Displaying 11-20 letters out of 189 published
Re:Is it really ischemic?
I have 2 points to make here, and i also agree whether this patient had ischemia in the first place.
1)In case of ischemia it is known that the Echo shows regional wall motion abnormalities in 1 to 2 minutes, and much earlier than the ECG changes, but in this case, patient had no regional wall motion abnormalities and normal LV function.
2) This patient might be having a NSTEMI with a preexisting RBBB.
Conflict of Interest:
Is it really ischemic?
I would like to raise two specific questions with regard to the RBBB seen in this patient. Firstly, how are the authors certain that this patient did not have a pre-existing benign RBBB with a superimposed NSTEMI? Did they have an older ECG for comparison? Secondly, in addition to the presence of RBBB, this ECG also shows an S1Q3T3 pattern suggestive of RV volume overload, although the tachycardia seen in PE is absent. Did echocardiography show any evidence of RV dysfunction?
Conflict of Interest:
. Aborted sudden cardiac death associated with an anomalous right coronary artery
I thank Dr. Veloso for his comments regarding our case report . Directly from the consensus statement he cites , his opinion is valuable, but feel that aborted sudden death conveys a better picture due to successful resuscitation with CPR and defibrillation, a description already used by other authors .
Rienzi A Diaz, MD, FACC, EACVI, Professor of Cardiology
References: 1) Diaz RA, Valdes J. Aborted sudden cardiac death associated with an anomalous right coronary artery. BMJ Case Rep 2015; doi: 10.1136/bcr-2015- 210850. 2) Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology). Circulation 2006; 114(23):2534-70. 3) Kaushik S, Subramanian SR, Rafii S, Castillo R. Aborted sudden cardiac death (SCD) in a patient with hypertrophic cardiomyopathy (HCM) with low-risk factors for SCD. BMJ Case Reports 2013; doi: 10.1136/bcr-2012-006459
Conflict of Interest:
The expression "aborted sudden cardiac death" should be avoided.
I read with interest the case reported by Diaz and Valdez (1) regarding a patient who was successfully resuscitated from ventricular fibrillation cardiac arrest while running in a marathon race. The patient had a posterior diagnosis of anomalous right coronary artery arising from the aorta above the left sinus of Valsalva that subsequently runs between the aorta and the pulmonary artery, discovered by a 64-slice multidetector coronary computerized tomography. However, the title of this article is not in accordance with current standards defined by the American College of Cardiology, the American Heart Journal, and the Heart Rhythm Society (2). In this document, it was postulated that "sudden cardiac death should not be used to describe events that are not fatal", restricting the use of this term only to the events directly resulting in death, in order to avoid misinterpretations. Thus, I do believe that the best title for this interesting report would be: 'Cardiac arrest associated with an anomalous right coronary artery'.
References: 1) Diaz RA, Vald?s J. Aborted sudden cardiac death associated with an anomalous right coronary artery. BMJ Case Rep 2015; doi:10.1136/bcr-2015- 210850. 2) Buxton AE, Calkins H, Callans DJ, et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology). Circulation 2006;114(23):2534-70.
Conflict of Interest:
Re:Regional anesthesia and traumatic extremity fracture - can they safely coexist?
Thank you very much Mr M.A Warner for reviewing our article and sharing your views from the same. We do agree with your suggestion that, there in no 'strong' correlation between the use of peripheral nerve blockage and delay in diagnosis of acute compartment syndrome following surgical procedures on extremities. Among the reported cases of peripheral nerve blockage use in extremity surgeries and where the compartment syndrome was diagnosed and prompt fasciotomy preformed, all the patients were within the "hospital or clinical setting". The clinicians were vigilant with high index of suspension of acute compartment syndrome hence there were no delays in making the diagnosis nor in performing the fasciotomy surgery to adequately decompress the compartments, thus avoided the potential long-term complications and disabilities.
Our patient received 10mls of 0.25% Chirocaine and 13mls of 2% lignocaine with adrenaline 1:200000 strength, in total for his left axillary nerve block. The procedure was performed with ultrasound guidance and confirmed with nerve stimulator of adequate block in Radial, Ulnar, Median and Musculoskeletal nerve. He was discharged 8 hours following his surgery as he was quite comfortable with no pain in the operated limb and unfortunately there was no clear documentation with regards to distal muscular activity, prior to discharge .
We also agree with you in that, this patient underwent a revision procedure that would involve more soft tissue dissection and stripping, which itself contribute to increased post operative swelling compared to fractures with minimal displacement.
We believe, learning points in addition to aforementioned in the case report are, clinicians and all health care professional involved in providing care, should have awareness of compartment syndrome risk in extremity injuries and caution with clinical vigilance is needed when treating patients with extremity fractures and regional block is still in effect.
Conflict of Interest:
A case of misdiagnosis: chronic fluoride intoxication?
[Apologies for late edits to letter submitted yesterday, please note there are 3 new references addressing hepatotoxicity of fluoroquinolones that were not in orginal letter].
Lugg et al (2015) reported a case study of a 16 year old girl born who presented with signs of chronic joint pain, dizziness and non-specific abdominal pains after consuming 3 cups per day of imported herbal green tea (as tea bags) for a period of 3 months . There are a number of interesting points not addressed in the case study which physicians may not be aware of that are of clinical significance.
Firstly, the description of the ailments which the subject presented with strongly suggest chronic fluoride intoxication. Hallanger et al (2007) reported that the clinical features associated with fluoride intoxication resulting from habitual tea consumption can include joint pain and gastrointestinal complaints and that fluoride toxicity is often overlooked by clinicians . Despite the publication of a large number of reports addressing fluoride intoxication from habitual tea drinking  many health care professionals remain unaware of the risk of fluoride intoxication from tea and lack an understanding of the pathophysiology of fluoride toxicosis. The United States National Academy, National Research Council (2006) reported that excessive intake of fluoride will manifest itself in a musculoskeletal disease with associated symptoms including chronic joint pain and arthritic symptoms . However, perhaps one the most detailed explanations of the pathophysiology of fluoride toxicosis is provided by Professor Alexander V. Akleyev . In addition to musculoskeletal disorders, Akleyev reported that stage 2 fluorosis, the following symptoms are observed: subatrophic and atrophic rhinitis, pharyngitis, laryngitis, chronic conjunctivitis, retinal degeneration with visual impairment, hearing loss, increasing impairment of bronchial patency, and pulmonary insufficiency; mycrodial dystrophy with reduced contractility, chronic gastritis mainly with the reduction of secretory and acid forming function of the stomach, and chronic hepatitis with persistent liver failure; distinct astheno-vegetative syndrome, toxic polyneuritis and decrease in glucocorticoid function of adrenal cortex; and microhematuria and proteinura . Kessabi et al (1986) also reported that acute hepatitis and degeneration in the liver develop following chronic fluoride intake . Other studies have also found that fluoride toxicosis can induce hepatotoxicity and oxidative stress in humans [7-8] and animals .
In the case study described by Lugg and associates , the fluoride concentration in the tea samples ingested by the patient are unknown, as they were not tested. Chan et al (2013) reported high fluoride levels in tea infusions in the United Kingdom including green tea leaves which were found to contained up to 6.67mg/L when made with deionized water . The European Food Safety Authority (EFSA) have reported that drinking just 2 cups of tea per day (with a fluoride content of 5mg/l), combined with an average consumption of fluoridated drinking water and use of fluoridated tap water in the preparation of food, but excluding all other sources (including solid foods, toothpaste and dental products), would provide a daily dietary intake of 6 mg per day . The EFSA have established daily recommended intake levels (AI) and Tolerable Upper Intake Levels (ULs) for fluoride. For an adult female the AI is 2.9mg per day while the UL is 7mg per day [11-12]. Birmingham is the largest city in the England with artificially fluoridated water. Thus, the patient having consumed 3 cups of tea per day, is likely to have exceeded the recommended UL for fluoride, thereby increasing the risk of chronic fluoride intoxication.
Secondly, Lugg and associates noted that the condition of the subject worsened following prescribing of amoxicillin . Amoxicillin is a fluoroquinolone. The name fluoroquinolone comes from the presence of fluorine which is found in all fluoroquinolones. Hong et al (2005) reported that amoxicillin was associated with dental fluorosis in children . Thus, it is likely that administration of amoxicillin resulted in further contributing to chronic fluoride intoxication of the subject and a worsening of her condition. Other fluoroquinolones such as ciprofloxacin have been found to significantly increase plasma fluoride levels in individuals . Fluoroquinolones have also been found to be associated with severe hepatotoxicity [15-18]. It is likely that the toxicity of fluoroquinolones would be more immediate in persons with elevated background plasma fluoride levels.
Thirdly, on cessation of the herbal tea and treatment with intravenous fluids and N-acetylcysteine, her condition resolved . N- acetylcysteine is known to protect against fluoride-induced oxidative damage .
Overall the evidence indicates the symptoms reported may be due fluoride toxicosis caused by high fluoride intake from tea, combined with other fluoride sources such as fluoridated drinking water and medications. There is a need for healthcare workers to be aware of the pathophysiology of fluoride toxicosis as well as dietary fluoride sources, particularly among habitual tea drinkers in communities with artificially fluoridated drinking water. Urinary or blood fluoride levels should be routinely monitored in patients with muscleoskeletal and gastrointestinal disorders. Fasting serum fluoride concentrations ranging from 2.5 - 8.0 ?M/L can result in chronic fluoride intoxication and stage I and stage II skeletal fluorosis .
 Lugg ST, Menezes DB, Gompertz S. Chinese green tea and acute hepatitis: a rare yet recurring theme. BMJ Case Rep 2015, doi:10.1136/ bcr -2014-208534.
 Hallanger-Johnson JE, Kearns AE, Doran PM, Khoo TK., Wermers RA. Fluoride-related bone disease associated with habitual tea consumption. Mayo Clinic Proceedings 2007;82(6):719-24.
 Yi J, Cao J. Tea and fluorosis. Journal of Fluorine Chemistry, 2008, 129: 76-81.
 National Research Council, Review of Fluoride in Drinking Water, U.S. National Research Council 2006.
 Neurological Disorders of Non-Radiation Nature, Fluorosis, In Chronic Radiation Syndrome, Alexander V. Akleyev, Spriner-Verlag Berlin Heidelberg 2014. ISBN 978-3-642-45116-4.
 Kessabi M, Hamliri A. Experimental fluorosis in sheep: Alleviating effects of aluminum. Vet. Hum. Toxicol., 1986, 28: 300-304.
 Michael M, Barot VV, Chinoy NJ. Investigations of Soft Tissue Functions In Fluorotic Individuals of North Gujarat. Fluoride 1996, Vol.29 No.2 63-71.
 Medvedeva VN. Characteristics of the course of chronic hepatitis in workers coming in contact with flourine compounds. Gigiena Truda; Professional'nye Zabolevaniia, Jan 1985. pg 24-6.
 AL-Harbia MS, Hamzaa RZ, Dwarya AA. Ameliorative effect of selenium and curcumin on sodium fluoride induced hepatotoxicity and oxidative stress in male mice. J Chem Pharma Res, 2014, 6(4):984-998.
 Chan L, Mehra A, Saikat S, Lynch P. Human exposure assessment of fluoride from tea (Camellia sinensis L.) Food Res Internat. 2013; 51: 564-570.
 European Food Safety Authority, Scientific Opinion on Dietary Reference Values for fluoride, EFSA Panel on Dietetic Products, Nutrition, and Allergies: EFSA Journal. 2013;11(8):3332.
 European Food Safety Authority, Scientific Opinion of the Panel on Dietetic Products, Nutrition, and Allergies (NDA) on the tolerable upper intake level of fluoride. The EFSA Journal. 2005, 192, 1-65.
 Hong L, Levy SM, Warren JJ, Dawson DV, Bergus GR, Wefel JS. Association of Amoxicillin Use During Early Childhood With Developmental Tooth Enamel Defects, Arch Pediatr Adolesc Med. 2005;159:943-948, 995-996.
 Pradhan KM, Arora NK, Jena A, Susheela AK, Bhan MK. Safety of ciprofloxacin therapy in children: magnetic resonance images, body fluid levels of fluoride and linear growth. Acta Paediatr. 1995, 84:555-560.
 Hautekeete ML. Hepatotoxicity of antibiotics. Acta Gastroenterol Belg. 1995 May-Aug;58(3-4):290-6.  Vial T, Biour M, Descotes J, Trepo C. Antibiotic-associated hepatitis: update from 1990. Ann Pharmacother. 1997 Feb;31(2):204-20.
 Thiim M, Friedman LS. Hepatotoxicity of antibiotics and antifungals. Clin Liver Dis. 2003 May;7(2):381-99, vi-vii.
 Robles M, Andrade RJ. Hepatotoxicity by antibiotics: update in 2008. Rev Esp Quimioter. 2008 Dec;21(4):224-33. Article in Spanish.
 Paw?owska-G?ral K, Kurzeja E, Stec M. N-acetylcysteine protects against fluoride-induced oxidative damage in primary rat hepatocytes. Toxicology in Vitro, December 2013, Volume 27, Issue 8, Pages 2279-2282. doi:10.1016/j.tiv.2013.09.019.
 Xiang QY, Chen LS, Chen XD., Wang CS, et al. Serum Fluoride And Skeletal Fluorosis In Two Villages In Jiangsu Province, China. 178 Fluoride 2005;38(3):178-184
Conflict of Interest:
Claims of effects of green tea without analysis for tea contamination
I have read with surprise the case report which makes rather wide sweeping claims about green tea being of health concern. After a quick literature review there have been rare cases after prolonged ingestion of green tea extract - but none ever analyzed the extract for components besides green tea. It is not a secret that there are problems with food safety in china, especially pesticide use, so making claims about the plant instead of doing at least a rough test for chemicals in the extract (or in that case the tea) seem in my opinion very much warranted prior to claims with such impact.
Conflict of Interest:
Misleading sentence in Summary
In the summary of this article is the following:
"Only following specific questioning did she reveal that she had, in the preceding 3 months, regularly consumed internet ordered Chinese green tea, which contained Camellia sinensis."
My issue with this sentence is the word "contained". Chinese green tea, or any other true tea, must come from Camellia sinensis.
The word "contained" gives the impression that this was added to the green tea.
Any "tea" from any other plant is considered an herbal tea.
I feel the article is well justified because the dangers of adulteration are very serious. I also agree with the dangers of supplements and liver toxicity from high levels of EGCG ingestion.
My concern is that green tea, oolong tea and black tea are all very healthy drinks and many bloggers will create misinformed conclusions from the summary which may derogate from the benefits of tea.
This misleading statement in the summary of this article has already been misinterpreted and published on "Grub Street" (http://www.grubstreet.com/2015/09/green-tea-hepatitis.html). A reader pointed out their mistake in the comments section and they have since retracted and corrected their error.
The real issue here is not the tea. It is the contaminants either sprayed on, or added to, the tea.
I think the sentence should be revised to prevent any further confusion.
Should this comment be posted on this or any other website, I ask that my email not be displayed.
Thank you for your time,
Conflict of Interest:
I run a green tea information website promoting the benefits of green tea consumption. I focus primarily on Japanese green tea. I don't believe there are any competing interests.
Green tea toxicity?
Lugg et al. present a case of acute hepatitis in a 16-year old girl and, using the CIOMS/RUCAM scale, conclude the probable cause as a 3-month exposure to a Chinese green tea ordered via the internet. Other case reports have associated an idiosyncratic hepatoxicity with green tea though other factors, including adulterants, can contribute to its causality (Blumberg et al.). Regrettably, like many of these reports, this one also fails to test the product and inappropriately presumes the product label is correct. Green tea adulterated with plant extracts and/or drugs is not green tea but an illegal product! A relatively simple analytical test would have revealed adulteration of this product and helped to remove it from the marketplace and prevent others from suffering a fate like this patient. Unsurprisingly, the story of this report carried widely by the media appear to have used only its title and summary to warn readers about the harm of drinking green tea, despite a strong likelihood that this product was not simply green tea. Thus, many people may now choose to forego what Lugg et al. note is "a very safe and healthy drink".
Jeffrey B. Blumberg Tufts University
Blumberg, JB, Bolling BW, Xiao H, Chen C-YO. Review and perspective on the composition and safety of green tea extracts. Eur J Nutr Food Safety 2015;5:1-31
Conflict of Interest:
Response to eLetter submitted to BMJ Case ReportsWe are grateful for your comments in our images in medicine article in BMJCR entitled "'Neonatal duodeno-duodenostomy and missed duodenal stenosis with windsock deformity: a rare intraoperative error of technique and judgement by an unwary surgeon"1 We agree that finding bile in what is considered a distal segment of an atretic duodenum does not exclude all possible pathology. We are in agreement with your statement that duodenal atresia diagnosed prenatally and presenting at birth with distal bowel gas (on abdominal radiograph) via an anomalous bifurcated bile duct connection is more common than initially thought and occurs more frequently than duodenal stenosis2. We agree with you that a perforated duodenal windsock web would allow a greater amount of air to pass through (and more gas appearing in the abdomen) particularly when bile passes freely through. We reviewed the abdominal radiograph with our radiology team and indeed there was greater amount of air in the right and transverse colon as seen in figure 1. The gas in the left transverse colon was still visible one week post-operatively as shown in figure 2. We have considered the pathology of bifid distal bile duct with openings proximal and distal to the web and therefore have performed upper gastrointestinal series and followed it for 24 hours in an attempt to demonstrate this as there is risk for cholestasis, possibly due to duodeno-biliary reflux through the abnormal ampulla2. Upper gastrointestinal contrast studies delineated the windsock deformity and show the site of attachment of the diaphragm. Sometimes there is an indentation externally to mark the site of attachment of the diaphragm as shown with arrows in figure 3. At operation, there was no duodenal atresia or annular pancreas. WE routinely use flexible neonatal endoscope during the operation to see any visible bile duct opening or the wind shock deformity with or without an opening and provide air distention and transillumination to see shouldering at the attachment of the diaphragm as reported earlier3-4. In this case we could not see any anomalous bile duct opening and a single normal ampulla opening was seen just above the attachment of the diaphragm medially and the eccentric opening in the duodenal wind shock deformity was abutting the medial wall of the duodenum obstructing it completely. At the first operation, consultant paediatric surgeon was available in the theatre suite and in fact popped in and requested for any help required but the operating senior registrar with special interest in paediatric surgery was confident as has seen dark green bile as confirmation of being distal to the site of obstruction. He did repent his decision not to allow paediatric surgeon to join and learn during first operation when he joined us at second operation and apologized to the parents admitting his ignorance and arrogance. Patel RV, Govani D, Patel R, Dekiwadia DB Department of Surgery, PGICHR, KTCGH and PDUMC, Rajkot, India References: 1. Patel RV, Govani D, Patel R, Dekiwadia DB. Neonatal duodeno-duodenostomy and missed duodenal stenosis with windsock deformity: a rare intraoperative error of technique and judgement by an unwary surgeon. BMJ Case Rep 2014. 15 Jan 2014 doi:10.1136/bcr-2013-202782 2. Komuro H1, Ono K, Hoshino N, Urita Y, Gotoh C, Fujishiro J, Shinkai T, Ikebukuro K. Bile duct duplication as a cause of distal bowel gas in neonatal duodenal obstruction. J Pediatr Surg. 2011; 46(12):2301-4. 3. Patel RV, Kumar H, More B. Preampullary duodenal web simulating gastric outlet obstruction. J Neonat Surg. 2013; 2: 13. 4. Patel RV, Philip I. Distal duodenal stenosis in Down's syndrome-a rare diagnostic and therapeutic challenge. J Pediatr Surg Specialities (in press) Legends to illustrations Figure 1. Abdominal radiograph showing greater gas in the right and transverse colon between arrows. Figure 2. Post-operative chest radiograph demonstrating gas in the left transverse colon Figure 3. Post-operative upper gastrointestinal contrast at 24 hours depicting indentation at the site of diaphragm attachment (arrows
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