Displaying 207-231 letters out of 774 published
Paramedic Airway Skills
I was extremely interested in these papers in this months EMJ. [Joint Royal College Ambulance Liaison Committee Airway Working Group commentary The College of Paramedics (British Paramedic Association) position paper regarding the Joint Royal Colleges Ambulance Liaison Committee recommendations on paramedic intubation (Prehospital airway management)].
I wonder if anyone could tell me what are the professional credentials of the members of the Airway Working Group in Pre-hospital care and their experience in working outside the comfort of the resus room or theatres. I have worked since the mid/late 70's on the roadside, was involved at the same time as Robin Glover in teaching Ambulance personnel advanced procedures such as cannulation, intubation and defibrillation. He to the Cambridge area and I to the Suffolk area. I have also taught proper paramedics in Suffolk, East Anglian and Kent ambulance services.
I still do BASICS, teach ATLS, ALS, in the past BTLS and PHTLS as well as Instruct instructors, so am very familiar with the Principles of Education and training. I have also been involved in teaching on human simulators as well. I have done probably more prehospital and resus room intubations over 33 years than any of the 'experts' on the panel. I have also done Anaesthetics in my even earlier years. Intubating in a Race gravel trap also features strongly in my 30 years on the circuits.
It beggars belief that they can base their decisions on such poor quality research and literature reviews, especially American papers. Also that they are not even attempting to investigate the new technologies that have been and are available for making ET intubation safer.
As an A/E consultant I have had the benefit of working night and day, summer and winter, hot and freezing cold, wet and dry at roughly more than 10,000 call outs plus working on many of these patients in my unit together with countless more to which I was not called out to the scene.
I really feel that the comments I have made about the experience of the panel are made from the standpoint of being infinitely more skilled than anyone around today. I have been on call 24/7 since the 70's except when on annual leave.
I sincerely trust someone somewhere will take your papers to heart and do some proper research
Conflict of Interest:
Effects of bed height on the performance of chest compressions- Clinical application of results
Editor- I would like to start by congratulating Cho and colleagues (1) on undertaking a study that addresses an area of cardiopulmonary resuscitation (CPR) which potentially, could for such a simple intervention have such a dramatic impact on the quality of CPR delivered. There are surprisingly few papers published on this area, and the 2005 ILCOR guidelines (2) were based largely on expert opinion with little evidence base.
The statistical relationship between a bed height at the knee level and the effectiveness of CPR is clear. The concern is the application of these results to the clinical setting. Having recently completed similar work within this area, I would suggest you would find it difficult to locate a hospital bed/trolley with mattress which is able to drop to the average person's knee level. So as a result, we may be continually subjecting patients to sub-optimal chest compressions, even if the beds are dropped to their lowest levels. Perkins et al suggested resuscitation carried out on the floor when compared to the bed is superior (3). Again, application of this not really possible on a daily basis and certainly not advocated by ILCOR guidelines.
The solution may be to eliminate the human component to chest compression all together, by using one of the various automated devices available now. Initial studies were very encouraging and demonstrated not only their safety but also possible survival benefits (4,5). The slow uptake of these devices probably stems from not only their cost implication, but the results of the large randomised prospective ASPIRE trial (6), which demonstrated that the use of Autopulse was associated with a worse neurological outcome and a trend towards worse survival, when compared to manual CPR.
So the answer in the mean time is a little bit more low-tech and a little bit more 'ER' esque; I would suggest we go back to kneeling on the bed when performing CPR. In this position the clinician can keep their arms straight and with the advantage of their upper body weight can perform effective chest compressions. It is always worth remembering, that in the real world good quality chest compressions are not simply dependent on the depth of chest compression. The vital role of chest recoil and the thoracic pump effect are not addressed with compression plates and manikin studies and form a key component of successful resuscitation.
1. Cho J, Oh JH, Park YS, et al. Effect of bed height on the performance of chest compressions. Emer Med J 2009: 26; 807-810
2. International Liaison Committee on Resuscitation. International Consensus on cardiopulmonary resuscitation and emergency cardiovascular science with treatment recommendations. Part 2. Adult basic life support. Resuscitation 2005; 67: 187-201
3. Perkins GD, Smith CM, Augre C, et al. Effects of a backboard, bed height, and operator position on compression depth during simulated resuscitation. Intensive Care Med 2006;32:1632-5
4. Casner M, Andersen D, Isaacs SM. The impact of a new CPR assist device on rate of return of spontaneous circulation in out-of-hospital cardiac arrest. Prehosp Emerg Care. 2005 Jan-Mar;9(1):61-7.
5. Krep H, Mamier M, Breil M, Heister U, Fischer M, Hoeft A. Out-of- hospital cardiopulmonary resuscitation with the AutoPulse system: a prospective observational study with a new load-distributing band chest compression device. Resuscitation. 2007 Apr;73(1):86-95. Epub 2007 Jan 24.
6. Hallstrom A, Rea TD, Sayre MR, et al: Manual chest compressions vs. use of an automated chest compression device during resuscitation following out-of-hospital cardiac arrest. JAMA 2006. 295(22):2620-2628.
Conflict of Interest:
Blended learning in the ED, and national guidance.
I read the article by Roe et al with great interest, particularly because as a trainer of junior doctors in the Emergency Department I recognise many of the barriers to effective teaching as described in the article.
Locally we have appreciated the poor attendance by Foundation trainees at weekly teaching sessions, mainly as a consequence of increasingly anti-social rotas. The delivery of high quality work-place based training is also becoming more difficult due to increasing service demand, Foundation doctors working 4-month posts, and the limits imposed by the EWTD.
To address this we have introduced a blended learning package consisting of core e-learning modules and a series of linked work-place based assessment (WPBA) templates. The modules and WPBAs have been selected to allow us to deliver all the competencies outlined in the NICE guidance "Acutely Ill Patients in hospital (CG50)". Foundation trainees in our department are given protected time at work (equivalent to approximately 34 hours dedicated study time in 4 months) to complete the e -learning modules, and then to return to the shopfloor to spend time with a senior doctor completing the linked WPBAs. This time can also be used to reflect on the e-learning session, and allows further discussion and an opportunity to answer questions. To make this process more robust the senior doctors are allocated timetabled afternoon sessions to deliver the WPBAs. At the end of the sessions the trainees are invited to update their eportfolios with the recently completed WPBAs.
What feedback have we received? The blended learning package was introduced in August 2009, and feedback from the first cohort of FY2s was very positive. 16 of 20 FY2s completed a questionnaire at the end of their 4 month post. 88% stated that the modules were appropriate to their learning needs and were of a high standard, 82% felt that the WPBA templates were appropriate to their learning needs, 93% said that feedback from the WPBA sessions was useful, 82% stated that the blended learning package provides high quality education. Overall, 87% of the FY2s would recommend the training they received in our department to colleagues, and 67% stated that teaching in our department was of a higher quality than experienced in previous posts.
And what do our senior doctors think of blended learning? Most have found the delivery of training on a one-to-one basis in the work-place to be a satisfying experience, and the timetabled sessions provide evidence of active personal involvement in teaching and training, which is increasingly important for our CPD returns!
In conclusion, the development of our blended learning package has allowed us to deliver a comprehensive education programme following national guidance in a 4 month period. Feedback from trainers and trainees is encouraging, and we endorse blended learning as an effective mode of delivery of postgraduate medical training in the ED in the 21st Century.
Conflict of Interest:
Re:A Seventy-Five Year Old Mistake
I read your letter and understand that you say r22 cant cause phosgene gas. It would be easier to believe this statement if almost everyone that has been soldering in the hvac field weren't overcome with some type of toxin in the process. I just today was soldering in a freezer that uses hp-80 refrigerant and all of the sudden could not breathe. It felt like my lungs weren't working for a half hour or so and I felt dizzy for more than an hour after with my lungs still not feeling right many hours after. This is not the first time this has happened to me, nor every time with hp80, and the reason everyone in the field thinks that phosgene gas is being produced, is they have probably experienced the same fearful, and possibly damaging condition. Also, the hvac field rarely uses propane or butane, almost always actlyene and oxygen. If you say that it isn't being caused by r22 than what is it? Since system lubrication is carried in refrigerant, is this the toxin causing agent? Is it something with the two soldering gases? It is easy to say something "isn't". Giving a reason always seems to be skipped and proves much more difficult.
Conflict of Interest:
Another case of asthma near death averted by chest compression
The article by Dr. Harrison reminds me of a similar case I treated years ago. A young adult with no prior history of asthma had the first, violent attack of asthma at home and went into respiratory arrest during transport to the emergency service of the small hospital I was working in at the time. The patient arrived unconscious but with carotid pulse still present. The thorax was obviously hyperexpanded and immediate intubation did not allow ventilation: attempts to inflate with air met with great resistance. I therefore proceeded to apply the chest squeezing manouvre: straddling the patient, very gradual but firm pressure with flat, wide-open hands was applied to the anterior thorax pushing the ribs both medially and posteriorly, with air flowing out until the diameter of the rib cage was significantly reduced; expiration by chest squeezing was alternated with inflation of air from the endotracheal tube. As soon as possible adrenaline was administered as well as endovenous hydrocortisone and subsequently salbutamole. Reaction to treatment was swift: spontaneous breathing started little after the use of adrenaline, and in less than ten minutes the patient started reacting to the tube, was extubated and became completely vigilant.
In less than an hour only mild bronchospasm was present. The patient was transferred for observation and further workup to the main hospital of the area and was subsequently discharged with no untoward effects, in particular no discomfort of the rib cage due to the compressions. I confirm that in the case described chest compression expelled air with relative ease, and that ventilation would not have been possible without this manouvre as no significant expiration was observed after intubation, notwithstanding the evidently hyperinflated thorax. I believe the hyperexpansion to have been due to a muscular effect, perhaps a spasm of expiratory muscles due to fatigue as occurs in common muscular cramps.
Conflict of Interest:
The value of taking a history in patients with chest pain
In introducing Goodacre et al's paper on low risk chest pain patients, the Primary Survey of the December 2009 issue prompts emergency physicians to reflect on "why [they] take histories at all in this patient group".(1,2) This is, in our opinion, an inappropriate reaction to the results of the study. The patients under investigation were those with a potential diagnosis of a cardiac cause of chest pain, and according to the exclusion criteria were only enrolled if the history and examination in the emergency department had ruled out other serious treatable causes of chest pain such as pulmonary embolism or aortic dissection. As discussed at the end of the paper, it is likely that many patients who had been diagnosed as having a benign non-cardiac cause of chest pain were not included in the study. Additionally, the majority of patients with typical presentations of other conditions such as pneumonia, pericarditis, pneumothorax, cholecystitis, pancreatitis or chest trauma were presumably not included even if chest pain was a major component of the presenting complaint. Therefore the study cohort comprised only those patients with chest pain whose clinical assessment had failed to suggest an obvious alternative diagnosis. Such assessment necessarily involves taking a careful history(3). Of the entire set of patients presenting with chest pain, the study group represents the subset that retains some diagnostic uncertainty despite a careful history.
To ask why we take a history at all in a group of patients that have already been defined by their history is begging the question. Suggesting to your readers that they may wish to reflect on whether they should take a history at all in this group not only overlooks this point, but invites them to miss other obvious and important treatable illnesses in the rush to "exclude MI". It must be remembered that there are many more diagnostic categories than "acute coronary syndrome" and "non-specific chest pain".
Only a minority of acute coronary syndromes present with a non- diagnostic ECG(4). What Goodacre's study illustrates is that if we take a group of patients with acute chest pain in whom the underlying diagnosis is not clear, a small proportion will be due to unusual presentations of acute coronary syndromes, and that this subset is not identifiable in advance by their symptoms alone. This is useful because it highlights that if an alternative diagnosis is not obvious then there is scope for doubt and that caution is advisable. It is not an argument for abandoning a careful history, which remains in everyday practice our most useful clinical assessment tool.
1. Clinical diagnosis of acute coronary syndrome in patients with chest pain and a normal or non-diagnostic electrocardiogram Emerg Med J 2009 26: 866-870 S Goodacre, P Pett, J Arnold, et al.
2. Primary Survey Emerg Med J 2009;26:843 Kevin Mackway-Jones
3. Evaluating the Patient with Chest Pain: The Value of Comprehensive History. Journal of Cardiovascular Nursing. July/August 2005; 20(4): 226-231 Reigle J
4. Prognostic Value of a Normal or Nonspecific Initial Electrocardiogram in Acute Myocardial Infarction JAMA. 2001;286:1977-1984 Robert D. Welch, MD; Robert J. Zalenski, MD; Paul D. Frederick, MPH, MBA; Judith A. Malmgren, PhD; Scott Compton, PhD; Mary Grzybowski, PhD, MPH; Sophia Thomas, MD; Terry Kowalenko, MD; Nathan R. Every, MD, MPH; for the National Registry of Myocardial Infarction 2 and 3 Investigators
Conflict of Interest:
Simple buckle fracture? Are you sure of the diagnosis before discharge with no follow up?
I read with interest the Best Evidence Topic report by May G, Grayson A regarding the follow up of buckle fractures. I agree that buckle fractures should not require routine follow up, however systems need to be robust to ensure that the correct diagnosis has been made. Diagnosis may not be as simple as often believed; several studies researching this topic have inadvertently included fractures other than buckle fractures in their trials, later having to withdraw them.[2,3,4] Misdiagnosis occurred across the board; by emergency medicine, orthopaedic and radiology clinicians.[2,3,4] Others have warned of the need of safety nets to be in place, with emphasis on training and hot reporting. With the reassurance that these measures are in place, we should be able to safely treat and discharge buckle fractures from the emergency department.
1. May G, Grayson A. BET 3: Do Buckle Fractures of the Paediatric Wrist require follow up? Emerg. Med. J. 2009 26:819-822; doi:10.1136/emj.2009.082891
2. Plint AC, Perry J, Correll R, Gaboury I, Lawton L. A Randomized, Controlled Trial of Removable Splinting Versus Casting for Wrist Buckle Fractures in Children. Pediatrics 2006;117:691-7.
3. Davidson JS, Brown DJ, Barnes SN, Bruce CE. Simple treatment for torus fractures of the distal radius. J Bone Joint Surg [Br] 2001;83- B:1173-5.
4. Oakley EA, Ooi KS, Barnett PL. A Randomized Controlled Trial of 2 Methods of Immobilizing Torus Fractures of the Distal Forearm. Pediatr Emerg Care 2008;24:65-70.
5. Guly HR. Injuries initially misdiagnosed as a sprained wrist (Beware the sprained wrist). Emerg Med J 2002;19:41-2.
Conflict of Interest:
On the philosophy of diagnosis: Authors' responseDear Editor,
We welcome the thoughtful responses of Dr. Challen and Dr. Cattermole to our paper entitled: On the philosophy of diagnosis: is doing more good than harm better than primum non nocere? Dr. Challen makes two principle criticisms of our review to which we would like to respond.
1. The existence of reality
Dr. Challen correctly states that outside the medico-scientific realm, the post-positivist concept that one indisputable reality truly exists is not universally accepted. This is particularly so in the social sciences where, by way of an example, constructivists hold that absolute reality exists only in the form of societal and social constructs. While this may be a helpful aid to certain forms of research, it is seldom of benefit in the scientific evaluation of diagnostic technology.
In order to provide a diagnosis, we must first accept that there is a disease to be diagnosed. While it is perfectly reasonable to investigate and debate the existence of that disease beforehand we, as physicians, must ultimately accept that specific diseases do exist, that they threaten health and happiness and indeed may lead to death. We must also accept that it is possible for us to recognise the presence or absence of those diseases, albeit imperfectly. This, by definition, is the post-positivist paradigm that must by necessity underpin our scientific approach to diagnosis.
2. The individualised approach to diagnosis as a refutation of utilitarian ideals
Dr. Challen comments that, while utilitarian ideals are inescapably embraced in the practice of clinical medicine and can be applied to population-based diagnostics such as screening, they should not be applied to individuals when pursuing a diagnosis. We can certainly appreciate this perspective, but we do not agree.
Our present approach to diagnostics involves the evaluation of the technology in a sample from a population, from which we may calculate estimates of sensitivity and specificity. These are population-based estimates which we do then apply (probabilistically) to individual patients. This underlies the principle of clinical probability scoring as a supplement to D-dimer testing in patients with suspected venous thromboembolism. Indeed, we may apply similar Bayesian principles to the diagnosis of individual patients on a day to day basis (for example, we may ignore the fact that the chest radiograph is normal if our patient appears to have a high clinical probability of aortic dissection).
The utilitarian approach we advocate relies on similar principles. As the sensitivity and specificity for all diagnostic tests are imperfect, there is an inevitable compromise to be drawn between false positive and false negative diagnoses. The relative weight that we assign to each of these is currently subjective.
However, by mapping the sensitivity and specificity to projected outcomes for the patients, it may be possible to appreciate the consequences of implementing any particular diagnostic test more objectively. Further, it would be possible to compare the anticipated consequences using different diagnostic tests and lead to a more informed judgement about which is the preferred investigation.
In doing this we are certainly not reinventing the wheel. We are simply trying to put it on a better vehicle.
In response to Dr Cattermole we would say that much of diagnostics and therapeutics is exactly as he describes utilitarianism: the right test or diagnostic strategy, or treatment is one which maximises the aggregate good outcome. In myocardial infarction with ST elevation we could never know for that individual whether thrombolysis would be of benefit, or might be harmful. Looking at the population as a whole more would benefit than be harmed. The same applies for many treatments and diagnostic strategies. Vaccination is inherently utilitarian. The fact that utilitarianism can be used to justify acts which by other standards are immoral does not invalidate the concept.
Modern medical ethics is not about a single unifying ethical theory. It combines elements of deontology (beneficence and non-maleficence) with justice and autonomy. The NHS is inherently utilitarian in that it aims to maximise the good. We do not have unlimited resources for each patient. We do our best, but there are constraints. Rule out strategies are not infallible but they aim to maximise the good.
Utilitarianism, as applied to diagnostics or therapeutics, is about the interests of the patient. For most treatments the number needed to treat is more than one. A priori we do not know which patient of the cohort will benefit, so they all get it because overall patients do better with than without that treatment. This is done in the interests of the patient, not of the State.
Richard Body and Bernard Foex
Conflict of Interest:
When the Good of the One outweighs the Good of the Many
I would like to thank Body and Foex for their thought-provoking article, and also Cattermole and Challen for their replies. Too often in the culture of emergency medicine, the philosophical underpinnings of thought and action are neglected. When is there time to reflect?
One highlight of their discussion of utilitarianism is the inclusion of emotional factors into the weighing of what actions can be counted as Good (or cost-effective). False-positive tests occasion much suffering at times, and this needs to be recognized. Many of our strategies of care would be well served through this form of examination. For example, practitioners who treat indigent patients disrespectfully with the intention of making them reflect upon the error of their ways or use the emergency department less often.
The challenge of utilitarian analysis is the consideration of all possible ramifications of action, and the subsequent calculation of costs and benefits on all levels - physical, economic, emotional... Faced with such complexity, a return to "primum non nocere" becomes attractive. And yet there needs to be a balance between action guided by ideals and action guided by calculation. It is possible that Hippocrates also said "secundum, consider all consequences of your words and deeds."
Conflict of Interest:
Don't we have a service concept?
The article by Higginson made me think about our specialty and whether we have got a missing link. However, it reminded me to look at the Way Ahead document produce by the UK College of Emergency Medicine in 2008. Surely this provides an excellent service concept for our specialty? The document provides clear guidance as to what our core and extended services should be and how we should consider delivering them. I wonder whether the author had read this....maybe he should.
Conflict of Interest:
Sensitivity or specificity?
With great interest we read the recent article by Bevan and colleagues reporting how predictive ALT is for liver injury in children with blunt abdominal trauma. In the result section the authors describe the following: "The presence or absence of liver injury can be predicted with a sensitivity of 96% and a specificity of 80%". In their conclusion they reported: "a threshold of >104 IU/L gave a 96% specificity for the detection of liver injury". We would like to emphasize the difference and think the authors mean 96% sensitivity in their conclusion section.
Shenaida R. Oemar
Assessment and risk stratification of patients with acute chest pain
We read with interest Manini et al’s 1 recent paper suggesting ischaemia-modified albumin assays could assist in decreasing the rate of inappropriate discharges from the ED, and that further studies into diagnostic tools for use in chest pain are warranted.
We conducted an audit at Ealing Hospital that also supports the need for developing new diagnostic algorithms for chest pain. Medical histories of 147 patients admitted to the Emergency Department’s Chest Pain Unit for monitoring were studied. All patients gave a history consistent with chest pain of cardiac origin. We studied whether positive troponin-T results correlated with the presence of Framlingham cardiovascular risk factors, or with a past medical history of cardiac or vascular disease (i.e. a history of angina, coronary artery bypass grafting, previous MI, stroke, TIA, heart failure, previous angiography or history of claudication).
In our patient group the percentage of positive troponin results did not increase in line with the number of Framlingham risk factors present, however these patients were highly likely to receive further in-patient investigation. Conversely, while past medical history of cardiac or vascular disease did not appear to have a bearing on the emergency physician’s decision to admit a patient for investigation, those patients with 1-3 conditions appeared to form the majority of patients with positive troponin results (this group made up 55.9% of patients with positive troponin results, but only contributed 36.9% of those with negative troponins).
This data supports a number of other studies on this topic 2,3, and we believe that physicians should consider treating chest pain patients with significant cardiovascular history with a higher index of suspicion that is currently the case. We also believe that further research into the use of past medical history in the assessment and risk stratification of acute chest pain is required.
- Manini AF, Ilgen J, Noble VE et al.. Derivation and validation of a sensitive IMA cutpoint to predict cardiac events in patients with chest pain. Emerg Med J 2009;26:791-796.
- Body R, McDowell G, Carley S et al.. Do risk factors for chronic coronary heart disease help diagnose acute myocardial infarction in the Emergency Department? Resuscitation 2008;79:41-5.
- Cakir B, Blue K. How to Improve the Management of Chest Pain: Hospitalists and Use of Prediction Rules. South Med J 2007;100:242-7.
This case appears to be describing the Pellegrini-Stieda syndrome/lesion. This is, in fact, a well-known and fairly common finding, generally felt to reflect a post-traumatic ectopic ossification, either acute or chronic. MR is a useful test, as the signal void from the calcification can be seen in relation to the MCL. It may also uncover bone bruising from an associated avulsion fracture (the so-called Stieda fracture). As an academic exercise, MR can also subclassify the lesion into 4 different types, dependent on the exact pattern of ossification (although this has limited, if any, clinical importance).
Reference: Mendes et al. Skeletal Radiology (2006) 35(12):916-22.
Importance of log roll and careful spine evaluation
Dear Editor, I understand that it is very important to log roll and carefully evaluate the whole spine of the patient. By reading this article, I understand the importance of complete spinal evaluation but there are situations in which spinal injuries are missed as a result of incomplete evaluation or not adhering to systematic approach. I want to share one of the clinical cases in the management of which I was involved. A patient presented with hypotension, abdominal distension, bradycardia and unconsciouness in A&E after being involved in a high speed motor vehicle crash. The patient was taken for emergency laparotomy which proved negative. Despite that patient remained hypotensive and cervical spine x-rays were obtained which revealed atlanto-occipital dislocation. The patient died 2 days later but the lesson is to firmly adhere to A,B,C,D and E protocol of ATLS and don’t cut short corners. Unnecessary operations can be avoided and those who are unlikely to survive symptomatic treatment can be decided from the point of presentation.
Primum, non nocere.
I was disturbed to read the article by Body and Foex  advocating the embrace of Utilitarian values in medicine. I hope it was merely a misuse of words. All penguins are birds, but not all birds are penguins. Utilitarianism is a form of consequentialism, but not all ethical thinking that considers the consequences of one’s actions is Utilitarian. The authors of the article correctly make a clear case for efficiency and risk -benefit “consequential” thinking in medicine, and in particular in decision analysis. However, this is not Utilitarianism.
Utilitarianism is an ethical theory in which the “right” action is that which maximises the aggregate “good” outcome across a population. The “good” can variously be defined as pleasure, or preference satisfaction, or as in this article, health benefit. There are practical problems with the theory which are common to any consequential thinking: the difficulties of making predictions and calculating relative risk-benefits for people with different perceptions of what is good for them. However, the big problem with utilitarianism itself is that it justifies any action, so long as there is an aggregate net increase in what is considered good. Plagiarism, falsified research data, dishonest job applications, unfair discrimination - could all in some situations be justified. And so could bribery, theft, or murder. Of course, doctors would never be involved in inhuman human experiments, forced sterilisations, “eugenic” murder, or torture for the “greater good”… but they would, and they were, and it didn’t stop with Nazi Germany or Tuskegee. And why should it, if you accept Utilitarianism? Why not kill an unwilling patient in order to harvest his healthy organs to save five others who would otherwise die?
If we seek to do net good in medicine, the command to “do no harm” is a helpful warning against the evil of imposing a centrally defined, collective “good”, on vulnerable individuals. As such, it is good that Hippocrates is said to have made it a priority. Bentham might have considered rights to be “nonsense upon stilts”, but it is because consequence-based ethical thinking is so inherently dangerous, that we need human rights, and aphorisms such as “first, do no harm”.
No-one outside the extreme wing of the health-and –safety lobby would suggest that “do no harm” means that one must never perform an action that might be painful. Foex and Body are setting up a “straw man” by using examples such as venous cannulation to argue against the importance of non -maleficence. Patients consent to undergo discomfort or risk in order to achieve a later benefit: this expresses their right to choose for themselves (autonomy), and is a balance of good and harm (beneficence and non-maleficence). If the patient cannot consent, then we have to weigh up very carefully what is in the patient’s best interests (risk-benefit) – not primarily the interests of the State.
Utilitarianism can impose deliberate involuntary harm on an individual for others’ benefit. By reminding ourselves of the importance of autonomy and doing no harm, we would remember that the good we seek is that of the patient we are treating, that the harm that may ensue is accidental, and the risks agreed by the one facing them.
Consequence-based reasoning and good medicine are of course “inescapably intertwined”. But for goodness’ sake, do not call this “Utilitarianism”.
Sincerely, Giles N Cattermole.
Body R, Foex B. On the philosophy of diagnosis: is doing more good than harm better than “primum non nocere”? Emerg Med J 2009;26:238-40.
 Bentham J. Anarchical fallacies. In Bowring J (editor): The Works of Jeremy Bentham (Vol 2). Edinburgh, Wm Tait. 1843, p501. Viewed 26 May 2009. http://books.google.co.uk.
Propofol is not safe for sedation for hip relocation
University Department of Anaesthetics Level 2, University Block Glasgow Royal Infirmary 10 Alexandra Parade Glasgow G31 2ER
19 February 2009
We read with interest the clinically based study, on the use of propofol to sedate patients for relocation of hip prostheses in the emergency department. The authors rightly point out that there are problems with the safety and efficacy of using midazolam, and conclude that the described technique is both effective and safe. In another paper by the same authors they demonstrate this technique of “sedation” has a better success than midazolam, reduces the delay in these patients going to theatre, and therefore the patients discomfort (although there is no mention of pain scores of these patients). However we disagree strongly with the conclusions that adverse effects were acceptably uncommon, and argue that the authors have not demonstrated the safety of this technique.
First, we would like to comment on the sedation protocol. Disappointingly there is no attempt to describe the depth of sedation provided. The report of the Academy of Royal Colleges on Safe Sedation Practice states clearly that “verbal contact with the patient is maintained throughout the period of sedation”. To us, 1mg.kg-1 of propofol in this age group is a dose close to that required for induction of anaesthesia , and without documentation of the maintenance of verbal contact it cannot be termed sedation. By your own admission, many of the patients in this study were, in fact, anaesthetised. The Academy of Royal Colleges document (to which the Faculty of Accident and Emergency Medicine were party) again is quite clear that “provision of sedation deeper than this (verbal contact)… is bordering on anaesthesia. As such, this depth of sedation must be supervised by those with the same level of training and skills necessary to provide general anaesthesia”. Given that many of these patients may have been anaesthetised, we have several concerns regarding this protocol pertaining to training, monitoring, and fasting:
Training: the staff responsible for this procedure had only undergone one hour of in-house training. The Royal College of Anaesthetists mandate to its own trainees that they should undergo an initial assessment of competency before being allowed to give any anaesthetic not directly supervised. This assessment is usually after a full three months. Monitoring: the level of monitoring recommended for patients undergoing general anaesthesia should include capnography. Fasting: we find it incredible that in emergency patients suffering pain (and consequently at higher risk of pulmonary aspiration) that you stated that fasting guidelines were used “as a guide and not a rule”. Evidence on the necessity of fasting for elective procedures are clear after almost 40 years of evidence. Guidelines are less clear for emergency cases as normal fasting times may be insufficient, necessitating protection of the patients’ airway.
More worryingly we refute the interpretation of these data as evidencing safety. It would have been useful to present the incidence of adverse events with confidence intervals (CI). This allows one to estimate the true population incidence of a rare event, which could be as much as the upper level of the 95% CI. We have taken the liberty of doing this for you: 8% (95% CI 2.6 to 13.4) of patients suffered arterial oxygen desaturation, 4% (95%CI 0.2-8) required bag-valve-mask ventilation and 4% (95%CI 0.2 to 2.8) required vasopressors. Therefore your actual population rate may be anywhere between 2.6% and 13.4%. This rate of airway/respiratory events equates to 80/1000 (but could be anywhere between 26 and 134/1000 patients). This compares very unfavourably with those of other non anaesthetic groups (Australian GPs) of 4.1 (95%CI 3.3 to 4.9) /1000 and even less favourably with anaesthetists of 2.6 (95%CI 1.6 to 4.2) /1000. 9 Our department has trained non-medical sedationists to provide true conscious sedation for a different painful procedure (oocyte retrieval for assisted conception), and have audited experience of 3000 patients with an adverse incidence rate of 0.3 (95%CI -0.3 to +0.9) /1000patients. In this context your described results cannot be remotely construed as demonstrating safety. We would also point out that a sample size of thousands not hundreds would be necessary to convince us of the safety of this non-standard technique.
In conclusion we are not surprised that the hip relocation rate is higher with your technique as you have compared propofol anaesthesia with midazolam sedation. We can entirely understand the desire to reduce delays for your patients waiting in pain for hip relocation in theatre. However, our answer to the title of your article “Is propofol a safe and effective sedative for relocating hip protheses?” is a resounding no. It is our interpretation that this technique has not been demonstrated as safe, and would be difficult to justify in the event of a permanent serious complication.
Dr A Puxty, Dr M Sim, Dr KJ Anderson, Professor J Kinsella
References 1. Mathieu N, Jones L, Harris A, et al. Is propofol a safe and effective sedative for relocating hip prostheses? Emerg Med J 2009;26:37–38. 2. Gagg J, Jones L, Shingler G, et al. Door to relocation time for dislocated hip prosthesis: multicentre comparison of emergency department procedural sedation versus theatre-based general anaesthesia. Emerg Med J 2009;26:39–40. 3. UK Academy of Medical Royal Colleges and their Faculties. Implementing and ensuring Safe Sedation Practise for healthcare procedures in adults. Report of an Intercollegiate working party chaired by the Royal College of Anaesthetists. November 2001. http://www.rcoa.ac.uk/docs/safesedationpractice.pdf 4. Dundee JW, Robinson FP, McCollum JSC, Patterson CC. Sensitivity to propofol in the elderly. Anaesthesia 1986;41:482 – 485. 5. http://www.rcoa.ac.uk/docs/CCTptii.pdf 6. http://www.aagbi.org/publications/guidelines/docs/standardsofmonitoring07.pdf 7. Practice guidelines for preoperative fasting and the use of pharmacological agents for the prevention of pulmonary aspiration: application to healthy patients undergoing elective procedures. Anesthesiology 1999; 90; 896-905. 8. Eypasch E, Lefering R,Kum CK, Troidl H. Education and debate. Probability of adverse events that have not yet occurred: a statistical reminder. BMJ 1995;311:619-620 9. Clarke AC, Chiragakis l, HillmanLC, Kaye GL. Sedation for endoscopy: the safe use of propofol by general practitioner sedationists. Med J of Aust 2002;176:158-61 10. Craig DC, Wildsmith JA. Conscious sedation for dentistry: an update. Br Dent J 2007; 203(11): 629-31
ToPDoG is in progress
I commend the work of Geelhoed and MacDonald in their sentinel dose- finding studies regarding the minimum effective dose of dexamethasone for croup, it does seem to suggest a 'ceiling' effect. This work has been recently followed by a descriptive paper (accepted for publication, not yet published) outlining the experience over 27 years at their institution, clearly demonstrating the real-world effectiveness of the lower dose (0.15mg/kg), which became local policy more than two decades ago. Unfortunately, every Systematic Review by the Cochrane Collaboration has found the numbers of patients enrolled in the initial RCTs of Geelhoed and MacDonald too small to rigorously prove the efficacy of the lower dose of dexamethasone in croup. It is with this background that we have recently started recruiting subjects for a large RCT, the ToPDoG Study: Trial of Prednisolone / Dexamethasone oral Glucocorticoid. This trial aims to settle the question of dexamethasone dose (0.6 vs 0.15mg/kg), and compare the efficacy of prednisolone (1mg/kg)in a three-armed equivalence study. Details can be found at: http://www.anzctr.org.au/trial_view.aspx?ID=83722
Oral dexamethasone in the treatment of croup: 0.15 mg/kg versus 0.3 mg/kg versus 0.6 mg/kg. Geelhoed GC, Macdonald WB. Pediatr Pulmonol. 1995 Dec;20(6):362-8. PMID: 8649915
Sixteen years of croup in a Western Australian teaching hospital: effects of routine steroid treatment. Geelhoed GC. Ann Emerg Med. 1996 Dec;28(6):621-6. PMID: 8953950
Glucocorticoids for croup. Russell K, Wiebe N, Saenz A, Ausejo SM, Johnson D, Hartling L, Klassen TP. Cochrane Database Syst Rev. 2004;(1):CD001955. Review. PMID: 14973975
Basic Life Support should be kept basic.
Although the definition of Basic Life Support (BLS) does vary between sources, it is probably best regarded as, "a level of medical care that can be used to treat patients with life-threatening illness or injury without the use of any advanced or invasive medical procedures or intravenous access". It should be possible for any rescuer in any situation to render BLS simply by using hands and lungs, although simple improvised items (such as a handkerchief plus necktie or tights to apply local pressure to a bleeding wound) should also be allowed. Some would extend the list of permitted adjuncts to include a face shield/pocket mask or even an oropharyngeal airway. However, to stretch the concept of BLS to include the use of a bag-valve-mask device (BVMD), laryngeal mask airway (LMA) or laryngeal tube (LT) probably strays too far into the realms of advanced life support. If this is the case, then the title of the paper by Dixon et al. was inaccurately worded.
In reality, the BVMD is probably one of the trickiest items to use correctly in prehospital care, and some would say its use requires two persons – one to hold the mask securely against the patient’s face and the other to squeeze the bag. Certainly, to ventilate the lungs correctly with a BVMD without inflating the stomach requires considerable skill.
The authors failed to state which versions of the selected supraglottic airway devices (SADs) were used in the trial. The Laryngeal Tube is available with both a single lumen (LT & LT-D) and dual lumens (LTSII & LTS-D), the dual-lumen versions featuring a gastric drainage channel in addition to the airway tube. With its distal balloon inflated within the manikin’s upper oesophagus, it is hardly surprising that the authors found a low incidence of gastric insufflation with the LT, particularly if the device also featured a gastric drainage channel opening beyond the distal balloon. Also, the authors failed to state which type of LMA was used by way of comparison. If this was a basic LMA (e.g., the LMA Classic, LMA Unique, Ambu LM or Softseal LM) then a direct comparison with any LT device was probably unfair with respect to the rates of gastric insufflation. It would have been better to have compared the LT with either the LMA Proseal or the disposable LMA Supreme or i-Gel airways - all of which have gastric drainage channels like the LT-D. It should also be noted that the correct sizing of a supraglottic airway device is particularly important when attempting to ventilate manikins, and the same size of airway does not always provide the optimum fit with a particular manikin across the entire range of SADs from different manufacturers. An ill-fitting basic LMA will never be a match for a correctly-sized LT on any of its performance characteristics.
Bearing in mind all these points, the authors’ conclusions need to be viewed with a degree of caution.
REFERENCE: 1. Dixon M, Carmody N, O’Donnell C. The effectiveness of supraglottic airway devices in prehospital Basic Life Support airway management. Emerg Med J 2009; 26: 4.
A response from the International Academies of Emergency DispatchIn response to this article it is important to highlight that this system is not used by any ambulance services or EMS systems in the UK or the world - it is over 8 years old and has been replaced multiple times. Also, a later version of the system has demonstrated a sensitivity of 83% for Emergency Medical Dispatchers using MPDS stroke protocol (http://www.prioritydispatch.co.uk/uk/San_Diego_Accuracy_of_Stroke.pdf). A response by the International Academies of Emergency Dispatch to this EMJ article can be viewed at http://www.prioritydispatch.co.uk/uk/documents/StrokeStudyAMPDS.pdf
Whilst we feel that Lindford et al(1)’s work has many admirable points, we also feel it important to point out minor areas about the study which detract from its overall impact.
Whilst details of the subgroups in the sample size of 50 assessors is given, unfortunately there is no similar breakdown in the information about their answer regarding size of burn requiring resuscitation in adults and children, about the fluid used, or about the identity of the Parkland Formula. As burns nurses are not routinely involved in the prescription of fluid for burns resuscitation their inclusion as part of the sample group is questionable.
In the calculations of the correct value of resuscitation fluid, no information is given about who was incorrect in their calculations. Whilst it is stated that 72% correctly assessed the size of the burn we do not know if the 28% who did not were excluded from the assessment of correct fluid resuscitation values.
A separate chart is given for use in children under the weight of 36kg, including maintenance fluids, this does not specify a proportion to be given as Dextrose Saline, which would constitute a deviation from the normal Parkland formula. Whether this would result in clinically significant hypoglycaemia is debatable(2), but concerns have been raised in the management of infants undergoing fluid resuscitation for septic shock(3). It may be possible to include this weight-related value within the chart in each weight based row.
The chart makes it easy to select the correct amount of resuscitation fluid to infuse per hour if the patient proceeds directly from injury to Emergency Department with no pause, this is often not the case. Delay in commencement of resuscitation and inadequate initial management may result in a deficit which needs to be calculated and the infusion rate adjusted compared to the value derived from the table, as the authors acknowledge. This is an area where information technology in the form of a web based application hosted on the burns centre website would be ideal.
T.H. McKinnell, MB ChB, MSc, MRCS (Ed)*$
A. Hartley, MB BS, BSc$
K. Allison MB ChB, MD, FRCS (Plast)$
*Royal Victoria Infirmary, Newcastle $James Cook University Hospital, Middlesbrough
1 Lindford AJ, Lim P, Klass B, Mackey S, Dheansa BS, Gilbert PM (2009) Resuscitation tables: a useful tool in calculating pre-burns unit fluid requirements Emerg Med J;26:245-249
2 Murat I and Dubois MC (2008) Perioperative fluid therapy in pediatrics. Pediatric Anesthesia 18: 363–370
3 Parker, MM; Hazelzet, JA; Carcillo, JA (2004) Pediatric considerations. Crit Care Med; 32[Suppl.]:S591–S594)
More questions than answers
One major shortcoming of this comparison of monophasic and biphasic defibrillators for the treatment of out-of-hospital cardiac arrest, which was not fully addressed by the authors, concerns the fact that the defibrillators used were programmed to analyse and deliver up to three stacked shocks in accordance with the AHA guidelines of 2000. Guidelines 2005 revolutionised the treatment of VF cardiac arrest by emphasising the importance of the application of early chest compressions with minimal interruption to these compressions, together with the delivery of an initial single shock instead of stacked shocks. Guidelines 2005 also advised that the energy level for the initial shock from a monophasic defibrillator should be raised to 360 Joules, as opposed to the 200/300/360-Joule pattern used in the study.
Consequently, this study probably poses more questions than it answers. For example, there is no way of knowing if the use of the currently recommended higher energy level for the initial shock from a monophasic defibrillator might have elevated the first-time success rate for monophasic defibrillation in the study to that (or, for that matter, above that) demonstrated by the biphasic units. Therefore, it may be premature to scrap all monophasic defibrillators based on the findings of this study, although it may have driven one more nail into their communal coffin.
CONFLICT OF INTEREST STATEMENT: This author still carries his trusty manual monophasic defibrillator with its integral cardiac pacing facility, and has been reluctant to ditch it until there is clear evidence of the superiority of biphasic AEDs.
MCL calcification not described?
Is this not "Pelligrini-Stieda" disease?
It is correct priority, not diagnosis, that matters at telephone triage
I found the article by Deakin et al interesting but have to feel that the article seems to dwell on whether the Advanced Medical Priority Dispatch system (AMPDS) correctly identifies stroke when the emphasis should have been on whether it can correctly prioritise patients to a catagory A or B who are later found to have suffered a stroke.
The authors themselves identify the fact that ambulance prioritisation is more important for the patient than the actual categorisation made by the AMPDS software. Certainly any system that relies upon information supplied by a lay person cannot expect to make a "diagnosis" of stroke in all cases. If the patient has collapsed and is unconcious use of the appropriate AMPDS algorithm for this is more appropriate in ensuring that the correct response is sent. Based on this the underprioritisation of only 2.9% is not entirely unacceptable and further review could be done to look for any triggers in these calls to indicate a higher likelihood of stroke.
Given that the DH has acute stroke response time set at Catagory B (19 minutes) these patients are getting an appropriate priority of response 97.1% of the time which is the most important thing.
It would be interesting to know how many of these cases were diagnosed as a stroke by the ambulance staff on their arrival and subsequently handed over at the ED.
CT Urography: Clarification
We read with great interest the excellent article in the September 2008 issue of the journal by Ulahannan et al entitled “Benefits of CT Urography in patients presenting to the emergency department with suspected ureteric colic”. They employed a test designated a “non-contrast CT Urogram” and concluded that CT is the preferred test of choice for patients over 40 with suspected ureteric colic. We understand the authors aim, methods and fully agree with the conclusion. However we feel the title and nomenclature are incorrect and potentially misleading to practitioners.
Advanced 3D CT can now offer a number of distinct studies of the urinary tract with specific protocols which are designed around various clinical questions (e.g. Routine CT, Urinary Stone CT, Renal CT Angiography (CTA), Dynamic Renal Mass CT and CT Urography (CTU). Much has been written in the literature regarding CTU[2, 3], and there is more than one way to perform this test. There is however one common theme: in a CT Urogram, contrast material must be administered to demonstrate the urothelium-lined tract.
The CT Urography working group of the European Society of Urogenital Radiologists has recently provided very comprehensive and most welcome guidelines on CT Urography. They define a CTU as “a diagnostic examination optimized for imaging the kidney, ureters and bladder. The examination involves the use of multidetector CT with thin-slice imaging, intravenous administration of a contrast medium and imaging in the excretory phase”. ‘Direct’ CTU is performed by administering contrast through nephrostomy, urostomy or bladder catheter. Urinary stone CT performed for detection of renal, ureteric or bladder stones is a non- contrast study and should not be referred to as “non-contrast CT Urography”, as the authors repeatedly do in their article. Most institutions do not give intravenous contrast routinely to patients for investigation of acute ureteric colic.
CT Urography is reserved for those patients in whom it is important to define the urothelial tract with contrast (e.g. investigation of hematuria, urothelial neoplasms, differentiating parapelvic cysts and assessment of ileal diversion). In summary, CT performed for the evaluation of urolithiasis in the setting of acute renal colic is a renal or urinary stone CT and is not a CT Urogram. Labelling it as a CT Urogram is a patient safety issue under current guidelines. If a contrast-enhanced scan is performed instead of a urinary stone CT it is a reportable event as it involves a misadministration of a drug, radiation exposure for the wrong test and a possible needless IV access. While we welcome this paper, we also feel that nomenclature is important for all readers and hope this clarifies any confusion.
References: 1. Ulahannan D, Blakeley CJ, Jeyadevan N, Hashemi K. Benefits of CT urography in patients presenting to the emergency department with suspected ureteric colic. Emerg Med J, 2008. 25(9): p. 569-71. 2. McNicholas MM, Raptopoulos VD, Schwartz RK, Sheiman RG, Zormpala A, Prassopoulos PK et al., Excretory phase CT urography for opacification of the urinary collecting system. AJR Am J Roentgenol, 1998. 170(5): p. 1261-7. 3. Kawashima A, Vrtiska TJ, LeRoy AJ, Hartman RP, McCollough CH, King BF Jr. CT urography. Radiographics, 2004. 24 Suppl 1: p. S35-54; discussion S55-8. 4. Nolte-Ernsting C, Cowan N. Understanding multislice CT urography techniques: Many roads lead to Rome. Eur Radiol, 2006. 16(12): p. 2670-86. 5. Van Der Molen AJ, Cowan NC, Mueller-Lisse UG, Nolte-Ernsting CC, Takahashi S, Cohan RH. CT urography: definition, indications and techniques. A guideline for clinical practice. Eur Radiol, 2008. 18(1): p. 4-17.
A low GCS does not equate to a compromised airway reflex
Sibbald and colleagues raise the important point that sedation often verges on the edge of general anaesthesia during emergency department sedation in response to Vardy et al’s audit of ED sedation practice(1,2). They do, however, make the false assumption that a GCS of 8 or less is equivalent to the loss of airway reflexes.
Moulton et al(3,4), in two papers describing the relationship between the GCS and gag and cough reflexes in the same institution as Vardy’s study, showed that even in conscious patients with a GCS>8 who had been given narcotics, the gag reflex was suppressed in 64% compared to 8% of similar head injury patients. Even patients who had a GCS of 14 or 15 and were exposed to ‘tranquilisers’ (not defined) had an impaired gag reflex. Airway reflexes should be reassessed independently of the GCS as the GCS alone is unable to indicate a loss of airway reflexes.
The significance of present airway reflexes may be an indication of a reduced risk of aspiration, although even that is not completely assured(3). Duncan et al showed that even in poisoned patients with a decreased GCS, endotracheal intubation was not necessarily required(5).
The definition of coma as a GCS of 8 or less does not include any reference to airway reflexes. The assumption that comatose patients require intubation after head injury is not unreasonable, but this practice has often been uncritically extended to other conditions such as poisoning, in addition to head injured patients. It may be that we should be considering intubation for patients with a GCS of 12 or less, in specific situations such as poisoning, or avoiding it is other specific patient populations with impaired consciousness.
Much more basic research is needed to unravel the complex relationships between GCS, airway reflexes and the subsequent incidence of aspiration and intubation.
Dexter Y S Chan
Colin A Graham
Accident & Emergency Medicine Academic Unit Chinese University of Hong Kong Trauma & Emergency Centre, Prince of Wales Hospital Shatin, New Territories, Hong Kong
1. Sibbald NM, Jackson MJ, Howie A. How deep is your sedation? Emerg Med J 2009;26:389
2. Vardy JM, Dignon N, Mukherjee N, Sami Dm, Balachandran G, Taylor S. Audit of the safety and effectiveness of ketamine for procedural sedation in the emergency department. Emerg Med J 2008;25:579-582
3. Moulton C, Pennycook A, Makover R. Relation between Glasgow coma scale and the gag reflex. BMJ 1991;303:1240-1241
4. Moulton C, Pennycook AG. Relation between Glasgow coma score and cough reflex. Lancet 1994;343(8908):1261-2.
5. Duncan R, Thakore S. Decreased Glasgow coma scale score does not mandate endotracheal intubation in the emergency department. J Emerg Med 2009 Mar 7 [Epub ahead of print].
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