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Recent eLetters

Displaying 1-10 letters out of 216 published

  1. Cost-effective prescribing: Medical schools must take responsibility

    Nwulu and colleagues present a highly relevant analysis of the financial implications of prescribing by F1 doctors in a UK teaching hospital1.

    It seems that the most important of the recommendations they discuss are for undergraduate medical education. Whilst they mention that most of the 79 doctors they investigated graduated from the same medical school, they do not categorise this further. As their data indicate, the large majority of doctors performed to a very similar level to the reference doctor, with a minority on either end of the spectrum proving to be the most cost-effective and lavish prescribers. This raises the possibility that the doctors at the extremes of this range may have been the minority that trained at alternative medical schools.

    As they highlight, further studies are needed across the country, although they may prove to be more of a challenge in trusts that do not have electronic prescribing systems. Future work into this area may benefit from investigating the medical schools at which doctors trained. As these doctors are in their first year after graduating, conclusions may be drawn about the extent to which medical schools are covering the financial aspects of prescribing in their clinical pharmacology curricula. With the increasing importance of cost-effectiveness in the NHS, this important topic should be on the agenda of medical educators across the UK in order to breed a new generation of financially astute prescribers.

    1. Nwulu U, Hodson J, Thomas SK, et al. Variation in cost of newly qualified doctors' prescriptions: a review of data from a hospital electronic prescribing system. Postgrad Med J Published Online First: [30 March 2013] doi:10.1136/postgradmedj- 2012-131334

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  2. Lewy Body Dementia in the Emergency Department

    Sir,

    We applaud the timely study by Kennelly et al and agree fully that ED physicians generally lack proficiency for recognizing and managing behavioral complications of dementia. As they succinctly state, "Failure of physicians to identify and highlight cognitive impairment can lead to disastrous consequences".[1] We venture that ED physicians are even less aware of the unique and potentially lethal emergency management aspects of Lewy Body Dementia (LBD). LBD is a degenerative neurological disease manifested by cognitive impairment, variable Parkinsonism, and marked psychosis exhibiting both auditory and visual hallucinations. LBD is now considered the second most common cause of dementia following only Alzheimer's comprising up to 20-30% of all dementia based on autopsy studies.[2] Differentiating LBD from other dementias can be difficult but the key features are daily fluctuation in cognition and the prominent hallucinations (paradoxically they are not distressful to the patient). DLB strikes its victims from late middle age up and respects no boundaries as to gender or race.[3]

    ED patients with LBD require careful and distinctive pharmacologic management of their agitation and psychotic symptoms. Administering typical neuroleptics will precipitate serious complications ranging from extrapyramidal symptoms to severe sedation to the often lethal neuroleptic malignant syndrome (NMS). Up to 50% percent of individuals with LBD are at an increased risk of these acute reactions to neuroleptics.[2].

    The pathophysiology of this phenomenon is based on the finding that neurons of the basal nucleus of Meynert and substantia nigra are reduced in LBD thus preferentially depleting acetylcholine and dopamine neurotransmitters. The typical antipsychotics, such as haloperidol (Haldol), fluphenazine (Prolixin), and chlorpromazine (Thorazine), block postsynaptic mesolimbic dopaminergic D1 and D2 receptors which can typically be helpful for reducing delirium and hallucinations in most patients with Alzheimer's. The specific neurotransmitter deficits in LBD however prevent up-regulation of D2 receptors in the affected brain centers thus uniquely sensitizing these patients to the EPS adverse effects of antipsychotics.[2] Not only can this exacerbate acute problems but it may worsen cognitive ability of these patients over the long term. LBD experts recommend the use of newer and more selective atypical antipsychotic agents. Importantly, however, case reports show that even these newer agents are not immune to inducing NMS in LBD, so small and carefully titrated doses are advised.[4] Employing non- pharmacologic modalities and the judicious of short acting benzodiazepines is also advised. Because the Emergency Medicine community is largely unaware of these unique hazards, the Lewy Body Dementia Association provides helpful guidelines for ED staff to safely treat these unique patients at http://www.lbda.org.

    1. Kennelly SP, Morley D, Coughlan T, et al. Knowledge, skills and attitudes of doctors towards assessing cognition in older patients in the emergency department. Postgraduate medical journal 2012 doi: 10.1136/postgradmedj-2012-131226.

    2. Baskys A. Lewy body dementia: the litmus test for neuroleptic sensitivity and extrapyramidal symptoms. J Clin Psychiatry 2004;65 Suppl 11:16-22

    3. Latto J, Jan F. Dementia with Lewy Bodies: Clinical Review. British Journal of Medical Practitioners 2008;1(1):10 - 14

    4. Weintraub D, Hurtig HI. Presentation and management of psychosis in Parkinson's disease and dementia with Lewy bodies. Am J Psychiatry 2007;164(10):1491-8

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  3. the current world record for giant left atrium

    The 76 year old patient recently reported in this journal with left atrial diameter of 10 cm(1), has been superseded, in the record books, by a 40 year old man with left atrial diameter of 21.5 cm attributable to severe mitral stenosis(2). The latter patient presented with dysphagia, hoarseness, and exertional dyspnoea. References (1)Shah BN., Rubens M Giant left atrium: a forgotten cause of cardiomegaly Postgrad Med J 2012;88:673-4 (2) Puri A., Vijay SK., Chaudhary G et al A rare cause of cardiomegaly Journal of the American College of Cardiology dx.doi.org/10.1016/j.jacc.2012.04.061

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  4. In response to Dr Levine's letter (13th July 2012)

    We recognise and acknowledge the issues raised by Dr Levine in his letter (13th July 2012). Newly qualified doctors can expect to be as prepared as their undergraduate training allows and their level of clinical supervision facilitates. These are important additional factors when considering preparedness of medical graduates commencing work at foundation year 1 (F1) level. F1 doctors must be able to increase their level of competence in relation to the assessment of critically ill patients, by working in functional teams both during the day and also at night.

    NHS hospitals have traditionally relied on multiple tiers of postgraduate doctors in-training to provide immediate patient care at night, with consultants being non-resident but available on-call from home. This model was and still is the subject of continuing debate. Particular concerns were raised about the impact of working excessive hours on the mental and physical health of newly qualified doctors and the quality of care they provided to patients. The European Working Time Directive (EWTD) acted as a major catalyst for changing the working pattern of these F1 doctors and the Hospital at Night concept was rolled out across a number of NHS trusts in response. This scheme proposes that the way to achieve effective clinical care in the hospital at night is to have one or more multi-professional teams working who, between them, have the full range of skills and competences to meet patients' immediate needs. There is now huge variation across NHS trusts with some hospitals employing no F1 doctors at night. Provided the supervision is appropriate, significant training opportunities exist at night, which are additional to those experienced in the day [1] and we, like Dr Levine, have concerns about this reduction in training opportunities at night for undergraduates and F1 doctors. Over 90% of F1 doctors (n = 1,084) recently surveyed reported that night shifts improved their prioritisation, decision making and planning [1]. In conclusion, when considering preparedness of medical students for medical practice we must consider the environment in which they are asked to work, as well as the training they have received.

    [1] London Deanery Foundation Conference 2012 - submitted for publication. http://www.londondeanery.ac.uk/foundation- schools/conferences/2012-foundation-programme-conference

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  5. Unpreparedness

    Newly qualified doctors can expect to be as prepared as their undergraduate training allows. For the initial management of acutely ill patients, perhaps involving practical procedures, we have to ensure that training and assessment of both students and doctors occur, as far as possible, under similar conditions to those in which doctors will work. 4 days of shadowing help but are not enough. The reality for many newly qualified doctors may be dealing with very sick patients at night in unfamiliar surroundings, in poor light and without much immediate assistance from even nurses, let alone more experienced doctors. Many new doctors report that they are at their most anxious and feel least prepared under these conditions. It would be interesting to review how much acute work medical students are now made to experience at night. I suspect that the results of such a survey might make uncomfortable reading.

    Few formative or summative assessments are carried out at these times by colleagues who are properly trained both in assessment and discussion of the factors that can impair performance (as opposed to competence under controlled conditions). Feedback capable of boosting confidence or generating insight into unhelpful behaviour is best carried out as soon as possible after the event; criticism the next day often misses the point. Effective decision-making, particularly for novices, involves clinical reasoning techniques that are not on the curricula of enough medical schools. Being able to talk through these thought processes at the time is invaluable for both senior and junior doctors but is too often denied to the latter by circumstances. Tackling this sort of unpreparedness certainly benefits from simulation, particularly in teams, but, where real life conditions can be so chaotic and unsupported by anything resembling a team, we may have to do much more to improve the working conditions themselves. Assessing ill patients is difficult enough for experienced doctors who are supported by other staff and not being constantly interrupted by pagers. It should cause no surprise that performance and perception of acute work by very junior doctors is inadequate when working without such benefits. Competence and performance can be very different things.

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  6. "Xanthelasma palpebrarum -a cutaneous sign of increased cardiovascular risk"-still a misunderstanding

    Xanthelasma palpebrarum ia a sharply demarcated yellowish flat plaque om the upper and lower eyelid, mostly near the inner canthus.In a prospective study done in Copenhagen University revealed that xanthelasme palpebrarum predict risk of myocardial infarction, ischaemic heart disease, severe atherosclerosis, and death in the general population[1].In present study which is a cross-sectional study revealed that xanthelasma is associated with increased proatherogenic markers thus there may be increased risk.Another study revealed that in patients with xanthelasma, no increase was observed in the rate or risk of cardiovascular disease, Moreover, no relationship was found between Lp (a) levels and xanthelasma though hyperlipidemia is common in patients with xanthelasma[2]. so, i want to highlight few points.As xanthelasma is quite common in asian individuals we need a nation wide, age and sex match, cohort study to strenghthen the hypothesis.Another point is that we should go for an randomised controlled trial evaluating the role of statin in patients with xanthelasme palpebrarum without any other cardiovascular and cerebrovascular risk factors in reducing the risk of death due to cardiovascular and cerebrovascular causes compared to placebo.Thus we can strengthen our present view in support. References: 1. . Mette Christoffersen, Ruth Frikke-Schmidt, Peter Schnohr, Gorm B Jensen, B?rge G Nordestgaard, Anne Tybj?rg-Hansen. BMJ 2011; 343 doi: 10.1136/bmj.d5497.

    2. Ozd?l S, Sahin S, Tokg?zo?lu L. Xanthelasma palpebrarum and its relation to atherosclerotic risk factors and lipoprotein (a). Int J Dermatol. 2008 Aug;47(8):785-9.

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  7. Natriuretic peptide levels must be interpreted in the light of clinical probability of heart failure

    Given the recognition that "choosing appropriate thresholds[for serum natriuretic peptide] is problematic"(1), the best diagnostic strategy for obtaining maximum diagnostic "mileage" from natriuretic peptide levels might be that of interpreting any given result in the light of whether the patient has high, medium, or low clinical probability of heart failure. For that to come about, instead of reinforcing the idea that "Individual symptoms...and signs...are generally weak predictors of heart failure"(2), we should embrace the use of a scoring system such as the one recently compiled in the Netherlands which recognises the diagnostic value of physical examination by allocating points to individual clinical stigmata(3). We must also recognise that, as is the case with biomarkers(such as natriuretic peptides), even echocardiography is hedged in by caveats, not only in systolic heart failure(4), but also in diastolic heart failure(5). In the former context the redeeming feature is that, notwithstanding the fact that a subnormal left ventricular ejection fraction(LVEF) does not equate with clinically overt heart failure(6), in its own right, however, a subnormal LVEF does justify the use of modulators of the renin-angiotensin-aldosterone system(RAAS) such as angiotensin converting enzyme inhibitors(ACE-inhibitors) even if only to exert a favourable influence on the natural history of both subclinical and clinically overt heart failure(6). This means that, even if clinical symptoms and signs are not those of heart failure, ACE_inhibitors would still be justified in the event of a subnormal LVEF. A similar parallel does not exist for left ventricular diastolic dysfunction(when it does not co-exist with left ventricular systolic dysfunction) because there is no evidence base for justifying modulation of the RAAS through the use either of ACE inhibitors or spironolactone(or both) regardless of whether or not left ventricular diastolic dysfunction co-exists with symptoms attributable to heart failure. Accordingly, for patients with intact LVEF in whom echocardiographically validated left ventricular diastolic dysfunction coexists with "problematic" natriuretic peptide blood levels the central issue is whether or not associated clinical signs and symptoms signify clinical congestion and, hence heart failure, whether it be acute or chronic. Evidence-based parameters which have been utilised as criteria for clinical congestion include symptoms such as effort dyspnoea and orthopnoea, signs such as peripheral oedema, resting hugular venous distension, and the presence of a third heart sound, and radiographic stigmata such as cardiomegaly, pulmonary vascular redistribution, interstitial oeadema, and pleural effusion. All these have been evaluated for positive predictive value as well as for negative predictive value(7). We now need to optimise the accuracy of non-echocardiographic stigmata(3)(7) so as to respond constructively to the criticism levelled by a distinguished American physician at the "downplaying" of clinical evelaution in the NICE guidelines, when he said "Clinical evaluation is central to all complex clinical syndromes"(8), References (1)Al-Muhammad A., Mant J Republished technology and guidelines: The diagnosis and management of chronic heart failure: review following the publication of the NICE guidelines Postgrad Med J 2011;87:841-6 (2) Hobbs FDR., Doust J., Mant J., Cowie MR Diagnosis of heart failure in primary care Heart 2010;96:1773-7 (3) Kelder JC., Cramer MJ., van Wijngaarden J et al The diagnostic value of physical examination and additional testing in primary care patients with suspected heart failure Circulation 2011;124:2865-73 (4) Jolobe OMP Usefulness of left ventricular ejection fraction in patients with overt heart failure(letter) Mayo Clinic Proceedings 2006;81:1636-9 (5)Paulus WJ., Tschope C., Sanderson JE et al How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure with normal left ventricular ejection fraction by the Haert Failure and Echocardiography Association of the European Society of Cardiology Eur Heart J 2007;28:1539-50 (6)The SOLVD Investigators Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions N Engl J Med 1992;327:685-91 (7)Gheorghiade M., Follath F., Ponikowski P et al Assessing and grading congestion in acute heart failure: A scientific statement from the Acute Heart Failure Committee of the Heart Failure Association of the European Society of Cardiology and endorsed by the European Society of Intensive Care Medicine European Journal of Heart Failuer 2010;12;423-33 (8) Finucane TE NICE Guideline for Management of Chronic Heart Failure in Adults(letter) Annals of Inernal Medicine 2012;156:69

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  8. Perception

    I can well remember my feelings of unpreparedness in both the areas that current graduates identify as feeling most unready for.

    However, I suspect that having this perception is not a bad thing. I hope that they are able to maintain such a degree of insight and use it to the advantage of their patients and themselves in the long term.

    Should I be asked, I would encourage them to think on it in terms of having identified areas for development and to plan their continuing education accordingly.

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  9. Hazards inherent in the use of either nonsteroidals or paracetamol

    Notwithstanding the absence of robust evidence to justify the use of antipyretic analgesics either for reducing patient discomfort or for reducing morbidity and mortality in febrile illnesses(1), it is only in recent times(2)(3) that the issue of drug-related mortality has been adressed in patients receiving either nonsteroidal anti-inflammatory drugs(NSAIDs) or paracetamol for febrile illnesses. Due to insensible losses via the skin and also via the respiratory tract, patients with pneumonia seem to be uniquely predisposed to NSAID-related nephrotoxicity, as was the case in a five year old girl who received recommended doses of ibuprofen(presumably for its antipyretic action) over a period of 4 days before she developed acute renal failure, characterised by peak serum creatinine 171 mcmol/l, and peak serum urea 23 mmol/l. Following the discontinuation of ibuprofen these parameters took 3 days to revert to the normal range(4). Both hepatitis and non-oliguric renal failure were the cardinal complications of the administration of paracetamol, followed by ibuprofen, in a 5 year old girl with febrile convulsions and vomiting. The former was prescribed as 11 mg/kg/dose, two total doses, over 5 hours. This was followed by ibuprofen 5 mg/kg/dose every 8 hours, three total doses. Both drugs were administered by mouth. Although her renal function tests and liver function tests had been within the normal range on admisssion, on day six aspartate transaminase and gammaglutamyl transaminase had increased to 144 iu/l, and 1394 iu/l, respectively. Correspondigly, serum urea and serum creatinine had increased to 67.9 mg/dl and 6.34 mg/dl, respectively. By day 60 all the abnormal parameters had reverted to the normal range(5). In the non febrile context, recommended doses of paracetamol administerd to adult patients over a period of 4-5 days, have been documented as being the cause of acute liver failure(6). Accordingly, especially in the context of febrile illnesses where insensible loss of fluid via the skin is compouded by fluid loss via the respiratory tract(as in pneumonia)(4) or compouded by fluid loss via the gastrointestinal tract as in the second case(5), there should be a high index of suspicion for subsequent development of renal failure. Where paracetamol is administered to patients with poor nutritional status, clinicians should be alert to the risk of drug-related hepatotoxicity(6) References (1) Greisman L., Mackowiak PA Fever: beneficial and detrimental effects of antipyretics Current Opinion in Infectious Diseases 2002;15:241-5 (2) Plaisance Toxicities of drugs used in the management of fever Clinical Infectious Diseases 2000;31(Suppl 5): S219-23 (3)Jefferies S., Weatherall M., Young P., Eyers S., Beasley R Ssystematic review and meta analysis of the effects of antipyretic medications on mortality in Streptococcus Pneumoniae infections Postgraduate Medical Journal 2012;88:21-27 (4)Ulinski T., Guigonis V., Dunan O., Bensman A Acute renal failure after treatment with nonsteroidal antiinflammatory drugs Eur J Pediatr 2004;163:148-150 (5) Zaffanello M., Brugnara M., Angeli S., Cuzzolin L Acute non-oliguric kidney failure and cholestatic hepatitis induced by ibuprofen and acetoaminophen: a case report Acta Paediatrica 2009;96:901-9 (6)Claridge LC., Eksteen B., Smith A., Shah T., Holt AP Acute liver failure after administration of paracetamol at the maximum recommended daily dose in adults BMJ 2010;341:1269-1271

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  10. is it showing the exact picture of igA nephropathy?

    I want to highlight few points about the study.First, IgA nephropathy is seen in nearly 40% of renal biopsy specimens of acute glomerulonephritis patients in asia in various study.In this study it is comprising only 8.1% of cases.Second, it is an crossectional study, taking data from the renal biopsy report thus not showing the exact % of acute glomerulonephritis caused by IgA nephropathy.So the finding is quite exaggerated, though 10% of IgA nephropathy patient develop ESRD after 10 year & 20% after 20 years.

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