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Recent eLetters

Displaying 11-20 letters out of 140 published

  1. RE: McConnell's sign is not specific to PE nor should this finding alone prompt use of thrombolytics

    I am glad to receive comments on my previous publication on McConnell sign in which we had stressed upon the clinical relevance of this echocardiographic sign of pulmonary embolism. These comments are well taken and are acceptable to me. I wish to clarify my point which I wished to stress upon by means of this image publication.

    McConnell sign although is not a definitive evidence of massive embolism but is truly an indicator of haemodynamically significant embolus which is affecting the function of the right ventricle. After having gone through the reference given in the query, I agree that this sign has lesser specificity in the diagnosis of embolism but we wish to stress upon in usage for predicting an embolism to be haemodynamically significant which could help in guiding therapy.

    The indication of thrombolytic therapy in embolism is controversial and is often used even in intermediate risk group especially if the bleeding risk is low and essentially is a matter of decision of the treating physician.

    Although we do not suggest using McConnell sign alone as a marker to thrombolyse but it sure is a marker of significance of embolism which can be used along with other parameters.

    Your point is valid and is acceptable for us but I think our point is clear in this regard and I feel that the above sentences would make our perspective clear.

    I will be happy to discuss the issue further if need be.

    Conflict of Interest:

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  2. McConnell's sign is not specific to PE nor should this finding alone prompt use of thrombolytics

    To the Authors,

    I enjoyed reading your case report. It is indeed a classic example of what appears to be massive PE with echocardiographic findings of RV dysfunction. However, I have some concerns about the learning points in your conclusion.

    1) You state that McConnell's sign is "a distinct echocardiographic feature of acute massive PE". This conclusion is misleading since McConnell's sign has been shown in case series to lack specificity. In fact, it is no better than a "coin toss" in differentiating PE from other causes of RV dysfunction (e.g. RV infarct): Casazza et al. showed a sensitivity and specificity of 70% and 30%, respectively (Eur J Echocardiography (2005) 6, 11e14). What's more, McConnell's sign does not differentiate "submassive" or "intermediate risk" PE from "massive" PE. This clinical distinction is based on the presence of hypotension/shock (Journal of Intensive Care Medicine 26(5) 275-294)

    2) You state that thrombolytics should be given in acute PE when this sign is found. What is the evidence for this firm recommendation? McConnell's sign can also be seen in "sub-massive" or "intermediate risk" PE, which is not associated with shock or hypotension. In fact, 90% of the normotensive patients in the series you cite by Grifoni et al. did well in the short term with conventional therapy. Furthermore, we know from the recent PEITHO trial that thrombolysis for this category of patients might have a benefit but with significant risk of major bleeding (N Engl J Med 2014; 370:1402-1411). The decision to use thrombolytics should be a careful, individualized decision. On the contrary, in cases of massive PE (defined by shock, hypotension), thrombolysis is indicated and not based at all on echocardiographic findings.

    The learning points in your case report overly simplify 2 important steps in a nuanced clinical algorithm: the interpretation of McConnell's sign and the decision to use thrombolytics in VTE.

    Conflict of Interest:

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  3. Re: Re: "Histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis"

    We would like to thank the author/s for the comment made above with regards to our publication in January of 2013 entitled "Histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis"1. In this report we alleged, following a review of the current literature, that this was the first report of its kind where a histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis was made and that we did not find any such reports previously. We would like to thank the author/s of the above comment for bringing to our attention two previous sources that have documented similar pathological findings to ours. We were surprised to note that this was described as early as 1978 within the Atlas of Tumor Pathology published by the Armed Forces Institute of Pathology (although we ourselves have not been able to peruse a copy of this book). Furthermore, we confirm that the lipomatous lesions within the myocardium of our patient did not show any associated inflammation, fibrosis or a capsule surrounding it. More importantly, this comment brought to our attention a few important factors, which we believe may be useful for future authors who may believe theirs is a highly unique case which has not been described previously. These factors include: 1) A comprehensive literature search involving all possible variations in terminology. The reason we did not come across the publication in the Journal of Clinical Pathology referred to above, was because we did not use the term "fat cells" when performing out database search2. Rather, we only used the term "lipoma" when performing our search which resulted in the above study being excluded from our search. 2) When claiming primacy of findings, one should phrase this claim in "tentative" language. What we mean by this is that one should phrase the claim in such a way that they concede the possibility of the report having been made previously. Hence, we recommend using terminology such as "we believe this to be the first such case" or "the authors' believe this to be the first such case". This leaves open the possibility of other reports of a similar nature. Shehab Jabir Samir Al-Hyassat

    References

    1. Jabir S, Al-Hyassat S. Histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis. BMJ Case Rep. 2013 Jan 3;2013. doi:pii: bcr2012007484.10.1136/bcr-2012-007484.

    2. Adriaensen ME, van Oosterhout MF, Feringa HH, Schaefer-Prokop CM, Zonnenberg BA, Prokop M. Mature fat cells in the myocardium of patients with tuberous sclerosis complex. J Clin Pathol. 2011 Mar;64(3):244-5. doi:10.1136/jcp.2010.087676

    Conflict of Interest:

    None declared

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  4. RE: "Histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis"

    Hereby, we would like to comment on the case report, you published earlier this year entitled "Histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis complex" (1). The authors state that they presented the first case of an adult with tuberous sclerosis complex, where a histological diagnosis of cardiac lipoma was made. Therefore, we would like to draw your attention to the Atlas of Tumor Pathology published by the Armed Forces Institute of Pathology in 1978 (2) in which three adult TSC-patients with multiple lipomas in the myocardium were presented. Furthermore, in 2011 the Journal of Clinical Pathology published a report in which the histopathological findings of areas of mature fat cells in the myocardium of two adult TSC-patients were presented (3). The before mentioned areas of mature fat cells in the myocardium showed no associated inflammation, no associated fibrosis, no entrapped myocardial cells, and no capsule. As far as we can judge from Figure 1 in the BMJ case report, the presented area of adipocytes resembles the figures presented in the Journal of Clinical Pathology. Therefore, it would be interesting to know whether the authors of the BMJ case report can confirm that the presented solid population of adipocytes in their adult TSC-patient showed no associated inflammation, no associated fibrosis, and no capsule in keeping with the suggested unique finding for tuberous sclerosis complex of areas of mature fat cells in the myocardium presented in 2011.

    1. Jabir S, Al-Hyassat S. Histological diagnosis of cardiac lipoma in an adult with tuberous sclerosis complex. BMJ Case Rep. 2013 Jan 3;2013.

    2. McAllister HA, Fenoglio JJ. Tumors of the cardiovascular system. In: Atlas of Tumor Pathology. Armed Forces Institute of Pathology, editor. Washington D.C. 1978:40-46

    3. Adriaensen ME, van Oosterhout MF, Feringa HH, Schaefer-Prokop CM, Zonnenberg BA, Prokop M. Mature fat cells in the myocardium of patients with tuberous sclerosis complex. J Clin Pathol. 2011 Mar;64(3):244-5

    Conflict of Interest:

    None declared

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  5. Alcoholic Cardiomyopathy and Chest X- Rays

    Dear editor please delete the previous letter which I submitted one hour ago and consider this new letter for response to the article THE LETTER:

    Very nice case and I read with much attention the article " Alcoholic cardiomyopathy" by Antonio Mirijello, et al published in BMJ Case Reports 2013 :doi:10.1136/bcr-2013-201449. I think that the most important sign is the rapidity of myocardial recovery during abstinence of drinking with the rapidity of disappearing of the signs: "cardiomegaly and pulmonary edema" in chest x-ray after cessation of drinking. Perfusion MRI can play a role in differential diagnosis of non ischemic dilated cardiomegaly. It will be great if the authors can explain in more details the meaning of "typical signs of alcoholic cardiomyopathy" in one non dynamic chest x-ray and what is the difference from other chest x-ray signs of other causes of dilated hypertrophic cardiomyopathy? Best regards Suheil Artul EMMS Hospital Nazareth Israel, Radiology Department 26-10-2013

    Conflict of Interest:

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  6. Response

    Dear Editor,

    We thank the reader for the interesting comment on our recently published "Images in..." entitled Alcoholic Cardiomyopathy, describing a case of severe cardiomegaly found at a chest X-ray in an alcoholic patient. We agree on the utility of perfusion MRI in the differential diagnosis of non-ischemic dilated cardiomegaly. Unfortunately, the patient declined a perfusion MRI, thus we were not able to perform it. The rapid improvement of pulmonary oedema is surely a very important sign. We are cautious, however, with its diagnostic utility because we cannot attribute the improvement of ventricular volumes only to the cessation of drinking, since both abstinence from alcohol use and heart failure pharmacological treatment were started concurrently. We agree that cardiomegaly in a patient complaining of exertional dyspnoea, peripheral oedema and reduced effort tolerance is not specific per se and that obviously a "non dynamic" exam, such as chest X-ray cannot provide information on the cause of cardiomyopathy. However, in the reading and clinical interpretation of the X-ray, we also considered the medical history of this patient, i.e. the lack of risk factors for or history of cardiovascular disease as well as the positive history for alcoholism during the last 20 years. As such, it is reasonable that this chest X-ray connotes a specific image of alcoholic cardiomyopahty. In summary, while radiology exams may not be diagnostic per se, on the other hand their interpretation together with a complete medical history may help the clinician to guide the diagnosis.

    Sincerely,

    Antonio Mirijello Giovanni Addolorato

    Conflict of Interest:

    None declared

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  7. Re:No indeed

    Reply to reader's observation: The serotonin syndrome is a clinical diagnosis based on a broad spectrum of certain clinical signs and symptoms after the intake of serotonergic agents. Diagnosis of our case was based on the Hunter Criteria.1 Other sets of diagnostic criteria have been studied for the definition of the serotonin syndrome.2,3 However the Hunter Criteria were more accurate, sensitive (84 per cent vs. 75 per cent), specific (97 per cent vs. 96 per cent) and simpler compared to the original Sternbach Criteria.1,4 Diagnostic Hunter Criteria include spontaneous clonus; inducible clonus and agitation or diaphoresis; ocular clonus and agitation or diaphoresis; tremor and hyperreflexia; hypertonia and temperature above 38*C and ocular or inducible clonus.1,4,5 Not all clinical findings might be present in a single patient. Presentation depends on mild, moderate or severe toxicity.4-6 Our patient was on a dual serotonergic drug regimen of a normal dose of venlafaxine and an overdose of sumatriptan, when he developed spontaneous clonus resulting in head shaking with only mild symptoms of serotonin toxicity (confer video in the full text).7 Signs of neuromuscular hyperreactivity such as clonus (spontaneous or inducible) with serial involuntary, rhythmic, muscular contractions and relaxations are the most important diagnostic findings also to distinguish from the neuroleptic malignant syndrome, anticholinergic and sympathomimetic toxicity, or CNS infections.4,6 Bilateral occurrence of clonus is not mandatory for the diagnosis of serotonin toxicity, however bilateral Babinski signs may occur.4 Clonus is typically more pronounced in the lower extremities in contrast to our patient's twitching of the head.4-6 However, previous observations described a "peculiar head-turning behavior characterized by repetitive rotation of the head" in patients with serotonin syndrome.5 Moreover animal studies found a link between head movements and the serotonin system, where the head-twitch response is induced by activation of serotonergic 5-ht receptors in rodents.8-10 Other mild cases of serotonin toxicity were found to be "afebrile but tachycardic and with twitching or tremor".6,11 Fever higher than 38*C was not as strongly associated with the diagnosis of the serotonin syndrome.1, 5 Otherwise temperature increase over 38.5*C usually caused by muscular hyperactivity indicated severe life-threatening cases of serotonin toxicity.1,4,5 In our patient with mild symptoms and low muscular hyperactivity the temperature was not elevated. Symptoms in our patient started shortly after increase of sumatriptan dosage and typically resolved within 24 hours after the discontinuation of serotonergic drugs and the initiation of symptomatic therapy with benzodiazepines. Synoptical with the timing of onset and resolution of symptoms, the pattern of illness, and the results of investigations to rule out alternative causes we established the diagnosis of a serotonin syndrome aka serotonin toxicity. We did not rechallenge the patient with the drug as a last option to attribute causality to the suspected adverse drug reaction.12

    References

    1. Dunkley EJ, Isbister GK, Sibbritt D, et al. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM 2003; 96:635.

    2. Sternbach H. The serotonin syndrome. Am J Psychiatry 1991; 148: 705-13.

    3. Hegerl U, Bottlender R, Gallinat J, Kuss HJ, Ackenheil M, M?ller HJ. The serotonin syndrome scale: first results on validity. Eur Arch Psychiatry Clin Neurosci 1998; 248: 96-103.

    4. http://www.uptodate.com/contents/serotonin-syndrome (accessed October 21, 2013).

    5. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med 2005;352:1112-20.

    6. Iqbal MM, Basil MJ, Kaplan J, Iqbal MT. Overview of serotonin syndrome. Ann Clin Psychiatry 2012; 24: 310-8.

    7. Weiler S, Offinger A, Exadaktylos AK. Shaking head means "no". BMJ Case Rep 2013 Sep 10;2013.

    8. Darmani NA, Zhao W. Production of serotonin syndrome by 8-OH DPAT in Cryptotis parva. Physiol Behav 1998; 65:327-31.

    9. Reissig CJ, Eckler JR, Rabin RA, Rice KC, Winter JC. The stimulus effects of 8-OH-DPAT: evidence for a 5-HT2A receptor-mediated component. Pharmacol Biochem Behav 2008; 88:312-7.

    10. Fantegrossi WE, Simoneau J, Cohen MS, Zimmerman SM, Henson CM, Rice KC, Woods JH. Interaction of 5-HT2A and 5-HT2C receptors in R(-)-2,5- dimethoxy-4-iodoamphetamine-elicited head twitch behavior in mice. J Pharmacol Exp Ther 2010; 335:728-34.

    11. Radomski JW, Dursun SM, Reveley MA, Kutcher SP. An exploratory approach to the serotonin syndrome: an update of clinical phenomenology and revised diagnostic criteria. Med Hypotheses. 2000; 55:218-24.

    12. Edwards IR, Aronson JK. Adverse drug reactions: definitions, diagnosis, and management. Lancet 2000; 356:1255-9.

    Conflict of Interest:

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  8. Cervical spine trauma can be underestimated by CT/MRI scans.

    In this interesting article, I'd like to submit the hypothesis that deformations of the spine during the few msec of trauma can be temporary (e.g. temporary disc bulging) and not picked up by CT/MRI scans after injury.

    We conducted a laboratory study which lent support to this idea.

    http://www.ncbi.nlm.nih.gov/pubmed/8009357

    CONCLUSIONS:

    Two potential spinal cord injury-causing mechanisms in axial bursting injuries of the cervical spine are occlusion and shortening of the canal. Post-injury radiographic measurements significantly underestimate the actual transient injury that occurs during impact.

    Conflict of Interest:

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  9. No indeed

    If the abstract is representative of the report's contents then it would seem rather unlikely that it makes any sense to label this case as SS (aka ST). It would not appear that any of the symptoms to fulfil the hunter criteria are present. There is no mention of the key symptoms of bilateral clonus and hyperpyrexia.

    Conflict of Interest:

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  10. Congratulations

    This work will open many unknown horizons. My sincerest congratulations to authors well as to the Journal.

    Conflict of Interest:

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