We thank BV Kumar and S Prasad for their interest in our report
describing the successful treatment of macular oedema (MO) secondary to
branch retinal vein occlusion (BRVO) with intravitreal triamcinolone
injection (IVTI).[1]
Although definitively establishing a clinical diagnosis of posterior
vitreous detachment (PVD) may be problematic, our patient did not have a
Weiss ring and no eviden...
We thank BV Kumar and S Prasad for their interest in our report
describing the successful treatment of macular oedema (MO) secondary to
branch retinal vein occlusion (BRVO) with intravitreal triamcinolone
injection (IVTI).[1]
Although definitively establishing a clinical diagnosis of posterior
vitreous detachment (PVD) may be problematic, our patient did not have a
Weiss ring and no evidence of PVD in the macular region was visible on
serial optical coherence tomography (OCT) scanning before or following
treatment.
We believe it is unlikely that the primary mechanism of action of
IVTI in treating MO is the induction of a PVD. We have treated another
patient with OCT confirmed MO associated with BRVO which initially
responded rapidly to IVTI with restoration of normal foveal contour and
improvement in visual acuity. This patient subsequently developed
recurrence of MO and visual loss one year following the initial treatment.
Retreatment with IVTI resulted in a rapid improvement in visual acuity and
restoration of foveal contour confirmed with OCT.
If induction of a PVD were the primary mechanism of IVTI efficacy in
reducing MO, then repeated treatments with IVTI would not be expected to
be efficacious as it would not be possible to induce a PVD more than once.
This is at odds with our own frequent clinical experience of successful
repeated IVTI’s for the treatment of recurrent MO associated with
posterior uveitis or the reported efficacy of repetitive IVTI’s for MO
associated with diabetic retinopathy [2] and pseudophakic cystoid MO.[3]
It might be interesting to speculate on the effect that the presence
or absence of a pre-existing PVD may have on the efficacy of IVTA and we
agree that it is important that such factors are considered in future
reports.
References
(1) Prasad S, BV Kumar, S Prasad. How does intravitreal triamcinolone work? [electronic response to Chen et al. Intravitreal triamcinolone acetonide for ischaemic macular oedema caused by branch retinal vein occlusion] bjophthalmol.com 2004http://bjo.bmjjournals.com/cgi/eletters/88/1/154#275
(2) Martidis A, Duker JS, Greenberg PB, et al. Intravitreal
triamcinolone for refractory diabetic macular edema. Ophthalmology
2002;109:920-7
We greatly appreciate the inquiry of Dr Vendantham and are happy to reply to his questions.[1]
While Dr Vendantham is correct regarding the definition of
ophthalmia neonatorum including all infections acquired by an infant
during the first 30 days of life, for the purposes of our study,[2] we were
primarily interested in those cases resulting from neonatal exposure in
the birth canal. This...
We greatly appreciate the inquiry of Dr Vendantham and are happy to reply to his questions.[1]
While Dr Vendantham is correct regarding the definition of
ophthalmia neonatorum including all infections acquired by an infant
during the first 30 days of life, for the purposes of our study,[2] we were
primarily interested in those cases resulting from neonatal exposure in
the birth canal. This source of ophthalmia neonatorum is the one that
would be influenced mainly by a second drop of Povidone-Iodine placed
later on the day of birth. Infections postnatally that Dr Vendantham
listed arising, while technically still within the definition of
"ophthalmia neonatorum", would not be impacted by this second drop and
therefore would not be directly affected by this study. Indeed, Dr
Vendantham's interest in neonatal dacryocystitis
would also fall within the same question since the reflux from the tear
duct causing this infection generally does not arise until well after the
first day of life.
The proportion of ophthalmia neonatorum cases acquired postnatally
compared with those acquired during the birth process probably differs by
country. The difference in predominant causative organisms (Staph aureus
and enterococcus in the former situation as in India [3] vs. chlamydia and
gonococcus in the latter) probably reflects the origin of the infection.
Historically, in Kenya a high proportion of the infections probably arose
from the birth process as reflected in the type of infecting organism.
This, our Kenyan study was primarily directed toward those infections
acquired during birth.
The fact that ophthalmia neonatorum in some countries seems to peak
in certain seasons and not in other seasons should cause increased
vigilance for this disorder in those countries. Our study, however,
encompassed more than one full year of births in Kikuyu, Kenya. Therefore,
the study included both the peaks and valleys of the incidence of
ophthalmia neonatorum.
We thank Dr Vendantham for his interest and hope that in many
countries, including India, ophthalmia neonatorum prophylaxis will either
continue unabated or be initiated preferentially with the use of Povidone-
Iodine.
Sincerely,
Sherwin J. Isenberg, M.D.
Lantz Professor
Pediatric Ophthalmology
Leonard Apt, M.D
Professor of Ophthalmology
Director Emeritus, Division of Pediatric Ophthalmology
References
(1) Vedantham V. Prophylaxis of ophthalmia neonatorum [electronic response to SJ Isenberg, L Apt, M Del Signore, S Gichuhi, NG Berman; A double application approach to ophthalmia neonatorum prophylaxis] ophthalmol.com 2004http://bjo.bmjjournals.com/cgi/eletters/87/12/1449#245
(2) Isenberg SJ, Apt L, Del Signore M, Gichuhi S,Berman NG. A double
application approach to ophthalmia neonatorum prophylaxis. Br. J
Ophthalmol 2003;87(12):1449-1452.
(3) Verma M, Chhatwal J. Vareghese PV. Neonatal conjunctivitis: a
profile. Indian Pediatr 1994;31(11):1357-1361.
I read with interest the case report of Ashraff et al[1] where a
posterior chamber phakic intraocular lens (PCPIOL) was used in a
pseudophakic eye with axial myopia and pseudoexfoliation for the
management of anisometropia. I would like to highlight a potential
problem in such eyes: dislocation of PCPIOL into the vitreous cavity.
PCPIOLs are inserted blindly behind the iris and, depen...
I read with interest the case report of Ashraff et al[1] where a
posterior chamber phakic intraocular lens (PCPIOL) was used in a
pseudophakic eye with axial myopia and pseudoexfoliation for the
management of anisometropia. I would like to highlight a potential
problem in such eyes: dislocation of PCPIOL into the vitreous cavity.
PCPIOLs are inserted blindly behind the iris and, depending on the
design, allow their haptics to rest at the structures of the posterior
chamber or float in it. Ultrasound biomicroscopy (UBM) identified haptic-
zonules contact and lens rotation for the Implantable Contact Lens (ICL)[2]
and the Phakic Refractive Lens (PRL),[3] although these PCPIOLs are intended
to fixate at the ciliary sulcus and float in the posterior chamber
respectively. Because of this potential haptic-zonules contact and lens
rotation of PCPIOLs the entire zonular apparatus should be intact and
healthy.
Pseudoexfoliation is characterised by progressive zonular disruption
and axial myopia by zonular weakness and both conditions may lead to
zonular defects. Although phakodonesis and iridodonesis may point towards
zonular insufficiency, those signs may be absent in a number of eyes with
occult zonular defects as shown in UBM studies.[4] Such zonular defects may
result in spontaneous dislocation of the PCPIOL into the vitreous cavity.
Two cases have been described already where PCPIOLs dislocated into the
vitreous cavity through such defects. Kaya et al.[5] reported a case of
dislocation of a silicone PCPIOL into the vitreous cavity following mild
head injury three weeks postoperatively in a highly myopic eye (–19 DS).
Another case of dislocation of a myopic PRL into the vitreous cavity has
been reported by the European Clinical Trial with PRL group [Philipson B.
PRL (phakic posterior chamber IOL)-the 12 month results of the European
clinical trial. Presented at the XXI Congress of the ESCRS-Munich 2003].
I have recently reported a case of spontaneous dislocation of a PRL into
the vitreous cavity in a young healthy female with high myopia two months
postoperatively (spherical equivalent –19.5 D). (H Eleftheriadis, S
Amoros, R Bilbao, MA Teijeiro. “Spontaneous dislocation of a Phakic
Refractive Lens into the vitreous cavity”. Submitted for publication to
the J Cataract Refract Surg December 2003).
The reported cases stress the importance of health and integrity of
zonular apparatus in the long-term stability of PCPIOLs. Since
pseudoexfoliation is a progressive disease that may lead to progressive
zonular disruption and spontaneous IOL-bag dislocation into the vitreous
cavity even many years after cataract surgery,[6] I think that PCPIOLs
should not be used in pseudophakic eyes with pseudoexfoliation.
References
1. Ashraff NN, Kumar BV, Das A et al. Correction of pseudophakic
anisometropia in a patient with pseudoexfoliation using an implantable
contact lens. Br J Ophthalmol. 2004;88:309.
2. Trindade F, Pereira F, Cronemberger S. Ultrasound biomicroscopic
imaging of posterior chamber phakic intraocular lens. J Refract Surg.
1998;14:497-503.
3. Garcia-Feijoo J, Hernandez-Matamoros JL, Mendez-Hernandez C et al. Ultrasound biomicroscopy of silicone posterior chamber phakic
intraocular lens for myopia. J Cataract Refract Surg. 2003;29:1932-1939.
4. McWhae JA, Crichton AC, Rinke M. Ultrasound biomicroscopy for the
assessment of zonules after ocular trauma. Ophthalmology. 2003;110:1340-
1343.
5. Kaya V, Kevser MA, Yilmaz OF. Phakic posterior chamber plate
intraocular lenses for high myopia. J Refract Surg. 1999;15:580-585.
6. Jehan FS, Mamalis N, Crandall AS. Spontaneous late dislocation of
intraocular lens within the capsular bag in pseudoexfoliation patients.
Ophthalmology. 2001;108:1727-1731.
SDM Chen and colleagues present a case of successful treatment of
macular oedema in the setting of ischaemic branch retinal vein occlusion
(BRVO).[1]
Intravitreal triamcinolone is increasingly being used as part of
our therapeutic armaterium in a wide range of conditions. However it’s
mode of action is still to be fully elucidated. It is known that the
induction of a posterior vitreous detachme...
SDM Chen and colleagues present a case of successful treatment of
macular oedema in the setting of ischaemic branch retinal vein occlusion
(BRVO).[1]
Intravitreal triamcinolone is increasingly being used as part of
our therapeutic armaterium in a wide range of conditions. However it’s
mode of action is still to be fully elucidated. It is known that the
induction of a posterior vitreous detachment (PVD) may have an important
role in the resolution of macular oedema.[2] In patients undergoing an
arterio-venous sheathotomy procedure for BRVO, surgical detachment of
posterior hyaloid could be as important as the sheathotomy to improve
macular oedema.[3]
In the reported case, it is possible that the intravitreal injection
of triamcinolone may have induced a PVD and this may have contributed to
the resolution of the macular oedema. Thus, it would be useful to know the
status of the posterior hyaloid before and after triamcinolone injection
in this case.
We feel that it is important that all relevant factors such as this
are reported and discussed in this and similar reports in the literature.
This will help us to evolve treatment alogarithms to target newer
interventions such as intravitreal triamcinolone, to the patients most
likely to benefit.
References
1. Chen SDM, Lochhead J, Patel CK, Frith P. Intravitreal
triamcinolone acetonide for ischaemic macular oedema caused by branch
retinal vein occlusion. Br J Ophthalmol 2004 Jan; 88: 154-5.
2. Yamaguchi Y, Otani T, Kishi S. Resolution of diabetic cystoid
macular edema associated with spontaneous vitreofoveal separation. Am J
Ophthalmol 2003 Jan; 135: 116-8.
3. Charbonnel J, Glacet-Bernard A, Korobelnik JF, et al. Management
of branch retinal vein occlusion with vitrectomy and arteriovenous
adventitial sheathotomy, the possible role of surgical posterior vitreous
detachment. Graefes Arch Clin Exp Ophthalmol 2003 Dec 18 [Epub ahead of
print].
I thank Dr Tomsak for his reply[1] to my comments.[2]
In response to point one,we agree that historically CBS is a disorder
described in the elderly, but as we mentioned in our previous reply, this
can easily be explained by the higher incidence of visual loss in the
elderly. Further, without formal child pyschiatry review it is difficult
to give a incidence in the childhood of CBS. As you wo...
I thank Dr Tomsak for his reply[1] to my comments.[2]
In response to point one,we agree that historically CBS is a disorder
described in the elderly, but as we mentioned in our previous reply, this
can easily be explained by the higher incidence of visual loss in the
elderly. Further, without formal child pyschiatry review it is difficult
to give a incidence in the childhood of CBS. As you would expect the very
young may not be able to differentiate between complex visual
hallucinations described by most elderly patients as a very real
phenomenon. Children may simply regard these are real visual stimuli and
not hallucinations. The literature does not support the diagnosis of CBS
on age alone.
Secondly, we support the point that editorial constraints limited the
paper somewhat. However, point three still seems to be a point of
contention. In the abscence of Brimonidine drops, the diagnosis of CBS
would have been justified. However, the onset and remission of CBS with
starting and stopping of brimonidine drops leads to support the fact that
these hallucinations are simply a pyscho-pharmakinetic response, as would
be expected by any medication penetrating the blood-brain barrier.
Indeed, as we described in our previous reply Brimonidine, and drugs of
the same class, have been shown to cause neuropysciatric phenomenon
similar to CBS, and that this effect described by the authours support
this point of visual hallucinations as a side effect of brimonidine
tartrate.
We reiterate our point that these four patients suffered side effects and
not CBS, as current literature does not support this view.
References
(1) Tomsak RL. Charles Bonnet Syndrome - Author reply [electronic response to RL Tomsak, CR Zaret, and D Weidenthal; Charles Bonnet syndrome precipitated by brimonidine tartrate eye drops] bjophthalmol.com 2004http://bjo.bmjjournals.com/cgi/eletters/87/7/917#204
(2) Rahman I, Fernando BS, Harrison M. Charles Bonnet Syndrome and brimonidine: comments [electronic response to RL Tomsak, CR Zaret, and D Weidenthal; Charles Bonnet syndrome precipitated by brimonidine tartrate eye drops] bjophthalmol.com 2004http://bjo.bmjjournals.com/cgi/eletters/87/7/917#189
I appreciate Dr Van Gelder’s thoughtful comments regarding the
potential consequences of a UV+blue light absorbing intraocular lens (IOL)
on circadian rhythmicity.[1] I agree that the clinical importance of retinal
ganglion photoreceptors is currently unknown and that decreasing the
amount of blue light reaching them might affect their function.
Conversely, if photosensitive ganglia respond to circadia...
I appreciate Dr Van Gelder’s thoughtful comments regarding the
potential consequences of a UV+blue light absorbing intraocular lens (IOL)
on circadian rhythmicity.[1] I agree that the clinical importance of retinal
ganglion photoreceptors is currently unknown and that decreasing the
amount of blue light reaching them might affect their function.
Conversely, if photosensitive ganglia respond to circadian changes in
their blue light exposure rather than just the magnitude of that exposure,
a UV+blue light absorbing IOL may not impair ganglion function.
Dr Van Gelder re-emphasizes our finding that IOL chromophore
selection balances the potential loss of useful visual function against a
reduction in the risk of acute UV-blue phototoxicity. Our paper did not
state, however, that UV+blue absorbing IOLs were desirable for people with
outer retinal degeneration. Indeed, blue light is more important in
scotopic than photopic vision. Individuals with age-related macular
degeneration have greater nighttime visual problems than their peers
without it, and these scotopic problems may be exacerbated if a
significant amount of blue light is blocked by an IOL.
Reference
(1) Van Gelder RN. Blue light and the circadian clock [electronic response to Mainster MA and Sparrow JR; How much blue light should an IOL transmit?] bjophthalmol.com 2004http://bjo.bmjjournals.com/cgi/eletters/87/12/1523#257
Drs Mainster and Sparrow have provided an excellent perspective on
the relative merits and difficulties of extending IOL absorption into the
blue portion of the spectrum.[1]
However, they have not considered an unintentional consequence of
blockage of the blue portion of the spectrum: reducing the activity of
intrinsically photosensitive retinal ganglion cells.[2, 3] These cells
subserve se...
Drs Mainster and Sparrow have provided an excellent perspective on
the relative merits and difficulties of extending IOL absorption into the
blue portion of the spectrum.[1]
However, they have not considered an unintentional consequence of
blockage of the blue portion of the spectrum: reducing the activity of
intrinsically photosensitive retinal ganglion cells.[2, 3] These cells
subserve several non-visual ocular photoreceptive tasks, most prominently
the entrainment of the circadian clock to external light-dark cycles.[4]
Pupillary light responses in mice are also at least partially controlled
by this system, which appears to use a novel opsin (melanopsin) [5,6] and
possibly also a flavoprotein (cryptochrome) [7,8] as photopigments.
Experiments in mice have suggested that the action spectrum for these
photopigments peak in the blue, at approximately 480 nm, but with
substantial sensitivity to blue light to 430 nm.[9] This system appears
to be functional in humans as documented by the action spectrum for light
suppression of the pineal hormone, melatonin.[10,11]
The clinical importance of these photoreceptors is presently unknown,
although it appears that loss of retinal ganglion cells predisposes
children and young adults to disorders of sleep timing that outer retinal
disease does not.[12] While, as the authors note, there may be
substantial benefit in blocking blue-light phototoxicity, particularly for
patients with pre-existing outer retinal degeneration, these IOLS lenses
may have unintended consequences with respect to the timing of sleep and
wakefulness or levels of certain neuro-hormones.
References
1. Mainster MA, Sparrow JR. How much blue light should an IOL
transmit? Br. J. Ophthalmol. 2003;87:1523-9.
3. Berson DM, Dunn FA, Takao M. Phototransduction by retinal ganglion
cells that set the circadian clock. Science. 2002;295:1070-3.
4. Freedman MS, Lucas RJ, Soni B, et al. Regulation of mammalian
circadian behavior by non-rod, non-cone, ocular photoreceptors Science.
1999;284:502-4.
5. Panda S, Provencio I, Tu DC, et al. Melanopsin is required for non
-image-forming photic responses in blind mice. Science. 2003;301:525-7.
6. Hattar S, Lucas RJ, Mrosovsky N, et al. Melanopsin and rod-cone
photoreceptive systems account for all major accessory visual functions in
mice. Nature. 2003;424:75-81.
7. Van Gelder RN, Wee R, Lee JA, Tu DC. Reduced pupillary light
responses in mice lacking cryptochromes. Science. 2003;299:222.
8. Selby CP, Thompson C, Schmitz TM, Van Gelder RN, Sancar A.
Functional redundancy of cryptochromes and classical photoreceptors for
nonvisual ocular photoreception in mice. Proc. Natl. Acad. Sci. U. S. A.
2000;97:14697-702.
9. Lucas RJ, Douglas RH, Foster RG. Characterization of an ocular
photopigment capable of driving pupillary constriction in mice. Nat.
Neurosci. 2001;4:621-6.
10. Brainard GC, Hanifin JP, Greeson JM, et al. Action spectrum for
melatonin regulation in humans: evidence for a novel circadian
photoreceptor. J. Neurosci. 2001;21:6405-12.
11. Thapan K, Arendt J, Skene DJ. An action spectrum for melatonin
suppression: evidence for a novel non-rod, non-cone photoreceptor system
in humans. J. Physiol. (Lond). 2001;535:261-7.
12. Wee R, Van Gelder RN. Sleep disturbances in young subjects
with visual dysfunction. Ophthalmology. In press.
The authors report on LASIK surgery in five children with unilateral
high myopia who were presumed to have amblyopia. One subject had
bilateral high myopia.
Optic nerve hypoplasia is associated with high myopia. In addition,
anisometropic myopia is a common sequela of retinopathy of prematurity.
Thinning of the sclera with posterior staphyloma formation has long been
known to be associa...
The authors report on LASIK surgery in five children with unilateral
high myopia who were presumed to have amblyopia. One subject had
bilateral high myopia.
Optic nerve hypoplasia is associated with high myopia. In addition,
anisometropic myopia is a common sequela of retinopathy of prematurity.
Thinning of the sclera with posterior staphyloma formation has long been
known to be associated with high myopia. Best corrected visual acuity in
these patients is often limited by associated retinal and scleral
pathology.
None of the treated eyes obtained acuity better than 6/15. This
limited outcome following refractive surgery may only be due to optical
enlargement of the retinal image rather than enhanced neurosensory
function. In the 3 children who were less than 3 years old improved
literacy, familiarity with the test procedure, and the Hawthorn Effect,
were certainly important factors in their assumed improvement. The
absolute lack of progress in one child was a likely manifestation of pre-
existing retinal pathology rather than non-compliance with patching.
The authors advocate increased use of LASIK to thin the corneas of
highly myopic children who already have profound reductions in scleral
thickness. “From a clinical viewpoint, optic nerve hypoplasia should be
carefully looked for in all patients with unilateral bilateral high myopia
and visual loss.”[1] It may well be more appropriate to improve the quality
of retinal and optic nerve evaluations prior to performing irreversible
surgical procedures with unknown long term consequences for these abnormal
eyes.
References
(1) M O’Keefe and L Nolan
LASIK surgery in children
Br J Ophthalmol 2004; 88: 19-21.
(2)
Avery H. Weiss and Eric A. ROS Axial myopia in eyes with optic nerve
hypoplasia Graefe's Arch Clin Exp Ophthalmol (1992) 230:372-377
(3) McBrien NA, Gentle A. Role of the sclera in the development and
pathological complication of myopia. Progress in Retinal and Eye Research
22 (2003):307-338
(4) Wickstrom G, Bendix T. "Hawthorne effect"--what did the original
Hawthorne studies actually show? Scand J Work Environ Health. 2000
Aug;26(4):363-7
(5) Lied TR, Kazandjian VA.A Hawthorne strategy: implications for
performance measurement and improvement. Clin Perform Qual Health Care.
1998 Oct-Dec;6(4):201-4.
I am the surgeon who found the case in the Skarf article in 1983. The
patient was comatose with an acute subdural hematoma and we only found it
with the help of visual evoked responses. Our case had ipsilateral
blindness. We did not have MRI and our patient died. The very late onset
of contralateral blindness in your case gives me pause as to the actual
etiology of visual loss. One might incriminate a "do...
I am the surgeon who found the case in the Skarf article in 1983. The
patient was comatose with an acute subdural hematoma and we only found it
with the help of visual evoked responses. Our case had ipsilateral
blindness. We did not have MRI and our patient died. The very late onset
of contralateral blindness in your case gives me pause as to the actual
etiology of visual loss. One might incriminate a "double" injury with
recurrent SDH on the premise that the cumulative effect is not 10+10 but
rather 10x10. I am unaware of the plausibility of this mechanism as
perhaps there was another distinct cause of injury. Let us hope this
phenomenon remains rare, even if it is fascinating, enigmatic and stygian
all at the same time. Thank you for sharing this case; now I think I
understand less about the certainty of the genesis of this oddity.
I was delighted to read Dr Okada’s reply to my letter.[1] At the risk of
transgressing from the point of the original article [2] that dealt with a
novel technique to administer triamcinolone to a wide group of patients
with uveitis, I would like to reply:
1. The WHO guidelines are indeed silent on the treatment of latent
tuberculosis which can be defined as merely positive mantoux tests w...
I was delighted to read Dr Okada’s reply to my letter.[1] At the risk of
transgressing from the point of the original article [2] that dealt with a
novel technique to administer triamcinolone to a wide group of patients
with uveitis, I would like to reply:
1. The WHO guidelines are indeed silent on the treatment of latent
tuberculosis which can be defined as merely positive mantoux tests with no
clinical, microbiological, or radiographic evidence of active tuberculosis
(TB).[3] These patients may be treated with single or two drug therapy to
prevent progression to active TB [4] but patients with an active uveitis
would not fall within this definition and probably should be treated as
patients with active extrapulmonary TB irrespective of the detection or
otherwise of an infective focus. The absence of a detectable focus of
systemic TB (usually pulmonary) should not lead to a diagnosis of latent
tuberculosis.
In patients suspected of ocular TB, the findings of systemic TB especially
in those patients with infective manifestations (like choroidal tubercles)
, suggests the need to receive the full four drug regime but considerable
latitude exists in those patients in whom there is neither a detectable
systemic focus or microbiologic evidence. As ocular TB has been known to
occur even in the absence of systemic foci,[5] it may be prudent to
advise a full four drug course rather than one/ two drug regimes.
Inadequate regimes would lead to the development of microbial resistance
and subsequent therapeutic difficulties.
2. The authors theorize that certain cases may be due to an immune
reaction to
sequestered mycobacterial antigen. Recent mouse models have demonstrated
an initial pulmonary infection followed by the appearance of bacteria at
the draining lymph nodes, at which stage a T cell immune response is
generated.[6] Does this response lead to the release of antigen into the
bloodstream leading to the sequence of events we describe as ocular TB? A
mantoux test would probably be positive in these patients indicating
recent infection (but not necessarily active disease) but whether they
would need antitubercular (as opposed to only immunosuppressive agents)
drugs remains unknown.
References
1. Okada AA and Wakabayashi T. Trans-Tenon's retrobulbar triamcinolone infusions in uveitis [electronic response to Okada et al. Trans-Tenon’s retrobulbar triamcinolone infusion for the treatment of uveitis] http://bjo.bmjjournals.com/cgi/eletters/87/8/968#210
2. AA Okada, T Wakabayashi, Y Morimura, S Kawahara, E Kojima, Y Asano
and T Hida. Trans-Tenon’s retrobulbar triamcinolone infusion for the
treatment of uveitis. Br J Ophthalmol 2003; 87:968-971.
3. American Thoracic Society. Diagnostic Standards and Classification of
Tuberculosis in Adults and Children. Am. J. Respir. Crit. Care Med 2000;
161(4): 1376-1395.
4. Small PM. Fujiwara PI. Management of Tuberculosis in the United States.
N Engl J Med. 2001; 345:189-200.
5. Sarvananthan N, Wiselka M, Bibby K. Intraocular tuberculosis without
detectable systemic infection. Arch Ophthalmol. 1998;116(10):1386-8.
6. Chackerian AA, Alt JM, Perera TV, Dascher CC, Behar SM. Dissemination
of Mycobacterium tuberculosis Is Influenced by Host Factors and
Precedes the Initiation of T-Cell Immunity. Infection and Immunity.2002,
70(8): 4501-4509.
Dear Editor
We thank BV Kumar and S Prasad for their interest in our report describing the successful treatment of macular oedema (MO) secondary to branch retinal vein occlusion (BRVO) with intravitreal triamcinolone injection (IVTI).[1]
Although definitively establishing a clinical diagnosis of posterior vitreous detachment (PVD) may be problematic, our patient did not have a Weiss ring and no eviden...
Dear Editor
We greatly appreciate the inquiry of Dr Vendantham and are happy to reply to his questions.[1]
While Dr Vendantham is correct regarding the definition of ophthalmia neonatorum including all infections acquired by an infant during the first 30 days of life, for the purposes of our study,[2] we were primarily interested in those cases resulting from neonatal exposure in the birth canal. This...
Dear Editor
I read with interest the case report of Ashraff et al[1] where a posterior chamber phakic intraocular lens (PCPIOL) was used in a pseudophakic eye with axial myopia and pseudoexfoliation for the management of anisometropia. I would like to highlight a potential problem in such eyes: dislocation of PCPIOL into the vitreous cavity.
PCPIOLs are inserted blindly behind the iris and, depen...
Dear Editor
SDM Chen and colleagues present a case of successful treatment of macular oedema in the setting of ischaemic branch retinal vein occlusion (BRVO).[1]
Intravitreal triamcinolone is increasingly being used as part of our therapeutic armaterium in a wide range of conditions. However it’s mode of action is still to be fully elucidated. It is known that the induction of a posterior vitreous detachme...
Dear Editor
I thank Dr Tomsak for his reply[1] to my comments.[2]
In response to point one,we agree that historically CBS is a disorder described in the elderly, but as we mentioned in our previous reply, this can easily be explained by the higher incidence of visual loss in the elderly. Further, without formal child pyschiatry review it is difficult to give a incidence in the childhood of CBS. As you wo...
Dear Editor
I appreciate Dr Van Gelder’s thoughtful comments regarding the potential consequences of a UV+blue light absorbing intraocular lens (IOL) on circadian rhythmicity.[1] I agree that the clinical importance of retinal ganglion photoreceptors is currently unknown and that decreasing the amount of blue light reaching them might affect their function. Conversely, if photosensitive ganglia respond to circadia...
Dear Editor
Drs Mainster and Sparrow have provided an excellent perspective on the relative merits and difficulties of extending IOL absorption into the blue portion of the spectrum.[1]
However, they have not considered an unintentional consequence of blockage of the blue portion of the spectrum: reducing the activity of intrinsically photosensitive retinal ganglion cells.[2, 3] These cells subserve se...
Dear Editor
The authors report on LASIK surgery in five children with unilateral high myopia who were presumed to have amblyopia. One subject had bilateral high myopia.
Optic nerve hypoplasia is associated with high myopia. In addition, anisometropic myopia is a common sequela of retinopathy of prematurity. Thinning of the sclera with posterior staphyloma formation has long been known to be associa...
Dear Editor
I am the surgeon who found the case in the Skarf article in 1983. The patient was comatose with an acute subdural hematoma and we only found it with the help of visual evoked responses. Our case had ipsilateral blindness. We did not have MRI and our patient died. The very late onset of contralateral blindness in your case gives me pause as to the actual etiology of visual loss. One might incriminate a "do...
Dear Editor
I was delighted to read Dr Okada’s reply to my letter.[1] At the risk of transgressing from the point of the original article [2] that dealt with a novel technique to administer triamcinolone to a wide group of patients with uveitis, I would like to reply:
1. The WHO guidelines are indeed silent on the treatment of latent tuberculosis which can be defined as merely positive mantoux tests w...
Pages