Thanks for the comments on our manuscript entitled "Plexiform neurofibromatosis of penis: a rare presentation of type 1 neurofibromatosis."
We think that this is a very good suggestion for treating such cases. Selumetinib has been found to be effective to treat neurofibromatosis type 1 in children 2 years of age and older. It is an inhibitor of mitogen-activated protein kinase and has been recommended as a first-line therapy approved for paediatric neurofibromatosis patients who have inoperable and bulky lesions.
Selumetinib therapy was a good option for this particular child but there were several reasons to choose surgery for this patient. Firstly the deformity was unsightly and grotesque considering the almost double length of the penis was leading to social discrimination, peer pressure and solitary life for this child. The patient has been rehabilitated with just one surgical operation in which after debulking the penile size is within socially acceptable limits. S...
Thanks for the comments on our manuscript entitled "Plexiform neurofibromatosis of penis: a rare presentation of type 1 neurofibromatosis."
We think that this is a very good suggestion for treating such cases. Selumetinib has been found to be effective to treat neurofibromatosis type 1 in children 2 years of age and older. It is an inhibitor of mitogen-activated protein kinase and has been recommended as a first-line therapy approved for paediatric neurofibromatosis patients who have inoperable and bulky lesions.
Selumetinib therapy was a good option for this particular child but there were several reasons to choose surgery for this patient. Firstly the deformity was unsightly and grotesque considering the almost double length of the penis was leading to social discrimination, peer pressure and solitary life for this child. The patient has been rehabilitated with just one surgical operation in which after debulking the penile size is within socially acceptable limits. Secondly, there were financial issues in procuring the drug as the treatment is expensive considering the high monthly costs that are involved in therapy with this particular drug. Thirdly medical treatment with this drug if available would have taken some time for the lesion to regress and the patient's parents were looking for a treatment that could immediately restore normalcy to the deformity.
We will definitely consider drug therapy with Selumetinib for this patient in the follow-up period as it has been shown to be quite effective in treating extensive neurofibromatosis as was seen in this paediatric patient.
A close comparison of baseline and exercise ECGs show mild ST elevation in V1 and mild inferolateral ST depression. Though the ST depression is mostly slow upsloping type, in lead I and V6 it is almost horizontal. The magnified view of the ECG makes ST elevation in V1 quite clear.
The author proposes two possible mechanisms for Aza induced hyperglycemia 1. Impaired beta cell function in pancreas via epigenetic mechanism 2. Increased secretion of cortisol. I suggest another possibility. A recent paper by Strand et al reports that Aza, a DNMT1 inhibitor, is a potent inducer of PTEN (this work done in vascular smooth muscle cells). It is well known that PTEN is an inhibitor of downstream elements of the insulin pathway, specifically PI3K-AKT-mTOR pathway and this results in insulin resistance. I suggest that the hyperglycemic activity of Aza is by PTEN induction of insulin resistance.
Strand KA, Lu S, Mutryn MF, et al. High Throughput Screen Identifies the DNMT1 (DNA Methyltransferase-1) Inhibitor, 5-Azacytidine, as a Potent Inducer of PTEN. Arterioscler Thromb Vasc Biol. 2020;40:1854–1869.
We thank Dr Yap and colleagues for describing clearly the successful management of an unexpectedly challenging airway.1 We agree that the index case highlights the need for vigilance in all patients requiring airway management, particularly where an atypical presentation of a respiratory condition may indicate occult airway pathology.2 However, the case raises a number of important issues for airway assessment, intubation-related laryngeal pathology and the management of ‘can’t intubate, can’t ventilate’ scenarios which warrant further discussion, considered below.
Airway assessment can be encapsulated by the quote, “Hindsight is a wonderful thing but foresight is better, especially when it comes to saving life,” attributed the 19th Century English poet William Blake. Whilst subtle, there were a number of clues in the described case report that could, and perhaps should, have prompted a more thorough evaluation of the airway. It is surprising that the patient did not report their extreme prematurity at birth, or the fact that they spent the first year of their life in hospital. This would have almost certainly have involved prolonged ventilation and sequelae into childhood. Respiratory and airway complications are well recognised in premature neonates and may coexist.3 The authors highlight the Difficult Airway Society’s airway algorithms and the fact that any clinician managing an airway should prepare for failure.4-6 This should involve an examination of the front...
We thank Dr Yap and colleagues for describing clearly the successful management of an unexpectedly challenging airway.1 We agree that the index case highlights the need for vigilance in all patients requiring airway management, particularly where an atypical presentation of a respiratory condition may indicate occult airway pathology.2 However, the case raises a number of important issues for airway assessment, intubation-related laryngeal pathology and the management of ‘can’t intubate, can’t ventilate’ scenarios which warrant further discussion, considered below.
Airway assessment can be encapsulated by the quote, “Hindsight is a wonderful thing but foresight is better, especially when it comes to saving life,” attributed the 19th Century English poet William Blake. Whilst subtle, there were a number of clues in the described case report that could, and perhaps should, have prompted a more thorough evaluation of the airway. It is surprising that the patient did not report their extreme prematurity at birth, or the fact that they spent the first year of their life in hospital. This would have almost certainly have involved prolonged ventilation and sequelae into childhood. Respiratory and airway complications are well recognised in premature neonates and may coexist.3 The authors highlight the Difficult Airway Society’s airway algorithms and the fact that any clinician managing an airway should prepare for failure.4-6 This should involve an examination of the front of the neck, in case an emergency surgical airway is required. This may have revealed the tracheostomy scar, noted during the evolving airway crisis. Although we recognise that these scars often heal very well after childhood tracheostomy and may not always be visible.
Any previous intubation of the trachea is associated with a risk of laryngeal injury and dysfunction occurring even after a short general anaesthetic.7 Clinical symptoms of hoarseness, breathiness (audible breathing), stridor, vocal fatigue or even ‘shortness of breath’ may indicate significant occult laryngeal pathology, including arytenoid fibrosis or dislocation, vocal cord paralysis or (sub)glottic stenosis.8 Even without the full disclosure of the preterm birth and likely prolonged intubation/ventilation, the history of intensive care unit admission in childhood is potentially significant, particularly when combined with the ongoing symptoms.
Lastly, the international language around what constitutes a “can’t intubate, can’t ventilate” scenario and, more importantly, what to do about it is well established. Dr Yap and colleagues describe appropriate initial actions following a failure to intubate the trachea: the patient could be ventilated and therefore oxygenated throughout via the use of a supraglottic airway device. Whilst we commend the authors for highlighting a stepwise approach to managing an evolving airway crisis, two important points need clarification. Repeated laryngoscopy and attempted intubation of the trachea (five in this case) are: increasingly likely to fail; will lead to trauma, bleeding and oedema; and risk provoking catastrophic airway obstruction and subsequent failure of ventilation and oxygenation.9 Furthermore, should a ‘can’t intubate, can’t ventilate’ scenario become apparent, the most appropriate course of action is an immediate cricothyroidotomy, not a tracheostomy which takes significantly longer and requires considerable surgical expertise which may not be immediately available.10 Therefore, we are concerned that the take home message from this report is potentially confusing. The authors rightly point out that different approaches to emergency cricothyroidotomy are debated, but we strongly recommend that the final learning point from their report is that a ‘can’t intubate, can’t ventilate’ scenario should be dealt with immediately, by whoever is managing the airway, by performing emergency scalpel-bougie cricothyroidotomy.10 Waiting for an ENT surgeon, who may not be immediately available, to attend may cause life threatening delay. Reinforcing this message consistently and supporting airway practitioners with appropriate training should reduce the potentially catastrophic outcomes associated with difficult and failed airway management.
References
1. Yap T, Quick M, Moore P. Emergency tracheostomy for failed intubation due to glottic stenosis. BMJ Case Rep 2021;14(2) doi: 10.1136/bcr-2020-239806 [published Online First: 2021/02/28]
2. Garini G, Fecci L, Giacosa R, et al. Adult idiopathic subglottic stenosis: a diagnostic and therapeutic challenge. Ann Ital Med Int 2004;19(1):54-7. [published Online First: 2004/06/05]
3. Jones M. Effect of preterm birth on airway function and lung growth. Paediatr Respir Rev 2009;10 Suppl 1:9-11. doi: 10.1016/S1526-0542(09)70005-3 [published Online First: 2009/08/11]
4. Higgs A, Cook TM, McGrath BA. Airway management in the critically ill: the same, but different. British journal of anaesthesia 2016;117 Suppl 1:i5-i9. doi: 10.1093/bja/aew055
5. Higgs A, McGrath BA, Goddard C, et al. Guidelines for the management of tracheal intubation in critically ill adults. British journal of anaesthesia 2018;120(2):323-52. doi: 10.1016/j.bja.2017.10.021
6. Frerk C, Mitchell VS, McNarry AF, et al. Difficult Airway Society 2015 guidelines for management of unanticipated difficult intubation in adults. British journal of anaesthesia 2015;115(6):827-48. doi: 10.1093/bja/aev371
7. Mota L, de Cavalho G, Brito V. Laryngeal Complications by Orotracheal Intubation: Literature Review. International archives of otorhinolaryngology 2012;16(2):236-45. doi: 10.7162/S1809-97772012000200014
8. Ponfick M, Linden R, Nowak D. Dysphagia--a Common, Transient Symptom in Critical Illness Polyneuropathy: A Fiberoptic Endoscopic Evaluation of Swallowing Study. Critical care medicine 2015;43(2):365-72. doi: 10.1097/CCM.0000000000000705
9. Mort TC. Emergency Tracheal Intubation: Complications Associated with Repeated Laryngoscopic Attempts. 2004
10. Pracy JP, Brennan L, Cook TM, et al. Surgical intervention during a Can't intubate Can't Oxygenate (CICO) Event: Emergency Front-of-neck Airway (FONA)? British journal of anaesthesia 2016;117(4):426-28. doi: 10.1093/bja/aew221 [published Online First: 2016/09/21]
Giant aortic aneurysm is a rare clinical entity. They may present with typical features of chest pain or abdominal pain, or most feared complications with dissection and rupture. However, an asymptomatic and unruptured giant thoracic aneurysm is extremely rare with only two case reports in the literature.
I had a similar case which an 80-year-old lady admitted to a local district general hospital with a 5 day history of productive cough with shivers, which she was tested positive for COVID-19 on admission.
Diagnostic workup demonstrated an incidental finding of a giant TAAA. Her case was referred to a tertiary hospital for vascular Multidisciplinary Team (MDT) discussion and planning.
It was decided that for her to have pre-operative assessment and MDT discussion after her recovery from infection to have a definitive management of the TAAA. The patient is currently being managed supportively in hospital.
According to National Institute for Health and Care Excellence (NICE), asymptomatic and 5.5 cm or larger aneurysm should be considered for repair. The case should be discussed in terms of the overall balance of benefits and risks with repair and conservative management, based on the current status of health and the expected future health. In this case, it was deemed that the risk of proceeding with repair at present outweighed the benefits.
Incidental finding of a giant AAA/TAAA is rare. It emphasises the importance...
Giant aortic aneurysm is a rare clinical entity. They may present with typical features of chest pain or abdominal pain, or most feared complications with dissection and rupture. However, an asymptomatic and unruptured giant thoracic aneurysm is extremely rare with only two case reports in the literature.
I had a similar case which an 80-year-old lady admitted to a local district general hospital with a 5 day history of productive cough with shivers, which she was tested positive for COVID-19 on admission.
Diagnostic workup demonstrated an incidental finding of a giant TAAA. Her case was referred to a tertiary hospital for vascular Multidisciplinary Team (MDT) discussion and planning.
It was decided that for her to have pre-operative assessment and MDT discussion after her recovery from infection to have a definitive management of the TAAA. The patient is currently being managed supportively in hospital.
According to National Institute for Health and Care Excellence (NICE), asymptomatic and 5.5 cm or larger aneurysm should be considered for repair. The case should be discussed in terms of the overall balance of benefits and risks with repair and conservative management, based on the current status of health and the expected future health. In this case, it was deemed that the risk of proceeding with repair at present outweighed the benefits.
Incidental finding of a giant AAA/TAAA is rare. It emphasises the importance of MDT approach to direct and achieve appropriate management for a complex case. Care treatment prioritisation, surgical planning and full complement expertise are required in complex cases such as this.
To the authors:
We read with interest the article entitled “Sudden irreversible hearing loss post COVID-19”.1 In this article, the authors presented an unusual case of a 45 year-old gentleman with sudden-onset sensorineural hearing loss (SNHL) after COVID-19 infection and treatment. In their literature review, five other case reports were cited with hearing loss noted after COVID-19.2-6 The patient in the case report experienced a decrease in his left sided hearing 1 week after his intensive care unit stay for COVID-19 treatment. His initial hearing loss was evaluated at the bedside with a tuning fork examination showing negative Rinne’s test on the side of reported hearing loss, and Weber’s test lateralizing to the side opposite to his hearing loss, which is consistent with SNHL of the affected side. He then had a 7 day treatment course of 60mg oral Prednisone daily in addition to a series of intratympanic steroid injection. His hearing loss was documented with elevated hearing thresholds of 65, 75, 75, and 85 dB at 2, 3, 4, and 6 kHz.
As multiple countries across all continents are facing the effects of the pandemic, our understanding of the various immediate and long-term complications of COVID-19 is evolving. SNHL is one of these complications. The Coalition for Epidemic Preparedness Innovations (CEPI) has developed a Brighton Collaboration case definition of SNHL to be utilized in the evaluation of adverse events following immunization, which can also be...
To the authors:
We read with interest the article entitled “Sudden irreversible hearing loss post COVID-19”.1 In this article, the authors presented an unusual case of a 45 year-old gentleman with sudden-onset sensorineural hearing loss (SNHL) after COVID-19 infection and treatment. In their literature review, five other case reports were cited with hearing loss noted after COVID-19.2-6 The patient in the case report experienced a decrease in his left sided hearing 1 week after his intensive care unit stay for COVID-19 treatment. His initial hearing loss was evaluated at the bedside with a tuning fork examination showing negative Rinne’s test on the side of reported hearing loss, and Weber’s test lateralizing to the side opposite to his hearing loss, which is consistent with SNHL of the affected side. He then had a 7 day treatment course of 60mg oral Prednisone daily in addition to a series of intratympanic steroid injection. His hearing loss was documented with elevated hearing thresholds of 65, 75, 75, and 85 dB at 2, 3, 4, and 6 kHz.
As multiple countries across all continents are facing the effects of the pandemic, our understanding of the various immediate and long-term complications of COVID-19 is evolving. SNHL is one of these complications. The Coalition for Epidemic Preparedness Innovations (CEPI) has developed a Brighton Collaboration case definition of SNHL to be utilized in the evaluation of adverse events following immunization, which can also be used in the study of COVID-19 complications.7 The American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS), the National Institute of Deafness and Other Communication Disorders (NIDCD) and the American Speech-Language-Hearing Association (ASHA) endorse the definition of Sensorineural hearing loss (SNHL) as hearing loss of at least 30 decibels (dB) in three sequential frequencies in the standard pure tone audiogram. However, this definition is not universally utilized, and variations of the definition area used in various publications. The audiometry can be a limiting factor for a definitive diagnosis when adequate equipment and appropriately trained personnel are not available. The Brighton Collaboration case definition suggests the classification of SNHL cases in various levels of diagnostic certainty based on the availability and utilization of adequate diagnostic tools in addition to the clinical evaluation (see reference 7, Table 1). This case ascertainment and classification then allows for data comparability across hospitals, countries, and surveillance systems. In this case report, a level 1 of diagnostic certainty was achieved as the patient had a physical examination excluding a cause for conductive hearing loss (CHL) in addition to an audiometry result consistent with SNHL.
In light of this report, and in the context of the active development of COVID-19 vaccines, SNHL should be evaluated as an event of interest in post-infection complications and post-immunization safety assessments. The Brighton Collaboration provides a consensus case definition for the standardized assessment of SNHL. It is our hope that the use of a standard definition will facilitate data interpretation and promote the scientific understand of SNHL following COVID-19.
Reference
1. Koumpa FS, Forde CT, Manjaly JG. “Sudden irreversible hearing loss post COVID-19.” BMJ Case Rep. 2020 Oct 13;13(11):e238419.
2. Kilic O, Kalcioglu MT, Cag Y, et al. Could sudden sensorineural hearing loss be the sole manifestation of COVID-19? An investigation into SARS-COV-2 in the etiology of sudden sensorineural hearing loss. Int J Infect Dis 2020;97:208–11.
3. Degen C, Lenarz T, Willenborg K. Acute profound sensorineural hearing loss after COVID-19 pneumonia. Mayo Clin Proc 2020;95:1801–3.
4. Rhman SA, Wahid AA. COVID-19 and sudden sensorineural hearing loss: a case report. Otolaryngol Case Reports 2020;16:100198.
5. Mustafa MWM. Audiological profile of asymptomatic Covid-19 PCR-positive cases. Am J Otolaryngol 2020;41:102483.
6. Sriwijitalai W, Wiwanitkit V. Hearing loss and COVID-19: a note. Am J Otolaryngol 2020;41:102473.
7. Liu YC, Ibekwe T, Kelso JM, et al. Sensorineural hearing loss (SNHL) as an adverse event following immunization (AEFI): Case definition & guidelines for data collection, analysis, and presentation of immunization safety data. Vaccine. 2020;38(30):4717-4731. doi:10.1016/j.vaccine.2020.05.019
We read the article published by Jaikaran O. et al on ‘Portomesenteric thrombosis after robotic sleeve gastrectomy’ with great interest. The reported about a morbid obese patient having porto-mesentric thrombosis after robotic sleeve gastrectomy due to obesity and mutation in methylenetetrahydrofolate reductase (MTHFR) mutation. However, we have few factors to report on this aspect.
Firstly, MTHFR enzyme dysfunction leads to hyperhomocysteinemia which leads to hypercoagulation state. Yet, the magnitude of this state is affected via degree of enzyme deficiency/dysfunction which is dependent on presence of heterogeneous/ homogenous mutation in enzyme gene. So, the authors must assess for the presence of hyperhomocysteinemia along with assessment of mutation.[1,2] Also the genetic homogeneity of the mutation must be assessed as heterogeneous mutation will have less effect on blood homocysteine levels.[3]
Next, the importance of folic acid for management of thrombotic state due to hyperhomocysteinemia must be considered. The patient has undergone sleeve gastrectomy which may further aggravate her vitamin and micronutrient deficiency. The administration of folic acid (instead of aspirin) will decrease the blood homocysteine levels and reduce the risk of hypercoagulation.[4]
References:
1. Friso S, Girelli D, Trabetti E, Stranieri C, Olivieri O, Tinazzi E, Martinelli N, Faccini G, Pignatti PF, Corrocher R. A1298C methylenetetrahydrofolate reductase mu...
We read the article published by Jaikaran O. et al on ‘Portomesenteric thrombosis after robotic sleeve gastrectomy’ with great interest. The reported about a morbid obese patient having porto-mesentric thrombosis after robotic sleeve gastrectomy due to obesity and mutation in methylenetetrahydrofolate reductase (MTHFR) mutation. However, we have few factors to report on this aspect.
Firstly, MTHFR enzyme dysfunction leads to hyperhomocysteinemia which leads to hypercoagulation state. Yet, the magnitude of this state is affected via degree of enzyme deficiency/dysfunction which is dependent on presence of heterogeneous/ homogenous mutation in enzyme gene. So, the authors must assess for the presence of hyperhomocysteinemia along with assessment of mutation.[1,2] Also the genetic homogeneity of the mutation must be assessed as heterogeneous mutation will have less effect on blood homocysteine levels.[3]
Next, the importance of folic acid for management of thrombotic state due to hyperhomocysteinemia must be considered. The patient has undergone sleeve gastrectomy which may further aggravate her vitamin and micronutrient deficiency. The administration of folic acid (instead of aspirin) will decrease the blood homocysteine levels and reduce the risk of hypercoagulation.[4]
References:
1. Friso S, Girelli D, Trabetti E, Stranieri C, Olivieri O, Tinazzi E, Martinelli N, Faccini G, Pignatti PF, Corrocher R. A1298C methylenetetrahydrofolate reductase mutation and coronary artery disease: relationships with C677T polymorphism and homocysteine/folate metabolism. Clin Exp Med. 2002 May;2(1):7-12.
2. McQuillan BM, Beilby JP, Nidorf M, Thompson PL, Hung J. Hyperhomocysteinemia but not the C677T mutation of methylenetetrahydrofolate reductase is an independent risk determinant of carotid wall thickening. The Perth Carotid Ultrasound Disease Assessment Study (CUDAS). Circulation. 1999 May 11;99(18):2383-8.
3. Zetterberg H, Regland B, Palmér M, Ricksten A, Palmqvist L, Rymo L, Arvanitis DA, Spandidos DA, Blennow K. Increased frequency of combined methylenetetrahydrofolate reductase C677T and A1298C mutated alleles in spontaneously aborted embryos. Eur J Hum Genet. 2002 Feb;10(2):113-8.
4. Serapinas D, Boreikaite E, Bartkeviciute A, Bandzeviciene R, Silkunas M, Bartkeviciene D. The importance of folate, vitamins B6 and B12 for the lowering of homocysteine concentrations for patients with recurrent pregnancy loss and MTHFR mutations. Reprod Toxicol. 2017 Sep;72:159-163.
Some more information will make the Case Presentation more Illuminating and Educative, such as:
1) What was Central Venous Pressure,
2) If patient was, presumably Conscious, Oriented, Able to take Food and Fluids by Mouth, could the Intravenous Administration of Fluids be avoided,
3) How did the Elevated Blood Pressure evolved during Hospitalization, either with or without Medications,
4) What was Patient's Diet and Fluid Intake Both Quantitative and Qualitative during the Hospitalization,
5) Whether the Patient took any Formal or Alternative Medicines or Home Remedies for Coryza he had Two Weeks before Episode of Shortness of Breath, that could have caused Autoimmune Hemolysis.
5) If the Patient's Blood Pressure before Present Illnesses was known and if he took any medications for it and any other conditions eg Bleeding per Rectum,
6) What were the instructions including those regarding medications diet and follow-up given to the Patient at the time of Discharge.
The Authors need to be complimented for seeing the patient through the crisis and The BMJ be thanked for bringing it up to the Readers.
Dear editor,
The case report of published in BMI Case Reports 2020 Oct 29;13(10):e236017 by Ong et al. further expanded the knowledge of cheiro-oral syndrome, an incomplete sensory disorder, in clinical practice. Regarding to the classification of cheiro-oral syndrome, authors cited for Satpute et al. (2013), who clearly described the vascular anatomy of thalamus relating to the clinical picture of sensory and other neurological deficits, including some incomplete sensory syndromes. Bogousslavsky et al. (1988) had reported similar results before. However, to my understanding, the four types of cheiro-oral syndrome was firstly suggested by Chen WH (2009).
1.Bogousslavsky J, Regli F, Uske A. Thalamic Infarcts: clinical syndromes, etiology, and prognosis. Neurology. 1988;38:837–848.
2.Chen WH. Cheiro-Oral Syndrome: A Clinical Analysis and Review of Literature. Yonsei Med J. 2009;50(6):777–783.
3.Satpute S, Bergquist J, Cole JW. Cheiro-Oral syndrome secondary to thalamic infarction: a case report and literature review. Neurologist 2013;19:22–5.
To the editor,
The authors of this article appear to be unaware that the cause of "EVALI" was identified almost a year ago. To quote Dr Ann Schuchat, Principal Deputy Director of CDC in December, 2019: "we can conclude that what I call the explosive outbreak of cases of EVALI can be attributed to exposure to THC-containing vaping products that also contained Vitamin E acetate." (1). This followed publication in NEJM of a study which noted that "Vitamin E acetate was identified in BAL fluid obtained from 48 of 51 case patients (94%) in 16 states but not in such fluid obtained from the healthy comparator group." It also noted that "47 of 50 (94%) had detectable tetrahydrocannabinol (THC) or its metabolites in BAL fluid or had reported vaping THC products." It is widely known that people who have become ill due to use of illicit products, such as THC vapes, do not always tell the truth about the illegal products they used. The NEJM study also reported that "9 of 11 patients who reported no use of THC-containing e-cigarette products in the 90 days before the onset of illness had detectable THC or its metabolites in their BAL fluid." These and numerous other studies have clarified that EVALI is caused by vaping THC products contaminated by vitamin E Acetate. Since the cause became clear in December 2019, identification of new cases of this disease dropped markedly, and in February 2020 CDC stopped reporting new cases. We...
To the editor,
The authors of this article appear to be unaware that the cause of "EVALI" was identified almost a year ago. To quote Dr Ann Schuchat, Principal Deputy Director of CDC in December, 2019: "we can conclude that what I call the explosive outbreak of cases of EVALI can be attributed to exposure to THC-containing vaping products that also contained Vitamin E acetate." (1). This followed publication in NEJM of a study which noted that "Vitamin E acetate was identified in BAL fluid obtained from 48 of 51 case patients (94%) in 16 states but not in such fluid obtained from the healthy comparator group." It also noted that "47 of 50 (94%) had detectable tetrahydrocannabinol (THC) or its metabolites in BAL fluid or had reported vaping THC products." It is widely known that people who have become ill due to use of illicit products, such as THC vapes, do not always tell the truth about the illegal products they used. The NEJM study also reported that "9 of 11 patients who reported no use of THC-containing e-cigarette products in the 90 days before the onset of illness had detectable THC or its metabolites in their BAL fluid." These and numerous other studies have clarified that EVALI is caused by vaping THC products contaminated by vitamin E Acetate. Since the cause became clear in December 2019, identification of new cases of this disease dropped markedly, and in February 2020 CDC stopped reporting new cases. We do a disservice to the public and to our patients by being imprecise about this. EVALI is not caused by nicotine e-cigarettes, just as the epidemic of lethal overdoses associated with addictive pain medication use is not caused by Ibuprofen. We are correct to call that the "opioid epidemic", rather than the "analgesic epidemic". A THC vape is not the same as a nicotine e-cigarette, just as Vicodin is not the same as Tylenol and a joint is not the same as a cigarette. Lets call this serious respiratory disease what it is: THC-Vaping Associated Lung Injury (THCVALI) caused by vaping THC products contaminated by vitamin E acetate. We should inform our at-risk patients and the public tha tit is dangerous to use THC vapes, from the United States that came from informal sources (i.e. not directly from a licensed dispensary or via a doctor's prescription), and we should not confuse our patients or professional colleagues by referring to this illness as if it is caused by nicotine e-cigarettes. It is not. We should therefore call it THCVALI..
(2) Blount BC et al, For the Lung Injury Response Laboratory Working Group. Vitamin E Acetate in Bronchoalveolar-Lavage Fluid Associated with EVALI. N Engl J Med 2020; 382:697-705 DOI: 10.1056/NEJMoa1916433
A close comparison of baseline and exercise ECGs show mild ST elevation in V1 and mild inferolateral ST depression. Though the ST depression is mostly slow upsloping type, in lead I and V6 it is almost horizontal. The magnified view of the ECG makes ST elevation in V1 quite clear.
The author proposes two possible mechanisms for Aza induced hyperglycemia 1. Impaired beta cell function in pancreas via epigenetic mechanism 2. Increased secretion of cortisol. I suggest another possibility. A recent paper by Strand et al reports that Aza, a DNMT1 inhibitor, is a potent inducer of PTEN (this work done in vascular smooth muscle cells). It is well known that PTEN is an inhibitor of downstream elements of the insulin pathway, specifically PI3K-AKT-mTOR pathway and this results in insulin resistance. I suggest that the hyperglycemic activity of Aza is by PTEN induction of insulin resistance.
Strand KA, Lu S, Mutryn MF, et al. High Throughput Screen Identifies the DNMT1 (DNA Methyltransferase-1) Inhibitor, 5-Azacytidine, as a Potent Inducer of PTEN. Arterioscler Thromb Vasc Biol. 2020;40:1854–1869.
We thank Dr Yap and colleagues for describing clearly the successful management of an unexpectedly challenging airway.1 We agree that the index case highlights the need for vigilance in all patients requiring airway management, particularly where an atypical presentation of a respiratory condition may indicate occult airway pathology.2 However, the case raises a number of important issues for airway assessment, intubation-related laryngeal pathology and the management of ‘can’t intubate, can’t ventilate’ scenarios which warrant further discussion, considered below.
Airway assessment can be encapsulated by the quote, “Hindsight is a wonderful thing but foresight is better, especially when it comes to saving life,” attributed the 19th Century English poet William Blake. Whilst subtle, there were a number of clues in the described case report that could, and perhaps should, have prompted a more thorough evaluation of the airway. It is surprising that the patient did not report their extreme prematurity at birth, or the fact that they spent the first year of their life in hospital. This would have almost certainly have involved prolonged ventilation and sequelae into childhood. Respiratory and airway complications are well recognised in premature neonates and may coexist.3 The authors highlight the Difficult Airway Society’s airway algorithms and the fact that any clinician managing an airway should prepare for failure.4-6 This should involve an examination of the front...
Show MoreDear Editor,
Giant aortic aneurysm is a rare clinical entity. They may present with typical features of chest pain or abdominal pain, or most feared complications with dissection and rupture. However, an asymptomatic and unruptured giant thoracic aneurysm is extremely rare with only two case reports in the literature.
I had a similar case which an 80-year-old lady admitted to a local district general hospital with a 5 day history of productive cough with shivers, which she was tested positive for COVID-19 on admission.
Diagnostic workup demonstrated an incidental finding of a giant TAAA. Her case was referred to a tertiary hospital for vascular Multidisciplinary Team (MDT) discussion and planning.
It was decided that for her to have pre-operative assessment and MDT discussion after her recovery from infection to have a definitive management of the TAAA. The patient is currently being managed supportively in hospital.
According to National Institute for Health and Care Excellence (NICE), asymptomatic and 5.5 cm or larger aneurysm should be considered for repair. The case should be discussed in terms of the overall balance of benefits and risks with repair and conservative management, based on the current status of health and the expected future health. In this case, it was deemed that the risk of proceeding with repair at present outweighed the benefits.
Incidental finding of a giant AAA/TAAA is rare. It emphasises the importance...
Show MoreTo the authors:
Show MoreWe read with interest the article entitled “Sudden irreversible hearing loss post COVID-19”.1 In this article, the authors presented an unusual case of a 45 year-old gentleman with sudden-onset sensorineural hearing loss (SNHL) after COVID-19 infection and treatment. In their literature review, five other case reports were cited with hearing loss noted after COVID-19.2-6 The patient in the case report experienced a decrease in his left sided hearing 1 week after his intensive care unit stay for COVID-19 treatment. His initial hearing loss was evaluated at the bedside with a tuning fork examination showing negative Rinne’s test on the side of reported hearing loss, and Weber’s test lateralizing to the side opposite to his hearing loss, which is consistent with SNHL of the affected side. He then had a 7 day treatment course of 60mg oral Prednisone daily in addition to a series of intratympanic steroid injection. His hearing loss was documented with elevated hearing thresholds of 65, 75, 75, and 85 dB at 2, 3, 4, and 6 kHz.
As multiple countries across all continents are facing the effects of the pandemic, our understanding of the various immediate and long-term complications of COVID-19 is evolving. SNHL is one of these complications. The Coalition for Epidemic Preparedness Innovations (CEPI) has developed a Brighton Collaboration case definition of SNHL to be utilized in the evaluation of adverse events following immunization, which can also be...
We read the article published by Jaikaran O. et al on ‘Portomesenteric thrombosis after robotic sleeve gastrectomy’ with great interest. The reported about a morbid obese patient having porto-mesentric thrombosis after robotic sleeve gastrectomy due to obesity and mutation in methylenetetrahydrofolate reductase (MTHFR) mutation. However, we have few factors to report on this aspect.
Firstly, MTHFR enzyme dysfunction leads to hyperhomocysteinemia which leads to hypercoagulation state. Yet, the magnitude of this state is affected via degree of enzyme deficiency/dysfunction which is dependent on presence of heterogeneous/ homogenous mutation in enzyme gene. So, the authors must assess for the presence of hyperhomocysteinemia along with assessment of mutation.[1,2] Also the genetic homogeneity of the mutation must be assessed as heterogeneous mutation will have less effect on blood homocysteine levels.[3]
Next, the importance of folic acid for management of thrombotic state due to hyperhomocysteinemia must be considered. The patient has undergone sleeve gastrectomy which may further aggravate her vitamin and micronutrient deficiency. The administration of folic acid (instead of aspirin) will decrease the blood homocysteine levels and reduce the risk of hypercoagulation.[4]
References:
Show More1. Friso S, Girelli D, Trabetti E, Stranieri C, Olivieri O, Tinazzi E, Martinelli N, Faccini G, Pignatti PF, Corrocher R. A1298C methylenetetrahydrofolate reductase mu...
Some more information will make the Case Presentation more Illuminating and Educative, such as:
1) What was Central Venous Pressure,
2) If patient was, presumably Conscious, Oriented, Able to take Food and Fluids by Mouth, could the Intravenous Administration of Fluids be avoided,
3) How did the Elevated Blood Pressure evolved during Hospitalization, either with or without Medications,
4) What was Patient's Diet and Fluid Intake Both Quantitative and Qualitative during the Hospitalization,
5) Whether the Patient took any Formal or Alternative Medicines or Home Remedies for Coryza he had Two Weeks before Episode of Shortness of Breath, that could have caused Autoimmune Hemolysis.
5) If the Patient's Blood Pressure before Present Illnesses was known and if he took any medications for it and any other conditions eg Bleeding per Rectum,
6) What were the instructions including those regarding medications diet and follow-up given to the Patient at the time of Discharge.
The Authors need to be complimented for seeing the patient through the crisis and The BMJ be thanked for bringing it up to the Readers.
Dear editor,
The case report of published in BMI Case Reports 2020 Oct 29;13(10):e236017 by Ong et al. further expanded the knowledge of cheiro-oral syndrome, an incomplete sensory disorder, in clinical practice. Regarding to the classification of cheiro-oral syndrome, authors cited for Satpute et al. (2013), who clearly described the vascular anatomy of thalamus relating to the clinical picture of sensory and other neurological deficits, including some incomplete sensory syndromes. Bogousslavsky et al. (1988) had reported similar results before. However, to my understanding, the four types of cheiro-oral syndrome was firstly suggested by Chen WH (2009).
1.Bogousslavsky J, Regli F, Uske A. Thalamic Infarcts: clinical syndromes, etiology, and prognosis. Neurology. 1988;38:837–848.
2.Chen WH. Cheiro-Oral Syndrome: A Clinical Analysis and Review of Literature. Yonsei Med J. 2009;50(6):777–783.
3.Satpute S, Bergquist J, Cole JW. Cheiro-Oral syndrome secondary to thalamic infarction: a case report and literature review. Neurologist 2013;19:22–5.
To the editor,
Show MoreThe authors of this article appear to be unaware that the cause of "EVALI" was identified almost a year ago. To quote Dr Ann Schuchat, Principal Deputy Director of CDC in December, 2019: "we can conclude that what I call the explosive outbreak of cases of EVALI can be attributed to exposure to THC-containing vaping products that also contained Vitamin E acetate." (1). This followed publication in NEJM of a study which noted that "Vitamin E acetate was identified in BAL fluid obtained from 48 of 51 case patients (94%) in 16 states but not in such fluid obtained from the healthy comparator group." It also noted that "47 of 50 (94%) had detectable tetrahydrocannabinol (THC) or its metabolites in BAL fluid or had reported vaping THC products." It is widely known that people who have become ill due to use of illicit products, such as THC vapes, do not always tell the truth about the illegal products they used. The NEJM study also reported that "9 of 11 patients who reported no use of THC-containing e-cigarette products in the 90 days before the onset of illness had detectable THC or its metabolites in their BAL fluid." These and numerous other studies have clarified that EVALI is caused by vaping THC products contaminated by vitamin E Acetate. Since the cause became clear in December 2019, identification of new cases of this disease dropped markedly, and in February 2020 CDC stopped reporting new cases. We...
Pages