerable to damage caused by the UV radiation?[2]
3. Various in-vitro studies suggest that down-regulation of
inflammatory
markers and changes in the endothelial cell permeability are probably
the
modes of action of triamcinolone in exudative ARMD, but all these
actions
are probably only for the duration when the steroids are in high
concentration in the vicinity. To maintain high concentrations
triamcinolone should be injected repeatedly and probably that is the
reason the improvement fades with time in many patients. Moreover none
of the studies published so far have been long enough to actually give a
fair idea about the long term outcome. The longest duration for which
the follow up has been done is 18 months. [3,4]
We need data from multicenter, placebo-controlled trials on a much larger population with long-term follow-up to establish the efficacy of the drug and assess possible side effects and complications. Until then we should probably reserve this therapy for those cases where
there is recurrence after laser treatment.[5]
References
(1) Danis RP, Ciulla TA, Pratt LM, Anliker W. Intravitreal triamcinolone acetonide in exudative age-related macular degeneration. Retina 2000; 20(3):244-50.
(2) Challa JK, Gillies MC, Penfold PL, Gyory JF, Hunyor AB, Billson FA. Exudative macular degeneration and intravitreal triamcinolone: 18 month follow up. Aust N Z J Ophthalmol. 1998 Nov;26(4):277-81.
(3) Penfold PL, Gyory JF, Hunyor AB, Billson FA. Exudative macular
degeneration and intravitreal triamcinolone. A pilot study. Aust N Z J
Ophthalmol 1995 Nov;23(4):293-8.
(4) Jonas JB, Kreissig I, Degenring R. Intraocular pressure after
intravitreal injection of triamcinolone acetonide. Br J Ophthalmol 2003 Jan;87(1):24-7.
(5) Ranson NT, Danis RP, Ciulla TA, Pratt L. Intravitreal
triamcinolone in subfoveal recurrence of choroidal neovascularisation
after laser treatment in macular degeneration.
Br J Ophthalmol 2002 May; 86(5):527-9.
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...
Dear Editor
We read with interest the paper by Tan et al. [1] on Charles Bonnet Syndrome (CBS) in Asian patients. Their finding of a lower CBS prevalence than European or North American surveys demands further investigation, although this may reflect the stringent criteria of hallucination complexity they used in making the diagnosis (thus excluding the commonest CBS hallucinations of coloured blobs and gri...
Dear Editor
I would like to congratulate Abugreen et al.[1] for publishing an interesting article on the relationship between choroidal neovascularisation (CNV) in one eye and age related maculopathy (ARM) in the opposite eye. However, the required data to support some of the authors’ conclusions were not given in the paper.
The authors stated in the abstracts that ‘the area occupied by the CNV in t...
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...
Dear Editor
In his second eLetter (1), Dua continues his criticism of our proposed modification of the classification of ocular surface burns(2) but once again fails to understand our motivation, which is to simplify the grading of such injuries in the light of recent advances in the management of ocular surface disease (3-6). The result is a modification of a well established classification, which is easily reme...
Dear Editor
I read the article by Pun et al.[1] with interest. My experience with ketamine is (thankfully) limited to operating in Bosnia after the war. Out of the six patients one vomited on the field. Difficulty is encountered in re-ops due to lack of muscle paralysis. Ketamine also has well known after effects. In my opinion it is neither safe nor effective. Learning and using safe anesthesia techniques...
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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...
Dear Editor
We read with interest the report by Henderson et al.[1] The title of the paper includes the word "early" and the median time to leak is 3.5 days, but the range of time taken for bleb leakage to develop extends to 408 days postoperatively. We do not think this is early nor a postoperative complication.
Wound leakage complicates the management of trabeculectomy: some eyes develop anter...
Dear Editor
First of all let me congratulate the authors for their work on exudative ARMD. But there are still some issues which need to be brought into account:
1. Some published studies show that even 4.0 mg of intravitreal triamcinolone has significant side effects in terms of increased IOP and more so for eyes which needed the second dose of the triamcinolone, with a few of them even needing a filtratio...
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...
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