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Recent eLetters

Displaying 1-10 letters out of 235 published

  1. Thoracic heat exchange

    I enjoyed the important and educational case report submitted by Dr. Little, and congratulate him on a successful outcome using aggressive resuscitation techniques. One additional option to transfer heat efficiently to the patient's core is via a device recently introduced that allows warming through the esophagus using a closed-system silicone tube connected to standard water blanket heat exchanger.[1] This approach has been shown to provide sufficient heat to patients to avoid hypothermia in the operating room during challenging burn cases that are prone to substantial heat loss.[2] As such, esophageal warming may allow avoidance of a more invasive thoracotomy in some patients, although in the extreme case described, it is likely that adding esophageal rewarming using this modality would instead be supplementary to the thoracotomy.

    1. Kulstad E, Metzger AK, Courtney DM, Rees J, Shanley P, Matsuura T, McKnite S, Lurie K: Induction, maintenance, and reversal of therapeutic hypothermia with an esophageal heat transfer device. Resuscitation 2013, 84(11):1619-1624. 2. Williams D, Leslie G, Kyriazis D, O'Donovan B, Bowes J, Dingley J. Use of an esophageal heat exchanger to maintain core temperature during burn excisions and to attenuate pyrexia on the burns intensive care unit. Case Rep Anesthesiol. 2016;2016:6.

    Conflict of Interest:

    Co-inventor of a device, and equity holder in Attune Medical developing device mentioned in response.

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  2. Rest tremor due to hypoglycaemic injury?

    Title Page: Rest tremor due to hypoglycaemic injury? 1Halil Onder, 2 Javid Jahanroshan

    1Department of Neurology, Yozgat State Hospital, Yozgat, Turkey 2Department of Neurology, Hacettepe University Hospital, Turkey

    Corresponding author: Halil Onder Department of Neurology, Yozgat State Hospital, Yozgat, Turkey Post Code: 66000 Telephone number: 4442066 email: halilnder@yahoo.com

    Key words: Hypoglycaemic injury; Rest tremor; Neuroimaging; Pathophysiology. Manuscript word count: 555

    Rest tremor due to hypoglycaemic injury? Letter to Editor: We read with great interest the article by Boylan et al. in which they report an interesting patient with severe hypoglycaemic injury presenting with continuous symmetric low amplitude 3-4 Hz pill-rolling type rest tremor of both hands (1). We agree with the interesting aspect of this patient, however, I would like to comment on the article for a better understanding of the report and avoid misleading conclusions. First, as the authors state, rest tremor in deep coma is an unexpected finding as only one prior case has been reported showing rest tremor in a patient following brain death (2). Therefore, for reporting such an atypical presentation, detailed documentation of the clinical manifestations is crucial to make a proper diagnosis. For instance, propriospinal myoclonus, a form of spinal myclonus is known to involve limbs with a frequency of 1-6 Hz which is similar to the frequency range of the described movements in this case (3). Another type of myoclonus is anoxic myoclonus that is a widely recognized finding after cardiac arrest and viewed as an ominous sign (4). Remarkably, myoclonus has also been reported to be present in hypoglycaemic encephalopathy in addition to hypoxic brain injury (5, 6). Although the underlying mechanisms and responsible neurons are not properly understood, generally, myoclonus has been associated with abnormal function of either cortical and/or subcortical structures (7). On the other hand, epileptiform discharges have been reported to lead anoxic-myoclonus in some sub-group of patients and EEG monitoring is suggested to be performed in early anoxic myoclonus for determination of underlying possible ictogenesis well as neuroprognostication of the patients (4, 8). Taken together these knowledges, we think that diagnosing the defined movement disorder (low- amplitude, 3-4 Hz) as 'rest tremor' can be strictly challenging. Hence, we think that electrophysiologic evaluation of the defined symptoms in this patient might give substantial contributions in identification of the abnormal movements in terms of phenomenological aspect. Also, EEG recording which is lack in the report might also give important insights regarding the underlying mechanisms as also mentioned by Elmer et al (4). Based on these points, we think that there may be some crucial limitations in the documentation of this manifestation, as tremor video was unavailable in the report. Second, I would like to remark the devastating neuroimaging findings, affecting prominently striatum, cerebral cortex (including occipital cortex) and hippocampus. However, unlike hypoxic damage, occipital cortex and hippocampus have rather been resistant to hypoglycaemic injury (9), which was not the case in this case. Hence, I wonder if the authors might state if there had been a concurrent hypoxic injury or not in this case. Finally, although the points mentioned above need to be clarified, I agree with the strictly interesting aspect of this report mentioning a patient with rest tremor due to hypoglycaemic injury. As there are some major hypotheses trying to explain the pathophysiology of rest tremor, such as basal ganglia and the cerebello-thalamo-cortical circuitry dysfunctions, the exact mechanims remain to be unknown (10). Besides, rest tremor occurring secondary to a brain lesion is an extremely rare entity, as not a detailed documentation of such a patient is present in literature. Future reports of these rare manifestations of movement disorders in symptomatic circumstances may add substantial contributions to our currently understanding of underlying pathophysiologies. Bullet Points - Were electrophysiologic evaluations of the defined movement disorders conducted? - Might a video demonstration of the defined 'rest tremor' be involved ? - Might the authors state if there had been a concurrent hypoxic injury or not in this case?

    Acknowledgements: None. Conflict of interest: None. References 1. Boylan LS. Hypoglycaemic injury spares thalamus, spoils striatum and leaves only a rest tremor. BMJ Case Rep. 2016;2016. 2. Araullo ML, Frank JI, Goldenberg FD, Rosengart AJ. Transient bilateral finger tremor after brain death. Neurology. 2007;68(16):E22. 3. Kojovic M, Cordivari C, Bhatia K. Myoclonic disorders: a practical approach for diagnosis and treatment. Ther Adv Neurol Disord. 2011;4(1):47 -62. 4. Elmer J, Sandroni C. A nuanced view of post-anoxic myoclonus. Resuscitation. 2017;115:A4-A5. 5. Kida Y, Sawada T, Naritomi H, Kuriyama Y, Ogata J, Kashiwagi A, et al. [A case of hypoglycemic coma associated with myoclonus, periodic synchronous discharges and progressive cerebral atrophy resembling Creutzfeld-Jakob disease]. Nihon Naika Gakkai Zasshi. 1988;77(3):419-24. 6. Nicoli F, Bartolomei F, Swiader L, Gastaut JL. [Diffuse, segmental, asynchronous myoclonus, manifestations of severe hypoglycemia]. Presse Med. 1991;20(36):1783-4. 7. Gupta HV, Caviness JN. Post-hypoxic Myoclonus: Current Concepts, Neurophysiology, and Treatment. Tremor Other Hyperkinet Mov (N Y). 2016;6:409. 8. Aicua Rapun I, Novy J, Solari D, Oddo M, Rossetti AO. Early Lance-Adams syndrome after cardiac arrest: Prevalence, time to return to awareness, and outcome in a large cohort. Resuscitation. 2017;115:169-72. 9. Cho SJ, Minn YK, Kwon KH. Severe hypoglycemia and vulnerability of the brain. Arch Neurol. 2006;63(1):138. 10. Helmich RC, Hallett M, Deuschl G, Toni I, Bloem BR. Cerebral causes and consequences of parkinsonian resting tremor: a tale of two circuits? Brain. 2012;135(Pt 11):3206-26.

    Conflict of Interest:

    None.

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  3. Re:Antenatal management of Cystic Pulmonary adenomatoid malformation

    Dear Dr Kumar,

    Thank you for your letter.

    In relation to the points raised:

    1. Much of the evidence for successful use of steroids in CPAMs relates to microcystic lesions. In this case, the lesion was a large macrocystic CPAM. The case was discussed at an antenatal MDT, and the decision not to treat with steroids was reached.

    2. We thank you for your comment on measuring baseline and subsequent cyst volume ratio, to monitor progression/resolution. That was not measured in this case.

    Conflict of Interest:

    None declared

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  4. Antenatal management of Cystic Pulmonary adenomatoid malformation

    We read case report by Cullen et al and found it very interesting. It was a successfully managed case however, I have certain queries regarding management in the index case.

    1. In a prenatally detected CPAM (previously known as CCAM) with hydrops detected prior to 32 weeks, there is a well-defined role of maternal steroids.(1) Even multiple courses of betamethasone can be tried. Whether it was thought off in index case or not.

    2. Instead of two-dimensional size, measurement of baseline, as well as subsequent Cyst volume ratio (CVR), is a good indicator of progression/ resolution of the cyst.

    References: 1. David M, Lamas-Pinheiro R, Henriques-Coelho T. Prenatal and Postnatal Management of Congenital Pulmonary Airway Malformation. Neonatology. 2016 Apr 13;110(2):101-15.

    Conflict of Interest:

    None declared

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  5. Rheumatic fever with chronic carditis: still prevalent in Germany

    Dear Sir,

    1953 born I was never treated with antibiotics as child.

    1985 a post-streptococcal-myocarditis was diagnosed in the University -hospital Goettingen. Treatment with penicillin and oral penicillin- prophylaxis. Many episodes of respiratory infections, complicated by arrhythmias.

    2004 atrial fibrillation.

    2017, July 4., anticoagulation with heparin/coumarin changed the intra-articular pressure at once: Less pain in hand and foot. A severe polyneuropathy was caused by unknown agents (Could this be a post- streptococcal-neuritis 2003, in the heat-wave of Southern France, combined with severe Myocarditis.)

    And so many of my patients, seen in 40 years, suffered from recurrent rheumatic fever attacks. Very often penicillin V could change the disease.

    We are all one. Suffering from streptococcal-reactive diseases.

    And penicillin/coumarin still is the best. Cheap and good.

    Best wishes

    Yours Friedrich

    Conflict of Interest:

    None declared

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  6. A field level reality

    I am impressed by the straight forward write up with giving emphasis on practical aspects in field.

    Conflict of Interest:

    None declared

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  7. Re:isolated gastric sarcoidosis

    Dear Reader,

    Thank you for your comments and review of our case. You raise an interesting point regarding the connection between coniosis and sarcoidosis. Mineral particles were not originally commented on in our pathology samples, although the patient did not have characteristic occupational exposures.

    Best, Ronak V. Patel, MD

    Conflict of Interest:

    None declared

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  8. isolated gastric sarcoidosis

    A very intriguing and well described case !

    I just think useful some further diagnostic qualification starting from the following description of the histological characterization of the disease.

    "Gastric biopsies revealed severe chronic active granulomatous gastritis (figure 3). Additional studies from her gastric biopsies,including gram stain, fungal stain and acid-fast stain, were negative."

    Possible to research and, if present, characterize mineral particles inside the biopsed granulomas, following recent hypotheses interpreting sarcoidosis like a peculiar form of coniosis ?

    Conflict of Interest:

    None declared

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  9. Case verification

    Hello, how recent is the case that's just been published about Anisakiasas? Is it recent?

    Do you have more details on the case I can read?

    Conflict of Interest:

    None declared

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  10. cutis aplasia congenita and amniotic band syndrome

    I have read the phenotype description of a child with aplasia cutis congenita as well as transverse limb defects; although this association is not common it is the presentation of Adams Oliver syndrome [OMIM 100300]; in this condition both manifestations are present and often the limb defects resemble the damage caused by the amniotic band sequence. The identification is important as patients with Adams Oliver have an identifiable genetic etiology as well as are at risk of further medical issues ivcluding congenital heart defects; neuronal migration disorders; ocular manifestations etc

    Conflict of Interest:

    None declared

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