I read with interest the recently published case report by Frazer and
coworker.1 History of decompensated alcoholic liver disease with gross
ascites and presence of right sided pleural effusion raise the clinical
suspicion of hepatic hydrothorax. The transudative nature of pleural fluid
confirms this diagnosis. In absence of any cytological analysis of pleural
fluid (total and differential count) it is difficult to understa...
I read with interest the recently published case report by Frazer and
coworker.1 History of decompensated alcoholic liver disease with gross
ascites and presence of right sided pleural effusion raise the clinical
suspicion of hepatic hydrothorax. The transudative nature of pleural fluid
confirms this diagnosis. In absence of any cytological analysis of pleural
fluid (total and differential count) it is difficult to understand why the
authors thought about the alternative differential diagnosis i.e.
parapneumonic effusion.
BTS guideline had recommended to put the chest tube in "safe triangle".2
In the present case, X-ray showed that the chest tube was placed at lower
level and the end of tube can be identified below the dome of diaphragm.
Draining of 7.0 l fluids from pleural cavity and followed by
development of hypotension, raise the suspicion that part of chest
tube was in the abdominal cavity. Re expansion pulmonary edema following
drainage of large effusion is rare but well documented.2 BTS guideline
suggested not to drain more than 1.5 l at one time or 500 ml per hour.
In this present case 2.0 l fluid was drained over initial 2 hours 45
minutes. So this case may be an example of near miss by the physician.
1. Frazer R, Deane C, Sabit R. A simple chest drain gone wrong: a near
miss! BMJ Case Reports 2011; doi:10.1136/bcr.12.2010.3563
2. Laws D et al, on behalf of BTS. BTS guidelines for the insertion of a
chest drain.Thorax 2003;58:ii53-ii59
Thank you to the authors for providing an interesting case study
suggesting an association between Roth spots and pyridoxine dependent
epilepsy. The documented causes of Roth spots include severe anaemia,
leukaemias, dysproteinaemia, HIV retinopathy and endocarditis (Kanski,
2002).
Within the manuscript, infection has been ruled out as the cause of
Roth spots. However, details on tests regarding the other diff...
Thank you to the authors for providing an interesting case study
suggesting an association between Roth spots and pyridoxine dependent
epilepsy. The documented causes of Roth spots include severe anaemia,
leukaemias, dysproteinaemia, HIV retinopathy and endocarditis (Kanski,
2002).
Within the manuscript, infection has been ruled out as the cause of
Roth spots. However, details on tests regarding the other differential
diagnoses for Roth spots are not available. The authors should consider
providing at least a full blood count to rule out gross anaemia and
leukaemias to strengthen their case, and other investigations as
clinically indicated.
Reference:
Kanski, J. Clinical Ophthalmology, a Test yourself Atlas. Butterworth-
Heinemann 2002.
Historically, the use of novel treatments, sometimes still in clinical trials, has led to significant breakthroughs in the management of incurable conditions. Highly active antiretroviral therapy (HAART) for HIV is a success story of modern medicine. But in the not so distant past (1988), HIV patients faced with certain death, campaigned for the fast-tracking of public access for drugs still in clinical trials at an attempt to sa...
Historically, the use of novel treatments, sometimes still in clinical trials, has led to significant breakthroughs in the management of incurable conditions. Highly active antiretroviral therapy (HAART) for HIV is a success story of modern medicine. But in the not so distant past (1988), HIV patients faced with certain death, campaigned for the fast-tracking of public access for drugs still in clinical trials at an attempt to save their lives. This, in turn, helped the development of HAART for HIV.
_(new paragraph)_One can draw a corollary between HIV treatments in 1988 with some targeted therapies at present. Targeted therapies represent a novel form of treatment for many oncological conditions, which are minimally responsive to current standard treatment regimes. One example is V600E metastatic melanoma and BRAF kinase inhibitor. Metastatic melanoma is notoriously resistent to standard chemotherapy, with around 5% response rate with dacarbazine. Compared to dacarbazine, the BRAF kinase inhibitor vemurafenib has a response rate of 48%.1 This gives hope for many patients with incurable metastatic melanoma.
_(new paragraph)_The place for bevacizumab in oncology is the subject of ongoing research. However, the careful observation that oncology patients receiving bevacizumab had improvement in their wet age related macular degeneration (ARMD) has led to a major breakthrough in ophthalmology. Now intravitreal bevacizumab and other anti-VEGF agents are the standard therapy for wet ARMD.
_(new paragraph)_The number of targeted therapies is only going to increase over time. Some will lead to major success, some will find soem specific targets, and some will be failures. Ethically, neither the regulatory bodies nor doctors should deny patients with incurable conditions from novel agents that are potentially life-saving. The challenge for clinicians here is to accept the inherent uncertainties with any novel therapies, and to carefully monitor and look out for the side effects (however rare) and potentially unexpected benefits for these agents.
_(new paragraph)_
1. Chapman PB, Hauschild A, Robert C, et al. Improved Survival with Vemurafenib in Melanoma with BRAF V600E Mutation. N Engl J Med 2011.
I would like to congratulate the authors on the publication of this
case report. Long term treatment of giant cell arteritis (GCA) with
prednisone in elderly patients is problematic with significant side
effects. An effective steroid sparing agent will help clinicians in the
long term management of GCA patients.
Although this case report provides compelling evidence that TCZ is
likely to be beneficial in the tr...
I would like to congratulate the authors on the publication of this
case report. Long term treatment of giant cell arteritis (GCA) with
prednisone in elderly patients is problematic with significant side
effects. An effective steroid sparing agent will help clinicians in the
long term management of GCA patients.
Although this case report provides compelling evidence that TCZ is
likely to be beneficial in the treatment of an acute exacerbation of GCA,
it is not clear from the information provided whether TCZ has a
significant steroid sparing effect in its long term management. The
patient continued to receive oral prednisone at 3.5 mg daily despite five
infusions of TCZ, 9 months after the initial flare up. Also, the dose of
prednisone before the patient's acute excerbation was not available, and
one cannot establish whether the prednisone dose after TCZ is any lower
than her pre exacerbation dose.
This case report shows that TCZ is probably beneficial in the
treatment of steorid refractory GCA. However, further studies should be
performed prior to the use of TCZ in uncomplicated GCA cases.
Editor Madam, it is very interesting case where the Lymphoblasts
appeared to cross over the blood brain barrier to appear in the CSF or a
leak from adjoining bone or capillary contributed it, and more
interestingly blast cells in CSF spared rest of the brain and nerves while
preferentially deposited in retinal layers formed by optic nerve, like of
the previous cases cited in the report. If any other significant reason
ap...
Editor Madam, it is very interesting case where the Lymphoblasts
appeared to cross over the blood brain barrier to appear in the CSF or a
leak from adjoining bone or capillary contributed it, and more
interestingly blast cells in CSF spared rest of the brain and nerves while
preferentially deposited in retinal layers formed by optic nerve, like of
the previous cases cited in the report. If any other significant reason
appeared than per chance juxta papillary deposit of lymphoblasts in
recurred leukaemia, authors may better comment.
thanks for sharing such a good case report,
but is there any way we can prevent calciphylaxis ? or serial checking the
calcium levels could do the job?
thanks.
Is it not a possibility that this patient coincidentally had an
internal laryngocoele and otalgia of a different cause?
You mentioned that she had dried blood in her external auditory
canal/tympanic membrane, where you able to find a reason for this? Could
this or the underlying reason for this have contributed to her pain?
Just because her otalgia resolved over the same 3 month time period,
that her...
Is it not a possibility that this patient coincidentally had an
internal laryngocoele and otalgia of a different cause?
You mentioned that she had dried blood in her external auditory
canal/tympanic membrane, where you able to find a reason for this? Could
this or the underlying reason for this have contributed to her pain?
Just because her otalgia resolved over the same 3 month time period,
that her laryngocoele was surgically treated, does not necessarily mean
that this was the cause of her pain.
The laryngocoele was probably an incidental finding on the MRI as she
was otherwise asymptomatic.
Maharshak I, Bourla D, Grinbaum A, Weinberger D, Axer-Siegel R.
Department of Ophthalmology, Rabin Medical Center, Beilinson Campus, Petah
Tiqva 49100, Israel. imaharshak@gmail.com
Sethiya et al presented a constellation of solid neurological signs
in a middle-aged male.
1. The author did not add a differential diagnosis list for this
constellation?
2. The MRI images do not "teach" anything. The right image is an
axial T2 FLAIR one while the left image is a sagittal T2-weighted one.
Hyper- or hypo-intense signals in the mesencephalon on these films; the
p...
Sethiya et al presented a constellation of solid neurological signs
in a middle-aged male.
1. The author did not add a differential diagnosis list for this
constellation?
2. The MRI images do not "teach" anything. The right image is an
axial T2 FLAIR one while the left image is a sagittal T2-weighted one.
Hyper- or hypo-intense signals in the mesencephalon on these films; the
potential cause(s) of this imaging abnormality? In addtion, there is a
striking C-shaped hyper-intense signal around the Sylvian aqueduct on the
FLAIR film. What are these, the readership might ask?
3. The autopsy addressed the lung as the cause of death; the
patient's brain undiagnosed disaster was ignored?
4. The case was published sometime ago in the website and the legend
for figure one was "corrected." I think the journal should mention that
there is an "erratum;" I have "2 PDFs" of his article!
So, after all, it's all about "Images In." As a neurologist who is
interested in teaching under- and postgraduates, I may ask: What have we
learned from this case's "images?"
Thanks!
Conflict of Interest:
None declared
Editor's Note - there was indeed a previous version of this article that contained significant errors so a correct version was published. We agree this should have been more transparent to the readers and a notice will be published shortly notifying readers to the previous publication
Yes, brain regression is known in certain infiltrative and
degenerative conditions, but, the problem as raised by Prof Agrawal S and
Nathani S here is, that Ursula von Schenk et al from Germany, when first
reported brain regression due to B12 deficiency followed by recovery
shortly on therapy, it contradicted the very concept of atrophy and
regression. And to the non radio/imaging experts it appeared simply that
two ima...
Yes, brain regression is known in certain infiltrative and
degenerative conditions, but, the problem as raised by Prof Agrawal S and
Nathani S here is, that Ursula von Schenk et al from Germany, when first
reported brain regression due to B12 deficiency followed by recovery
shortly on therapy, it contradicted the very concept of atrophy and
regression. And to the non radio/imaging experts it appeared simply that
two images at different planes were used to claim high signal image
pathology in their figure 1. Zekai Avci et al from Turkey 2003 presented
good images for the same claim, yet, to the non image experts there were
no visible fronto-parietal hyper intensive lesions appreciable in cortex.
It looked as if gray matter image was seen in the fist figure and white
with gray in second with no appreciable intensity differences. These
researches of course in the domain of Radio and Imaging, experts could be better interpretors. In the present case, since Agarwal and
Naithani pointed out, it appears that their opinion is scientifically
factual.
I read with interest the recently published case report by Frazer and coworker.1 History of decompensated alcoholic liver disease with gross ascites and presence of right sided pleural effusion raise the clinical suspicion of hepatic hydrothorax. The transudative nature of pleural fluid confirms this diagnosis. In absence of any cytological analysis of pleural fluid (total and differential count) it is difficult to understa...
Thank you to the authors for providing an interesting case study suggesting an association between Roth spots and pyridoxine dependent epilepsy. The documented causes of Roth spots include severe anaemia, leukaemias, dysproteinaemia, HIV retinopathy and endocarditis (Kanski, 2002).
Within the manuscript, infection has been ruled out as the cause of Roth spots. However, details on tests regarding the other diff...
I would like to congratulate the authors on the publication of this case report. Long term treatment of giant cell arteritis (GCA) with prednisone in elderly patients is problematic with significant side effects. An effective steroid sparing agent will help clinicians in the long term management of GCA patients.
Although this case report provides compelling evidence that TCZ is likely to be beneficial in the tr...
Editor Madam, it is very interesting case where the Lymphoblasts appeared to cross over the blood brain barrier to appear in the CSF or a leak from adjoining bone or capillary contributed it, and more interestingly blast cells in CSF spared rest of the brain and nerves while preferentially deposited in retinal layers formed by optic nerve, like of the previous cases cited in the report. If any other significant reason ap...
Dear author ,
thanks for sharing such a good case report, but is there any way we can prevent calciphylaxis ? or serial checking the calcium levels could do the job? thanks.
Conflict of Interest:
None declared
Is it not a possibility that this patient coincidentally had an internal laryngocoele and otalgia of a different cause?
You mentioned that she had dried blood in her external auditory canal/tympanic membrane, where you able to find a reason for this? Could this or the underlying reason for this have contributed to her pain?
Just because her otalgia resolved over the same 3 month time period, that her...
Dear Editor,
I have read the well written case report "Missile launch pad: an unusual consequence of airbag deployment" by Davies et al.
I believe that my article published in Cornea in 2005 (see details below), should be part of the reference list for this case report.
Best wishes, Idit Maharshak
Cornea. 2005 Jan;24(1):110-1. Airbag-induced bilateral corneal graft dehiscence.
...Dear Editor,
Sethiya et al presented a constellation of solid neurological signs in a middle-aged male.
1. The author did not add a differential diagnosis list for this constellation?
2. The MRI images do not "teach" anything. The right image is an axial T2 FLAIR one while the left image is a sagittal T2-weighted one. Hyper- or hypo-intense signals in the mesencephalon on these films; the p...
Yes, brain regression is known in certain infiltrative and degenerative conditions, but, the problem as raised by Prof Agrawal S and Nathani S here is, that Ursula von Schenk et al from Germany, when first reported brain regression due to B12 deficiency followed by recovery shortly on therapy, it contradicted the very concept of atrophy and regression. And to the non radio/imaging experts it appeared simply that two ima...
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