RAPID RESPONSES

Rapid Responses are electronic letters to the editor. They enable our users to debate issues raised in articles published on bmj.com. Although a selection of rapid responses will be included as edited readers' letters in the weekly print issue of the BMJ, their first appearance online means that they are published articles.

To RESPOND to a particular article: Click on the link 'Respond to this article' in the box at the top left hand corner of the article.

To READ responses to a particular article: Click on the link 'Read responses to this article' in the box at the top left hand corner of the article.

All responses published in the past 14 days are shown below. You can also read responses published in the past 2, 3, 4, 5, 6, 7, 14, or 21 days.


Rapid Responses published in the past 14 days:

158 Rapid Responses published for 91 different articles.

Articles    Rapid Responses
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EDITORIALS:
Improving patient safety through training in non-technical skills
Flin and Patey (23 September 2009) [Full text]
Jump to Rapid Response Life-long learning in non-technical skills
Richard FitzGerald   (15 November 2009)
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RESEARCH:
Selective serotonin reuptake inhibitors in pregnancy and congenital malformations: population based cohort study
Pedersen et al. (23 September 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Authors' reply
Lars H Pedersen, et al.   (12 November 2009)
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CLINICAL REVIEW:
Surgery for obesity in adulthood
Leff and Heath (22 September 2009) [Full text]
Jump to Rapid Response Acknowledgement
Dugal Heath   (12 November 2009)
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RESEARCH:
Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of 19 000 men in the Whitehall study
Clarke et al. (16 September 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Re: Life expectancy in relation to cardiovascular risk factors
L Sam Lewis   (12 November 2009)
Jump to Rapid Response Life expectancy in relation to cardiovascular risk factors
Robert J Clarke, et al.   (11 November 2009)
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NEWS:
Doctors’ view of care pathway for dying patients clashes with audit findings
Kmietowicz (16 September 2009) [Full text]
Jump to Rapid Response End of Life Care Using the Liverpool Care Pathway
Hilary Speller   (23 November 2009)
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OBSERVATIONS:
No power for the people
Heath (14 September 2009) [Full text]
Jump to Rapid Response No Triumph for 'the people' still
susanne stevens mccabe   (23 November 2009)
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VIEWS & REVIEWS:
Should I have an H1N1 flu vaccination after Guillain-Barré syndrome?
Price (9 September 2009) [Full text]
Jump to Rapid Response A good example of why those with an interest should publish
Peter M English   (13 November 2009)
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CLINICAL REVIEW:
Autoimmune liver disease for the non-specialist
Decock et al. (8 September 2009) [Full text]
Jump to Rapid Response Autoimmune hepatitis after long-termmethotrexate administration for rheumatoid arthritis
Ricardo Moreno-Otero, MD, et al.   (16 November 2009)
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PRACTICE:
Digoxin specific antibody fragments (Digibind) in digoxin toxicity
Ip et al. (3 September 2009) [Full text]
Jump to Rapid Response Authors' comments
Dorothy Ip, et al.   (17 November 2009)
Jump to Rapid Response 'Treatment of hyperkalemia & digoxin toxicity'
Faisal Khan, et al.   (12 November 2009)
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PRACTICE:
Tennis elbow
Mallen et al. (2 September 2009) [Full text]
Jump to Rapid Response decorator's elbow
Geraldine R lindley   (23 November 2009)
Jump to Rapid Response Family practice & specialism - the difference
peter mahaffey   (23 November 2009)
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CLINICAL REVIEW:
Pain management and sedation for children in the emergency department
Atkinson et al. (30 October 2009) [Full text]
Jump to Rapid Response Sedating unfasted children may be dangerous
david c crawford, et al.   (19 November 2009)
Jump to Rapid Response paediatric analgesia & sedation could be better
aruni sen   (15 November 2009)
Jump to Rapid Response Miscellaneous points intended to help
Steven Ford   (15 November 2009)
Jump to Rapid Response Intranasal Midazolam for sedation in emergency department
Angela De Cunto, et al.   (12 November 2009)
Jump to Rapid Response Its not always good to reassure
Liam G Mahoney   (10 November 2009)
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RESEARCH:
Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised trial
Stiell et al. (29 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response The existence of a previously published validated study along with restricted supervision are two confounding factors in the impact of the of Canadian C-spine rule
Vafa Rahimi-Movaghar, et al.   (15 November 2009)
Jump to Rapid Response Published validated study and restricted supervision are two confounding factors in implementation of C-spine rule
Vafa Rahimi-Movaghar, et al.   (12 November 2009)
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EDITOR'S CHOICE:
Gagging for it
Delamothe (29 October 2009) [Full text]
Jump to Rapid Response Response to Tony Delamothe's Article 'Gagging for it'
Helen Gavin   (17 November 2009)
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NEWS:
Twenty four risk factors responsible for nearly half of annual deaths, says WHO
Zarocostas (28 October 2009) [Full text]
Jump to Rapid Response Remembering Mental Illnesses
Madhavan Seshadri, et al.   (12 November 2009)
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ANALYSIS:
Lessons from the past decade for future health reforms
Ham (28 October 2009) [Full text]
Jump to Rapid Response Is there any altruistic political leader who will take us to the 21st. century?
Layla Jader   (19 November 2009)
Jump to Rapid Response Breaking the cycle
Stephen F Hayes, et al.   (17 November 2009)
Jump to Rapid Response Groundhog Day
Christopher L Manning   (17 November 2009)
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OBSERVATIONS:
The chilling effect of English libel law
Hurley (28 October 2009) [Full text]
Jump to Rapid Response Video now online
Richard Hurley   (12 November 2009)
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OBSERVATIONS:
The perversion of choice
Heath (27 October 2009) [Full text]
Jump to Rapid Response Why should choice drive inequality?
stephen black   (10 November 2009)
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SHORT CUTS:
All you need to read in the other general journals
(27 October 2009) [Full text]
Jump to Rapid Response Spironolactone is underused in people with heart failure.
Manish Ramlall, et al.   (12 November 2009)
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RESEARCH:
Differences in atherosclerosis according to area level socioeconomic deprivation: cross sectional, population based study
Deans et al. (27 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Atherosclerosis cannot be understood without knowledge of blood viscosity.
Les.O Simpson   (23 November 2009)
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FEATURE:
The price of silence
Gornall (27 October 2009) [Full text]
Jump to Rapid Response Re. ‘The price of silence’ (Vol.339 31 October)
Helen Gavin   (23 November 2009)
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EDITORIALS:
Migraine with aura and increased risk of ischaemic stroke
Loder (27 October 2009) [Full text]
Jump to Rapid Response Progesterone or progestogen or progestin; which is it?
M Joy Spark   (19 November 2009)
Jump to Rapid Response Author's reply
Elizabeth Loder   (15 November 2009)
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FEATURE:
Falling foul of gagging clauses
Cassidy (27 October 2009) [Full text]
Jump to Rapid Response Clarification of a clarification
Gerald Shaw   (16 November 2009)
Jump to Rapid Response Clarification on article: 'Falling Foul of Gagging Clauses'
Prof. Peter Rubin, et al.   (13 November 2009)
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PRACTICE:
Depression in adults, including those with a chronic physical health problem: summary of NICE guidance
Pilling et al. (27 October 2009) [Full text]
Jump to Rapid Response Depression: its pathophysiology and treatment.
Les.O Simpson   (20 November 2009)
Jump to Rapid Response Medical illnessess and depression.
Gnanie Panch   (20 November 2009)
Jump to Rapid Response Updates on treatment for depression: NICE in theory not always in practice.
June S. L. Brown, et al.   (12 November 2009)
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CLINICAL REVIEW:
Hyperkalaemia
Nyirenda et al. (23 October 2009) [Full text]
Jump to Rapid Response Re: Salbutamol unsafe in hyperkalaemia
Moffat J Nyirenda, et al.   (23 November 2009)
Jump to Rapid Response Salbutamol unsafe in hyperkalaemia
Simon B Dimmitt, et al.   (19 November 2009)
Jump to Rapid Response Damage to the juxta glomerular apparatus and impairment of aldosterone release.
Richard G Fiddian-Green   (11 November 2009)
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RESEARCH:
Mortality in renal transplant recipients given erythropoietins to increase haemoglobin concentration: cohort study
Heinze et al. (23 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response ESAs in Chronic Kidney Disease
Timothy J Littlewood   (12 November 2009)
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EDITORIALS:
Use of erythropoietins in patients with renal transplants
Treleaven and Clase (23 October 2009) [Full text]
Jump to Rapid Response ‘Normalisation of haemoglobin is hazardous, ineffective and costly.’
Eric J Will   (23 November 2009)
Jump to Rapid Response Anemia and kidney function are related
Jan Gossmann   (18 November 2009)
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RESEARCH:
The PRaCTICaL study of nurse led, intensive care follow-up programmes for improving long term outcomes from critical illness: a pragmatic randomised controlled trial
Cuthbertson et al. (16 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Cognitive Function assessment might improve the quality of life in intensive care survivors
David John Bowen Thomas   (19 November 2009)
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OBSERVATIONS:
The unpalatable truth about ethics committees
Sokol (14 October 2009) [Full text]
Jump to Rapid Response The need for evidence based ethics
Simon Hatcher   (10 November 2009)
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RESEARCH:
Rate of undesirable events at beginning of academic year: retrospective cohort study
Haller et al. (13 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Doctors’ transitions: critically intensive learning periods
Sue Kilminster, et al.   (11 November 2009)
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RESEARCH:
Effect of a multimodal high intensity exercise intervention in cancer patients undergoing chemotherapy: randomised controlled trial
Adamsen et al. (20 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Why extended follow-up periods are important in non-pharmacological RCT's
Niels Henrik Hjollund, et al.   (11 November 2009)
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LETTERS:
Paper or patient safety?
Sandler et al. (12 October 2009) [Full text]
Jump to Rapid Response Effective audit improves patient safety
Elizabeth A. Edwards, et al.   (11 November 2009)
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PRACTICE:
Chest radiographs in pregnancy
O’Connor et al. (9 October 2009) [Full text]
Jump to Rapid Response Chest Radiographs in Pregnancy - why not?
B D McCann, et al.   (17 November 2009)
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OBSERVATIONS:
Live and let die
McLean (7 October 2009) [Full text]
Jump to Rapid Response Clear Guidance on Capacity Assessment is Urgently Required
Joseph El-Khoury, et al.   (10 November 2009)
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RESEARCH METHODS & REPORTING:
The tyranny of power: is there a better way to calculate sample size?
Bland (6 October 2009) [Full text]
Jump to Rapid Response A different test ?
Peter H FITTON   (20 November 2009)
Jump to Rapid Response Unintended consequences of a boot-strap exercise?
Tony H. Reinhardt-Rutland   (18 November 2009)
Jump to Rapid Response Stopping power calculation? Yes, but not at any price.
Pierre Charles, et al.   (14 November 2009)
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RESEARCH:
Partial protection of seasonal trivalent inactivated vaccine against novel pandemic influenza A/H1N1 2009: case-control study in Mexico City
Garcia-Garcia et al. (6 October 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Authors’ response to Skowronski and colleagues
Jose Luis Valdespino-Gómez, et al.   (10 November 2009)
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EDITOR'S CHOICE:
The power of stories
Groves (20 November 2009) [Full text]
Jump to Rapid Response If thought corrupts language, language can also corrupt thought.
BM Hegde   (20 November 2009)
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NEWS:
Poor care in hospital is delaying discharge of patients with dementia, charity says
Kmietowicz (18 November 2009) [Full text]
Jump to Rapid Response Sound findings but confusing statistics
David E Stewart   (20 November 2009)
Jump to Rapid Response Caring for patients with Dementia
Reza Aghamohammadzadeh   (19 November 2009)
Jump to Rapid Response Poor care of patients with dementia: Root Causes
Bamidele Omotosho   (19 November 2009)
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EDITORIALS:
Is primary care research a lost cause?
Mar (18 November 2009) [Full text]
Jump to Rapid Response Neglected virgin areas in primary health care basic and applied research.
Rodolfo J. Stusser   (20 November 2009)
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NEWS:
Hospitals are criticised for yielding to pressure over human rights lecture
Dyer (17 November 2009) [Full text]
Jump to Rapid Response Pressures on UK medical institutions regarding coverage of Israel-Palestine
derek a summerfield   (20 November 2009)
Jump to Rapid Response Silencing debate is unhealthy
Nadeem Z Jilani   (19 November 2009)
Jump to Rapid Response Hospitals are criticised for yielding to pressure over human rights lecture
Judith Emanuel   (19 November 2009)
Jump to Rapid Response Paranoia about the truth
Christopher J Burns-Cox, et al.   (19 November 2009)
Jump to Rapid Response Correction
Clare Dyer   (18 November 2009)
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NEWS:
Patents on breast cancer genes are illegal and stymie research, say scientists
Lenzer (17 November 2009) [Full text]
Jump to Rapid Response Claims and uses are the real problem, not patenting
Robert M Cook-Deegan   (20 November 2009)
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VIEWS & REVIEWS:
Politics, science, and the White House
Smith (17 November 2009) [Full text]
Jump to Rapid Response Harold Varmus and The Art of Politics and Science
Felix ID Konotey-Ahulu   (20 November 2009)
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NEWS:
Poor service provision is blamed for overuse of antipsychotics in dementia patients
Mashta (17 November 2009) [Full text]
Jump to Rapid Response Antipsychotic treatment for dementia may now constitute 'serious medical treatment' under the Mental Capacity Act 2005
Tim Branton, et al.   (18 November 2009)
Jump to Rapid Response Beware of antipsychotics in the elderly
Hugh Mann   (18 November 2009)
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NEWS:
Australia operates "closed shop" to restrict doctors from overseas, say critics
Sweet (16 November 2009) [Full text]
Jump to Rapid Response Great Barriers
William McGuire   (19 November 2009)
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RESEARCH:
Concept of unbearable suffering in context of ungranted requests for euthanasia: qualitative interviews with patients and physicians
Pasman et al. (16 November 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response The difficulties of subjective suffering
Emma Phillips   (19 November 2009)
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NEWS:
WHO recommends early antiviral treatment for at risk groups with suspected swine flu
Zarocostas (13 November 2009) [Full text]
Jump to Rapid Response Does early antiviral treatment give a false sense of protection
Dr Irugal bandara Dissanayake   (15 November 2009)
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VIEWS & REVIEWS:
Dr Doom
Spence (12 November 2009) [Full text]
Jump to Rapid Response Re: Re: Re: Re: Re: This will hurt...
Des Spence   (19 November 2009)
Jump to Rapid Response Re: Re: Re: Re: This will hurt...
L Sam Lewis   (18 November 2009)
Jump to Rapid Response Re: Re: Re: This will hurt...
Des Spence   (17 November 2009)
Jump to Rapid Response Re: Re: This will hurt...
L Sam Lewis   (17 November 2009)
Jump to Rapid Response Re: This will hurt...
Des Spence   (16 November 2009)
Jump to Rapid Response This will hurt...
L Sam Lewis   (15 November 2009)
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VIEWS & REVIEWS:
Joking about cerebral palsy
Drife (12 November 2009) [Full text]
Jump to Rapid Response Passionate about CP
David JR Hutchon   (15 November 2009)
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VIEWS & REVIEWS:
Learning to teach
Jackson (12 November 2009) [Full text]
Jump to Rapid Response Practical Teaching Tips
Avtar Singh   (20 November 2009)
Jump to Rapid Response Being an effective clinical teacher
Asif M Bachlani   (15 November 2009)
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PRACTICE:
Investigating recurrent respiratory infections in primary care
Wood and Peckham (12 November 2009) [Full text]
Jump to Rapid Response HIV is a very relevant cause of recurrent respiratory bacterial infection and should be excluded
Paul Collini, et al.   (18 November 2009)
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OBITUARIES:
Jeremy Morris
Richmond (11 November 2009) [Full text]
Jump to Rapid Response Jeremy Morris
Michael D Warren   (19 November 2009)
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ENDGAMES:
Matching
Sedgwick (11 November 2009) [Full text]
Jump to Rapid Response Bias
L Sam Lewis   (15 November 2009)
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RESEARCH:
Evaluation of modernisation of adult critical care services in England: time series and cost effectiveness analysis
Hutchings et al. (11 November 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Improved results but why?
Christian P Subbe   (16 November 2009)
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EDITORIALS:
Clashes between the government and its expert advisers
Gossop and Hall (11 November 2009) [Full text]
Jump to Rapid Response Clashes between the government and its expert advisers
Makarand K Oak   (17 November 2009)
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PRACTICE:
Self diagnosis
Goyder et al. (11 November 2009) [Full text]
Jump to Rapid Response Prescriptions for worriers
Richard Bartley   (19 November 2009)
Jump to Rapid Response Self Diagnosis is a Noun not a Verb
Stephen H Raymond   (19 November 2009)
Jump to Rapid Response Jerome K Jerome syndrome
Michael Power   (19 November 2009)
Jump to Rapid Response Triggering diagnostic hypotheses........I don't think so
Brid Farrell   (14 November 2009)
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RESEARCH:
Income inequality, mortality, and self rated health: meta-analysis of multilevel studies
Kondo et al. (10 November 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Erratum
Naoki Kondo   (12 November 2009)
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RESEARCH:
Slow walking speed and cardiovascular death in well functioning older adults: prospective cohort study
Dumurgier et al. (10 November 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Good study; few questions
DR.Indranil Banerjee, et al.   (20 November 2009)
Jump to Rapid Response To walk, or to run: that is the question
Matteo Cesari, et al.   (14 November 2009)
Jump to Rapid Response m/s is equivalent to m·s−1
Michael Williams   (13 November 2009)
Jump to Rapid Response Clarifications regarding speed of walking units
Ralph Earle Jr   (12 November 2009)
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EDITORIALS:
Slow walking speed in elderly people
Harwood and Conroy (10 November 2009) [Full text]
Jump to Rapid Response Sprint your way to immortality
Michael O'Donnell   (20 November 2009)
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NEWS:
Battle against hospital acquired infections has been too limited, MPs’ report says
Mayor (11 November 2009) [Full text]
Jump to Rapid Response Infection Control - what is the point?
Jenna L Morgan, et al.   (20 November 2009)
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LETTERS:
Solutions to the August problem
Tate (10 November 2009) [Full text]
Jump to Rapid Response September, not August, for new staff - time for action?
Richard C Worth   (18 November 2009)
Jump to Rapid Response Sweeping statements?
Andrew Owens, et al.   (17 November 2009)
Jump to Rapid Response Echoes of the past
Karen E Groves   (12 November 2009)
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LETTERS:
Looking to rebuild Iraq’s healthcare system
Rawaf et al. (10 November 2009) [Full text]
Jump to Rapid Response Rebuilding or Building
Phil Geis   (15 November 2009)
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LETTERS:
Propofol is safely and widely used in emergency departments
Sen (10 November 2009) [Full text]
Jump to Rapid Response Propofol data sheet requires it is only given by anaesthetists or intensivists
Bernard J Norman   (16 November 2009)
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ANALYSIS:
Is haemoglobin A1c a step forward for diagnosing diabetes?
Kilpatrick et al. (10 November 2009) [Full text]
Jump to Rapid Response Totally agree
Abdelwahab Y babiker   (19 November 2009)
Jump to Rapid Response Haemoglobin A1c: a false step cystic fibrosis-related diabetes
Federico Marchetti, et al.   (16 November 2009)
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NEWS:
Activists call for public health to take central role in UN climate change talks
Jara (9 November 2009) [Full text]
Jump to Rapid Response A call to action on climate change
Jienchi Dorward, et al.   (19 November 2009)
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NEWS:
Reassure pregnant women over swine flu vaccine, health officials urge
Wise (9 November 2009) [Full text]
Jump to Rapid Response Practicing Medicine Under False Pretenses ?
Dr. Herbert Nehrlich   (10 November 2009)
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NEWS:
GMC clears research dean of dishonesty
Dyer (9 November 2009) [Full text]
Jump to Rapid Response An evolving understanding?
A Clark   (11 November 2009)
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RESEARCH:
Aspirin for primary prevention of cardiovascular events in people with diabetes: meta-analysis of randomised controlled trials
De Berardis et al. (6 November 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Re: Aspirin. A long life with always a new fashion
Les O. Simpson   (20 November 2009)
Jump to Rapid Response Aspirin. A long life with always a new fashion
Roberto G Carbone MD, FCCP, et al.   (19 November 2009)
Jump to Rapid Response Diabetes, blood viscosity and aspirin.
Les O. Simpson   (16 November 2009)
Jump to Rapid Response Aspirin to prevent cardiovascular disease in diabetes: time to rethink?
Soon H Song, et al.   (15 November 2009)
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FEATURE:
Dangers of listening to the fetal heart at home
Chakladar and Adams (5 November 2009) [Full text]
Jump to Rapid Response The dangers of home fetal heart monitoring: a personal perspective
Amy L Blake   (17 November 2009)
Jump to Rapid Response Dangers of listening to the fetal heart at home, that may be surmountable, should be weighed against the benefits
John A Crowe   (11 November 2009)
Jump to Rapid Response Re: A double tragedy - Inappropriate action after maternal perception of reduced fetal movements
Abhijoy Chakladar, et al.   (10 November 2009)
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EDITOR'S CHOICE:
Crunch time for doctors’ hours
Godlee (5 November 2009) [Full text]
Jump to Rapid Response Optimise surgical trainees' working time with Wikisurgery scripts
Michael Edwards   (12 November 2009)
Jump to Rapid Response Questionable Surgery Hours Calculation
Felix E May   (11 November 2009)
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EDITORIALS:
Working time regulations for trainee doctors
Pounder (5 November 2009) [Full text]
Jump to Rapid Response Surgeon training and physician assistants
Margaret E Allen   (10 November 2009)
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ANALYSIS:
How long does it take to train a surgeon?
Purcell Jackson and Tarpley (5 November 2009) [Full text]
Jump to Rapid Response Work on motivation, do not complain about hours!
Thomas Krasemann   (18 November 2009)
Jump to Rapid Response Learning to cut through a new swiss cheese
Rhys Jones   (17 November 2009)
Jump to Rapid Response Academic Surgery: It’s all about competency, flexibility, and being an adult learner
Alexander H Mirnezami, et al.   (17 November 2009)
Jump to Rapid Response Surgical training: Optimising operative work time with on-line scripts
Michael H Edwards, et al.   (17 November 2009)
Jump to Rapid Response Working hours directives changing working patterns from team based to shift based medicine
AJ Hay   (16 November 2009)
Jump to Rapid Response Kudos to Surgeons
Hugh Mann   (15 November 2009)
Jump to Rapid Response It depends what you want
benjamin dean   (15 November 2009)
Jump to Rapid Response How long does it take to train a surgeon? Less time then you think.
Christopher A Efthymiou, et al.   (14 November 2009)
Jump to Rapid Response Residency education
Thein H Oo   (13 November 2009)
Jump to Rapid Response Improving surgical training
Simon Paterson-Brown   (13 November 2009)
Jump to Rapid Response Number of hours required to maintain skills
Kirsten Duckitt   (12 November 2009)
Jump to Rapid Response The 10,000 hour rule and surgical training.
Donald MacDonald, et al.   (12 November 2009)
Jump to Rapid Response Doubling of training time
Kenneth YL Hon   (11 November 2009)
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VIEWS & REVIEWS:
The highs and lows of policy based evidence
Colquhoun (4 November 2009) [Full text]
Jump to Rapid Response Independent?
John Stone   (23 November 2009)
Jump to Rapid Response Our best chance ever!
Steven Ford   (15 November 2009)
Jump to Rapid Response Seeing the light
L Sam Lewis   (13 November 2009)
Jump to Rapid Response Re: A crisis of mistrust
John Stone   (12 November 2009)
Jump to Rapid Response Truth itself is the ultimate victim
stephen black   (12 November 2009)
Jump to Rapid Response A crisis of mistrust
Mark Struthers   (10 November 2009)
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NEWS:
Scientists want more protection after government adviser is sacked
Dyer (4 November 2009) [Full text]
Jump to Rapid Response Naive not to expect a backlash
Carl Curtis   (13 November 2009)
Jump to Rapid Response Does rejecting a particular scientific opinion mean a rejection of Science?
Felix ID Konotey-Ahulu   (10 November 2009)
Jump to Rapid Response Nutts to Alan Johnson
Jason Luty   (10 November 2009)
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FEATURE:
Reducing the burden of malnutrition in Bangladesh
Ahmed and Ahmed (4 November 2009) [Full text]
Jump to Rapid Response Simple strategy to reduce malnutrition in India through already existing special immunization campaigns
Nivedita Gupta, et al.   (11 November 2009)
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FEATURE:
Commercial solutions to malnutrition
Bland (4 November 2009) [Full text]
Jump to Rapid Response Breastfeeding in Bangladesh: national asset, national neglect
Khurshid Talukder, et al.   (12 November 2009)
Jump to Rapid Response Sprinkling the landscape for years to come?
Gabriele Pollara   (10 November 2009)
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PRACTICE:
Chest pain
Jelinek and Barraclough (3 November 2009) [Full text]
Jump to Rapid Response Stress Echo vs.Stress Electrocardiogram
Robert Matz   (10 November 2009)
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PRACTICE:
Using probabilistic reasoning
Doust (3 November 2009) [Full text]
Jump to Rapid Response Probabilistic reasoning in diagnosis
Huw Llewelyn   (10 November 2009)
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NEWS:
Glasgow hospital wins design award
Christie (3 November 2009) [Full text]
Jump to Rapid Response All fine architectural values are human values, else not valuable. (Frank Lloyd Wright)
Hugh Mann   (13 November 2009)
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NEWS:
English treatment centres are treating less complex patients than hospitals
Dobson (2 November 2009) [Full text]
Jump to Rapid Response ISTCs cherry pick easier cases, obviously enough
Stephen Hayes   (10 November 2009)
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LETTERS:
Author’s reply
Gilliat (2 November 2009) [Full text]
Jump to Rapid Response GMC’s guidance on confidentiality
Robert Lewis   (12 November 2009)
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LETTERS:
Role of plastic surgery
Abela et al. (2 November 2009) [Full text]
Jump to Rapid Response The role of Plastic Surgeons in Obesity Surgery
Ihab H. Hujazi, et al.   (11 November 2009)
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NEWS:
US drug agency is slow to exclude doctors who commit research crimes from further trials
Hopkins Tanne (2 November 2009) [Full text]
Jump to Rapid Response Rx for FDA
Hugh Mann   (11 November 2009)
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CLINICAL REVIEW:
The management of interstitial cystitis or painful bladder syndrome in women
Marinkovic et al. (31 July 2009) [Full text]
Jump to Rapid Response Its painful bladder in women.
irugal Bandara Dissanayake   (15 November 2009)
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CLINICAL REVIEW:
Sarcoidosis
Dempsey et al. (28 August 2009) [Full text]
Jump to Rapid Response Comments on sarcoidosis review
Jerome M Reich   (10 November 2009)
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PRACTICE:
Acute anterior uveitis
Khan et al. (25 August 2009) [Full text]
Jump to Rapid Response How to perform a red reflex?
M Ashwin Reddy, et al.   (17 November 2009)
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VIEWS & REVIEWS:
Shiny happy people?
Spence (20 May 2009) [Full text]
Jump to Rapid Response Legislation is needed to stop children using sunbeds
Catherine S Thomson, et al.   (14 November 2009)
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RESEARCH:
Community involvement in dengue vector control: cluster randomised trial
Vanlerberghe et al. (9 June 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response Re: Re: Simultaneous fumigation by everyone can kill all the adult mosquitoes at once
Neeru Gupta, et al.   (10 November 2009)
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RESEARCH:
Clinical effectiveness of health visitor training in psychologically informed approaches for depression in postnatal women: pragmatic cluster randomised trial in primary care
Morrell et al. (15 January 2009) [Abstract] [Full text] [PDF]
Jump to Rapid Response The PoNDER Trial: Analysed According to Protocol
Pauline Slade, et al.   (13 November 2009)
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SHORT CUTS:
All you need to read in the other general journals
(1 July 2008) [Full text]
Jump to Rapid Response New oral agents vs subcutaneous alternatives - has the DTB drawn the correct conclusion?
Dr Hannah Cohen, et al.   (19 November 2009)
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ANALYSIS:
Hookah smoking
Gatrad et al. (7 July 2007) [Full text] [PDF]
Jump to Rapid Response Re: Findings on Waterpipe Second Hand Smoke
Kamal Chaouachi   (11 November 2009)
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NEWS:
Thiomersal doesn't cause developmental disorders
Tanne (11 September 2004) [Full text] [PDF]
Jump to Rapid Response Old article/responses but still pertinent
Jas Singh   (15 November 2009)
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LETTERS:
Global medical knowledge database
Davison and Midgley (21 October 2000) [Full text]
Jump to Rapid Response The place to put it is now prepared
Adrian K Midgley   (19 November 2009)
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EDITORIALS:
Improving patient safety through training in non-technical skills
Flin and Patey (23 September 2009) [Full text]
Improving patient safety through training in non-technical skills
Life-long learning in non-technical skills
15 November 2009
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Richard FitzGerald,
Consultant Radiologist
Royal Wolverhampton Hospitals NHS Trust

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Re: Life-long learning in non-technical skills

Flin and Patey are to be congratulated for their timely editorial on the importance of non-technical skills training to improve patient safety.[1]

However I disagree with them when they state "it is too late to start delivering this training after undergraduate education has been completed and professsional attitudes are almost fully formed".

They imply this is also the conclusion of the Parliamentary Inquiry into Patient Safety .[2]

The House of Commons Health Committee states on page 63 of their report ..."Training in Human Factors skills such as teamwork and communication...should be mandated by regulation, taught and examined. The appropriate professional bodies should be active partners in examining and assessing competencies in non technical skills and Human Factors for both trainees and qualified staff".

On page 56 the report states "clinicians who persistently disregard these [safety] checklists should undergo retraining".

Doctors and other healthcare professionals acquire many new competencies and improve other skills during their working lives.

Flin and Patey should not underestimate the ability of doctors at all stages in their career to benefit from training in non-technical skills. The culture change we both want for the sake of patients requires ongoing training of all doctors.

[1] Flin R, Patey R. Training in non-technical skills to improve patient safety. BMJ 2009; 339: 985-986.

[2] House of Commons Health Committee: Patient Safety. Sixth report of Session 2008-09. London : Stationery Office, 2009

Competing interests: None declared

RESEARCH:
Selective serotonin reuptake inhibitors in pregnancy and congenital malformations: population based cohort study
Pedersen et al. (23 September 2009) [Abstract] [Full text] [PDF]
Selective serotonin reuptake inhibitors in pregnancy and congenital malformations:...
Authors' reply
12 November 2009
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Lars H Pedersen,
Research Assistant (1); Resident (2)
(1) Dept. Epidemiology, Aarhus University; (2) Dept. ObGyn, Aarhus University Hospital, Denmark,
Tine B. Henriksen, Mogens Vestergaard, Jorn Olsen, and Bodil H. Bech

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Re: Authors' reply

Various very important points and questions have been raised in response to our paper; ”selective serotonin reuptake inhibitors in pregnancy and congenital malformations: population based cohort study” (1).

Overall, caution is warranted in causal interpretation of observational studies if the exposure in question is potentially confounded by unobserved factors. We may have a strong potential association between the degree of underlying psychiatric disease and use of antidepressant medication. We have discussed this potential confounding by indication in the paper but this paramount limitation deserves much attention. With this in mind we still interpret the difference between the different SSRIs as suggestive of a drug effect but other explanations apply, as discussed in the paper, and further studies are needed. No randomized controlled trials are possible on most types of malformations, due to ethical and practical considerations, so we are stuck with the fairly foggy results from epidemiological studies. We present such data but believe that the results, interpreted with caution in the context of the existing literature, represent important information in the evidence- based treatment of depression during pregnancy.

Professor Einarson raises the important point of how data is presented in the abstract. With English as a second language we are humble to the fact that our wording could have been more elegant. However, we still believe the conclusion in the abstract is in line with what our data show. The estimate of the association between any SSRI and septal heart defects is not solely based on sertraline and citalopram but also on the (larger) association with the more than one type of SSRI. In the latter group some women did not use sertraline or citalopram, hence the wording “particularly sertraline and citalopram”. We do not present the result on paroxetine in the abstract, as the OR 0.76 was based on only one case and we were unable to consider dose as suggested by a previous study (2).

The study is based on information on malformation coded by hospital physicians and we used data from the first year after birth (with an additional analyses on malformations coded up to two years after birth). Professor Hoffman’s questions are essential in the understanding of the nature of the heart defects. The septal heart defects were defined as defects of either the atrial or ventricular wall (or both), excluding the atrioventricular canal defects (3). There was no routine use of echocardiography during the period and, because the children were born before the warning on the use of paroxetine, we expect no increased clinical investigation of the SSRI exposed children. Unfortunately, we have no further information on the nature of the septal heart defects. Regardless, even if all the defects were small we believe that the information is important to consider. Even ASDs with no symptoms for many years might eventually cause atrial hypertrophy and potentially pulmonary hypertension later in life. Importantly, more severe septal heart malformations do mandate surgical treatment but further studies with a larger sample size are needed to disentangle the potential differences in severity of the outcome.

References

1. Pedersen LH, Henriksen TB, Vestergaard M, Olsen J, Bech BH. Selective serotonin reuptake inhibitors in pregnancy and congenital malformations: population based cohort study. BMJ 2009;339:b3569.

2. Berard A, Ramos E, Rey E, Blais L, St-Andre M, Oraichi D. First trimester exposure to paroxetine and risk of cardiac malformations in infants: the importance of dosage. Birth Defects Res.B Dev.Reprod.Toxicol. 2007;80(1):18-27.

3. Louik C, Lin AE, Werler MM, Hernandez-Diaz S, Mitchell AA. First- trimester use of selective serotonin-reuptake inhibitors and the risk of birth defects. N.Engl.J Med. 2007;356(26):2675-83.

Competing interests: None declared

CLINICAL REVIEW:
Surgery for obesity in adulthood
Leff and Heath (22 September 2009) [Full text]
Surgery for obesity in adulthood
Acknowledgement
12 November 2009
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Dugal Heath,
Consultant Surgeon
Whittington Hospital

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Re: Acknowledgement

The authors of the article Surgery for Obesity in Adulthood would like to acknowledge the contribution of the following individuals who worked tirelessly to develop the North London Obesity Surgery Service and who work hard to ensure its continuing success and to maximise patient safety. More particularly, we wish to acknowledge their crucial role in developing the algorithm describing the pathway through which patients referred for bariatric surgery pass which was documented in the paper. The “core members” of the team are as follows:- anaesthesia and intensive care: A Badacsonyi, C Hargreaves , N Harper, M Kuper, S Makindie, H Montgomery, K Rauf, A Ziyad; bariatric service co-ordination: E Spencer, L Antoine; bariatric surgery: M Hashemi, P Sufi; cardiology: D Brull; gastroenterology: D Suri, C Onnie; management: S Harrington, K Slemick, D Sloman; metabolic and endocrine medicine: S Coppack, A Leeds, W May Kong; obstetrics: H Morgan; physiotherapy: J Benton, J Ross; plastic surgery: S Hamilton; psychiatry: C Gallagher, S Jacob, P Robinson; radiology: B Timmis; respiratory medicine: L Restrick; specialist dietetics: L Jones, E Segaran; specialist nurse practitioners: D Briner, K McDougall. We would also like to thank all those who are not “core members” (such as laboratory based, “out of hours” and support services) who have contributed to the development and to the smooth running of the bariatric service, who are too numerous to mention but whose contribution is greatly appreciated.

Yours sincerely

Dugal Heath

Competing interests: None declared

RESEARCH:
Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of 19 000 men in the Whitehall study
Clarke et al. (16 September 2009) [Abstract] [Full text] [PDF]
Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of...
Re: Life expectancy in relation to cardiovascular risk factors
12 November 2009
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L Sam Lewis,
GP
SA42 0TJ

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Re: Re: Life expectancy in relation to cardiovascular risk factors

"measurement of these risk factors on a single occasion at age 50 was associated with a 10 to 15 year shorter life expectancy."

Good Lord !! I really should steer clear of screening ..

Competing interests: Worry versus Wellness

Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of...
Life expectancy in relation to cardiovascular risk factors
11 November 2009
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Robert J Clarke,
Reader in Epidemiology and Public Health Medicine
Clinical Trial Service Unit and Epidemiological Studies Unit,
Martin J Shipley

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Re: Life expectancy in relation to cardiovascular risk factors

The objectives of our recent report from the Whitehall study were to estimate life expectancy in relation to cardiovascular risk factors (1).

In the 38-year follow-up of 19,019 middle aged men first examined in 1967- 1970, we estimated life expectancy in relation to smoking, blood pressure, and total cholesterol, separately and in combination in a risk score, also including body mass index, employment grade and diabetes mellitus/ glucose intolerance. The three main risk factors were selected for measurement in advance, as being modifiable risk factors that are causally related to cardiovascular disease (2). It would be prudent not to rank the risk factors associated with life expectancy to indicate their importance for disease prevention (3). Classification of participants on the basis of unequal groupings for smoking, diabetes and glucose intolerance and total cholesterol will preclude any such comparisons. Use of more extreme groups in a risk factor distribution will result in greater differences in life expectancy. Moreover, while smoking is causally related to both vascular and non-vascular mortality, total cholesterol is unrelated to non-vascular mortality (at least in part due to reverse-causality [4]). Despite substantial within-person variability in these risk factors (5), measurement of these risk factors on a single occasion at age 50 was associated with a 10 to 15 year shorter life expectancy. The results quantify the life-limiting effects of these risk factors and highlight the importance of having such risk factors measured at least once in middle age for prevention of cardiovascular disease.

References

1) Clarke R, Emberson J, Fletcher A, Breeze E, Marmot M, Shipley M J. Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of 19000 men in the Whitehall Study. BMJ 2009; 339: b 3513 doi: 104136/bmj.63513.

2) Rose G, Reid DD, Hamilton PJS, McCartney P, Keen H, Jarrett RJ. Myocardial ischaemia, risk factors and death from coronary heart disease. Lancet 1977;i: 105-9.

3) Lord JR. Curious display for multiple factors. BMJ (current issue).

4) Smith GD, Shipley MJ, Marmot M, Rose G. Plasma Cholesterol Concentration and Mortality: The Whitehall Study. JAMA 1992; 267: 70 - 76.

5) Clarke R, Shipley M, Collins R, Marmot M, Peto R. Underestimation of risk associations due to regression dilution in long-term follow-up of prospective studies. Am J Epidemiol 1999;150: 341-53.

Competing interests: None declared

NEWS:
Doctors’ view of care pathway for dying patients clashes with audit findings
Kmietowicz (16 September 2009) [Full text]
Doctors’ view of care pathway for dying patients clashes with audit findings
End of Life Care Using the Liverpool Care Pathway
23 November 2009
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Hilary Speller,
Former carer
N/A Home Address:SE11 4TJ

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Re: End of Life Care Using the Liverpool Care Pathway

I would like to comment on the experience of my father’s death which was managed using the Liverpool Care Pathway. He was in a dementia nursing home and could not communicate using words. After a series of strokes my father developed a chest infection. We took the difficult decision that he should be made comfortable, remain in the nursing home and not receive treatment to prolong his life. We were unaware of the practice of withdrawing fluids to a dying person, but it was explained that it was in his interests not to prolong the process of dying. My father survived for 11 days from the first ‘nil by mouth instruction’. His death certificate states that he died from a stroke and bronchial pneumonia, but we feel we witnessed a harrowing death from dehydration. We were at his bedside 24/7 for the final seven days.

The LCP was introduced to us several days after the initial decision was taken about his care We had not heard of it before; my interpretation of the document and our need to sign it was simply that it ensured all parties involved with my father’s care understood that he was dying.

Having previously never faced the dying process, we did not know what to expect and we felt very poorly supported. We feel there was a lack of continuity in monitoring him; perhaps that is inherent in a nursing home environment. During those eleven days he was seen by five different general practice doctors.

We explained to every person involved with his care that his left shoulder was clearly causing him a great deal of pain, especially when moved, although this was not investigated. It was in the last 24 hours of his life when my sister who is a physiotherapist arrived that we realised that my father had a dislocated shoulder.

What have we learnt? The LCP must be used by people with good experience and understanding of it as a tool in palliative care. More training is needed, especially for staff in care homes where the majority of residents do indeed end their lives. There must be access to expert palliative care on a 24/7 basis, beyond hospice and hospital settings. The dying person needs continuity of care; the LCP guidelines are meaningless if applied as a box ticking exercise. In addition, there are specific issues about end of life care for those with dementia which need to be considered. And relatives need more than kind words and cups of tea.

We are in no doubt that my father had a bad death. We hope that the painful process of recounting aspects his death mean that lessons are learnt.

Hilary and Rosemary Speller
22 November 2009

Competing interests: None declared

OBSERVATIONS:
No power for the people
Heath (14 September 2009) [Full text]
No power for the people
No Triumph for 'the people' still
23 November 2009
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susanne stevens mccabe,
retired
cf5 6su

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Re: No Triumph for 'the people' still

It is not pleasant to feel powerless but maybe demonising those with opposing strongly held views is not very useful. What should not happen is that residents of local communities become used as pawns in the sort of power games they are largely unaware of. As it turns out Rosa Curling, Solicitor for Leigh Day and Co. representing campaigners against the proposal to introduce a Polyclinic,has won a challenge to the legality of the Trust's proposal. They consulted only on locality and services without consulting as to whether it was wanted by the community in the first place. This could be described as a successful curb on the power of NHS Camden but it was achievable only with the help of large amounts of funding and the assistance of networks of people in influential positions. People in general in the community had very little information or knowledge, were mainly informed if at all, by those who opposed the introduction of the Polyclinics. It is not easy to weigh up information and come to an autonomous decision in this way.The ability of residents to seriously influence policy, as usual, is pretty negligible. Massive efforts have been put into this campaign against the Polyclinics but it has not been matched historically by any group from either side, practitioners of managers, by an interest in bringing people into a democratic process - whereby all with a stake could work together. 'The people' mainly get what coalitions of those in powerful positions, decide.

Reference: article by Gareth Iacobucci in 'Pulse' November 18th 2009

Competing interests: ex long term resident of Camden. Have been involved in NHS consultation and implementation processes

VIEWS & REVIEWS:
Should I have an H1N1 flu vaccination after Guillain-Barré syndrome?
Price (9 September 2009) [Full text]
Should I have an H1N1 flu vaccination after Guillain-Barré syndrome?
A good example of why those with an interest should publish
13 November 2009
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Peter M English,
Public Health Physician
Surrey KT19 9XF

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Re: A good example of why those with an interest should publish

It is sometimes felt that those with "too strong a personal interest" in something might, as a result of their interest, reach biased or otherwise invalid conclusions.

This article is an excellent example of the opposite. The author is somebody for whom the answer to a question is particularly important - and who has therefore taken the trouble to do a particularly good job of seeking out the available evidence (and she seems to have been well- trained in evidence-based medicine), in order to come to the best possible conclusions. Well done, Laura!

Competing interests: None declared

CLINICAL REVIEW:
Autoimmune liver disease for the non-specialist
Decock et al. (8 September 2009) [Full text]
Autoimmune liver disease for the non-specialist
Autoimmune hepatitis after long-termmethotrexate administration for rheumatoid arthritis
16 November 2009
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Ricardo Moreno-Otero, MD,
Chief, Hepato-Gastroenterology Service; Hospital de La Princesa and CIBEREHD, Universidad Autónoma
Mdrid-28006, Spain,
María Trapero-Marugan, MD, and Luisa García-Buey, MD

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Re: Autoimmune hepatitis after long-termmethotrexate administration for rheumatoid arthritis

We read the practical review on autoimmune liver disease (1) and considered of interest to emphasize the diverse forms of presentation of autoimmune hepatitis (AIH). This progressive liver disease of unknown etiology may be associated with immune-mediated disorders. Genetic predisposition, triggering factors such as viral infections or drugs, and altered immunoregulation are implicated in its pathogenesis (2-4).

Methotrexate (MTX), a folic acid antagonist, improves symptoms minimizing joint damage in rheumatoid arthritis (RA) (4). We describe the first RA patient receiving MTX who developed severe AIH resolved with corticosteroids.

A 57-year-old man with RA diagnosed in December-2000 received MTX, 15 mg weekly. On July-03 he presented with asthenia, jaundice, weight lost and liver tests (LFT) alterations: prothrombine time (PT) 15 sec, albumin 3.2 g/dl, total bilirubin (TB) 3.3 mg/dl, AST 1242 IU/l, ALT 1715 IU/l, gamma-GT 196 IU/l and alkaline phosphatase 167 IU/l. He was hospitalized with probable toxic hepatitis, remaining asymptomatic although LFT worsened (TB 6.8 mg/dl, AST 1175 UI/l, PT 17 sec and albumin 2.9 g/d).

Serology showed 1/160 ANA positivity ( previously negative), gammaglobulin 2.1 g/dl and IgG 1890. Biopsy found typical AIH: architectural distortion caused by perivenular and lobular confluent and bridging necrosis, portal tracts enlargement by intense inflammatory plasma cells infiltrate , foci of interface hepatitis, marked liver-cell damage within parenchyma with regenerative changes, and intra-acinar necrosis with plasma cells infiltration (Figure). Diagnostic score >7 denoted definite AIH (6). Metilprednisone (80 mg/day) was initiated: at day 3 a decrease of transaminases (AST 216 UI/l, ALT 644 IU/l) and TB (4.3 mg/dl) appeared, with PT (13 sec) and albumin (3.3) improvement. On tapering corticosteroids, at month 5 LFT normalized: TB 0.6 mg/dl, AST 26 UI/l, ALT 38 UI/l, PT 12 sec, albumin 3.5 mg/dl, gammaglobulin 1.7 g/dl and IgG 1670. After 6 years follow-up, LFT persist normal.

Liver involvement in RA is usually slight (7). Our patient received MTX for RA and developed severe liver damage. The damage induced by MTX range from steatosis to cirrhosis, being acute inflammation and necrosis rare (8). MTX causes liver folate depletion and, although its relationship with hepatic damage has not been established, folinic acid supplementation reduces AST/ALT levels. LFT changes and autoimmunity alterations (previously absent) occurred in this patient, and histology diagnosed AIH. As AIH appeared during MTX course and a successful corticosteroids response was attained, this hepatic autoreactivity could be more probably related to MTX than just a manifestation of RA. This case highlights that breakdown of immune tolerance by drugs may trigger liver autoreactivity (9-11), that difficulties in establishing a diagnosis of AIH instead of toxic damage exist, and that rapid corticosteroids therapy is effective.

Ricardo Moreno-Otero M.D., María Trapero-Marugán M.D. and Luisa García-Buey M.D.

Digestive Diseases Service and Centro de Investigación Biomédica en Red (CIBEREHD), Instituto De salud Carlos III, Madrid, Spain.

Hospital Universitario de La Princesa, Universidad Autónoma de Madrid, Madrid, Spain.

REFERENCES

1. Decock S, McGee P, Hirschfield G. Autoimmune liver disease for the non-specialist. BMJ 2009;339:686-91.

2.Czaja AJ. The variant forms of autoimmune hepatitis. Ann Intern Med 1996; 125: 558-98.

3.Medina J, Garcia-Buey L, Moreno-Otero R. Review article: immunopathogenetic and therapeutic aspects of autoimmune hepatitis. Aliment Pharmacol Ther. 2003 ;17:1-10.

4.Garcia-Buey L, Garcia-Monzon C, Rodriguez S, Borque MJ, Garcia-Sanchez A, Iglesias R, DeCastro M, Mateos FG, Vicario JL, Balas A, et al. Latent autoimmune hepatitis triggered during interferon therapy in patients with chronic hepatitis C. Gastroenterology. 1995 ;108: 1770-7.

5.Pincus T, ODell JR, Kremer JM. Combination therapy with multiple disease -modifying antirheumatic drugs in rheumatoid arthritis: a preventive strategy. Ann Intern Med 1999; 131: 768-74.

6.Hennes EM, Zeniya M, Czaja AJ, Parés A, Delekos GN, Krawitt EL, Bittencourt PL. et al Simplified criteria for the diagnosis of autoimmune hepatitis. HEPATOLOGY 2008; 48:169-176.

7.Abraham S, Begum S, Isemberg D. Hepatic manifestations of autoimmune rheumatic diseases. Ann Rheum Dis 2004; 63: 123-9.

8.Willkens RF, Leonard PA, Clegg Do, et al. Liver histology in patients receiving low dose pulse methotrexate for the treatment of rheumatoid arthritis. Ann Rheum Dis 1990; 49: 591-3.

9.Flax MH. Editorial:Drug-induced autoimmunity. N Engl J Med 1974; 291:414 -5.

10.Kamradt T, Mitchison NA. Tolerance and autoimmunity. N Engl J Med 2001; 344: 655-64.

11.Mackay IR, Leskovsek NV, Rose NR. Cell damage and autoimmunity: a critical appraisal. J Autoimmun 2008; 30: 5-11.

Competing interests: None declared

Editorial note
Patient consent obtained.

PRACTICE:
Digoxin specific antibody fragments (Digibind) in digoxin toxicity
Ip et al. (3 September 2009) [Full text]
Digoxin specific antibody fragments (Digibind) in digoxin toxicity
Authors' comments
17 November 2009
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Dorothy Ip,
SpR acute medicine
North Middlesex Hospital,
Dr Hafiz Syed and Dr Maurice Cohen

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Re: Authors' comments

In response to Dr Khan’s questions and comments, we would like to clarify a few points. Firstly, the presenting symptoms were 10 day history of dry cough, reduced fluid intake, 2 syncopal episodes, fall and vomiting whilst in the ambulance. Her admission electrolytes were sodium 128, potassium 6.1, urea 33 creatinine 601 (baseline urea 10.8 and creatinine 150). ECG showed atrial fibrillation with a rate 35 beats per minute, left bundle branch block and poor R wave progression. Her diagnoses were lower respiratory tract infection, dehydration, acute on chronic renal failure, syncope and fall secondary to bradycardia, digoxin toxicity and fractured left tibia and fibula.

The admitting medical team treated her hyperkalaemia with intravenous calcium gluconate, insulin and dextrose. They suspected digoxin toxicity and requested a digoxin level, which was 4.8 nmol/l on admission. Four hours after her admission, when patient became unresponsive, the digoxin level was recorded at 5.4 nmol/l.

As patient presented with bradyarrhythmia on presentation, it was difficult to distinguish whether this was due to hyperkalaemia or digoxin toxicity, given digoxin level was not immediately available. Clinicians should stabilise the myocardium with calcium gluconate, in the context of hyperkalaemia with bradyarrhythmia. In this case, we did not think that calcium gluconate administration contributed to the increase in digoxin toxicity. The digoxin levels pre and post administration were 4.8nmol/l and 5.4nmol/l respectively, with no change in her ECG.

Theoretically, digoxin toxicity could cause hyperkalaemia through its action on the Na+/K+ ATPase pump, but clinically, the cause of hyperkalaemia is often multifactorial. In this case, it is likely due to dehydration, renal impairment and medications.

Digoxin toxicity presents with non specific symptoms. Patients who are elderly and with hyperthyroidism are at increased risk of digoxin toxicity. We agree with you that clinicians should have a high index of suspicion of digoxin toxicity in patients who are on digoxin presenting with renal failure, hyperkalaemia and arrhythmias.

Competing interests: None declared

Digoxin specific antibody fragments (Digibind) in digoxin toxicity
'Treatment of hyperkalemia & digoxin toxicity'
12 November 2009
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Faisal Khan,
Specialty Trainee
Guy's & St Thomas' Hospitals NHS Foundation Trust,
SE1 9RT

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Re: 'Treatment of hyperkalemia & digoxin toxicity'

Dear editor,

In article on ‘Digoxin specific antibody fragments (Digibind) in digoxin toxicity’, Dr Dorothy Ip, Dr H Syed and Dr Cohen presented a case of elderly woman presented with renal impairment, hyperkalemia and digoxin toxicity who had treatment with digibind (digoxin – antibody fragments).

There are a few questions that, I think, need answering. I would like to know the values of electrolytes (including creatinine) on presentation in this patient and what did the baseline ECG show. Did ECG show sings of hyperkalemia? Did the patients have other symtoms to suggest digoxin toxicity (GI or visual symtoms)? Then authors did not comment on the treatment of hyperkalemia as it might have contributed to the digoxin toxicity (i-e calcium administration).

It is said that that calcium administered in the setting of digoxin toxicity can potentiate the effect of digoxin and may cause arrhythmia or cardiac arrest (1),(as in this case patient developed bradyarrythmia after treatment of hyperkalemia, but it is not clear from the article whether this patient had IV calcium or not), however this fact has been debatable (5,6). Secondly, as digoxin normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump, lowering of potassium level down (with conventional measures) in setting of digoxin toxicity can theoretically increase digoxin cardiac sensitivity.

Thirdly digoxin toxicity is associated with hyperkalemia (2,3). Therapy with digoxin antibody (Fab) fragments is indicated in this setting (4) and it will reduce the serum potassium (1).

There should be high index of suspicion of digoxin toxicity in digoxin taking patients who present with renal failure and hyperkalemia.

References;

1) M Davey; Calcium for hyperkalemia in digoxin toxicity (Emergency Medicine Journal 2002;19:183; doi:10.1136/emj.19.2.183)

2) Cardiac glycoside toxicity is frequently associated with hyperkalemia and dysrhythmias in patients with renal insufficiency. J Toxicol Clin Toxicol. 2003;41(4):373-6; Treatment of hyperkalemia in a patient with unrecognized digitalis toxicity (Van Deusen SK, Birkhahn RH, Gaeta TJ).

3) Ann Emerg Med. 1996 Oct;28(4):440-1. Hyperkalemia and digoxin toxicity in a patient with kidney failure. Fenton F, Smally AJ, Laut J.

4) GlaxoSmithKline. Digibind prescribing information. 2003. http://us.gsk.com/products/assets/us_digibind.pdf.

5) J Emerg Med. 2009 Feb 5. The Effects of Intravenous Calcium in Patients with Digoxin Toxicity;(Levine M, Nikkanen H, Pallin DJ).

6) J Toxicol Clin Toxicol. 2004;42(4):337-42: The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model (Hack JB, Woody JH, Lewis DE, Brewer K, Meggs WJ).

(faisalkhan@doctors.org.uk)

Competing interests: None declared

PRACTICE:
Tennis elbow
Mallen et al. (2 September 2009) [Full text]
Tennis elbow
decorator's elbow
23 November 2009
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Geraldine R lindley,
retired homoeopath
N/a

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Re: decorator's elbow

The grip tension may be the source of the problem if no other cause is obvious. Has your patient tried increasing the circumference of his brush handles with the use of padding( or changing the make of his brushes)? This will frquently give some relief as it may help relax his habitual grip and thus help resolve the problem

Competing interests: None declared

Tennis elbow
Family practice & specialism - the difference
23 November 2009
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peter mahaffey,
consultant (plastic & hand surgery)
bedford hospital mk42 9dj

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Re: Family practice & specialism - the difference

We in the hospital service are constantly told that its more efficient to retain patients in primary care, but honestly, most of that 'consultation' was flannel. And what did the patient get out of it at the end......nothing really. Tennis elbow is diagnosed following a complaint of persistent pain at the lateral epicondyle and is confirmed by focal tenderness 1 cm distal to the bony prominence. There is no proven treatment and the condition settles after about 1 year. Usually its fatuous to tell patients to "avoid" certain actions because they have to get on with their lives and pain will dictate what they can and cant do.

Steroids achieve nothing (Stahl, S., Journal of Bone and Joint Surgery 79:1648-52 (1997). Indeed if one believes the microtrauma theory, then to subject patients to "pepperpot" injections at the site is nonsense because anyone who's done appreciable amounts of minor surgery will be well familiar with the degree of bruising and bleeding one gets in local tissues from injections.

Competing interests: None declared

CLINICAL REVIEW:
Pain management and sedation for children in the emergency department
Atkinson et al. (30 October 2009) [Full text]
Pain management and sedation for children in the emergency department
Sedating unfasted children may be dangerous
19 November 2009
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david c crawford,
Consultant Anaesthetist
Newcastle upon Tyne Hospitals Trust, NE4 6BE,
Avinish Kapoor

Send response to journal:
Re: Sedating unfasted children may be dangerous

As consultant and registrar paediatric anaesthetists working in a large university hospital with substantial paediatric attendance in the ED we are concerned by some of the guidance offered specifically the use of intravenous anaesthetic induction agents Ketamine, (and Propofol and Midazolam) by ED doctors "appropriately trained" (our italics) in doses (2mgs/kg for ketamine) sufficient to induce general anaesthesia in unfasted children. Health care commissionaires are now requesting specific data regarding experience of anaesthetists treating children in acute trusts and some anaesthetic departments are restricting paediatric care to those with sufficient case load.

Our concern is that this review may be used as evidence that ED doctors who have completed a sedation course (unspecified) may safely use Ketamine (or Propofol, Midazolam with IV narcotics) on unfasted children for fracture manipulations or suturing of facial lacerations. Recognition of sick children and potential difficult airways requires experience. .Even for those ED doctors who have received anaesthetic training, paediatric exposure is usually limited and maintenance of practical skills e.g. airway manipulation is an accepted problem. Unlike benzodiazepines and narcotics there are no specific “antidotes” to Ketamine or Propofol.

All anaesthetists are aware that the international guidelines for fasting (6 hours for food, 4 hours for breast milk and 2 hours for clear fluids) may not guarantee an empty stomach especially in children with trauma who have delayed gastric emptying. However the suggestion that fasting is unnecessary based upon a 10 year old study of 257 procedures during which no child suffered aspiration pneumonitis is brave.

Anaesthesia is remarkably safe in the UK today. Despite the frustration caused by a six hour fast (breeching 4 hour ED stays?), general anaesthesia with a protected airway, given by a specialist must remain the safest option for many of these children.

Competing interests: None declared

Pain management and sedation for children in the emergency department
paediatric analgesia & sedation could be better
15 November 2009
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aruni sen,
Consultant in Emergency Medicine
Wrexham Maelor Hospital, LL13 7TD

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Re: paediatric analgesia & sedation could be better

Sir,

The authors need to be congratulated on clearing a lot of myth that surrounds this topic. Emergency Medicine Specialists are constantly drawing criticism from their paediatric colleagues and pharmacists who consider a loading dose of 20mg/Kg for paracetamol as excessive, while the authors quite correctly cite 30mg/Kg as a safe and effective initial dose. Our pharmacy is currently trying to ban the 20mg/Kg dose used in nurse triage. Sadly these misconcepts add to the reprehensible oligo-analgesia that is so rife in acute pain in the emergency setting.

Unfortunately, the authors have omitted two important points.

Firstly, in relation to Morphine, they forget to specify that the 100mcg/Kg dose is a TARGET for IV titration and NOT a fixed 3 or 4 hourly dose. Fixed dose of IV Morphine would cause either inadequate analgesia or oversedation. The acutal dose titrated to response may well be below or above this target.

Secondly, they make no mention of IM Ketamine given at 4mg/Kg as a good alternative to IV Ketamine (Ref 1,2) for procedural sedation. At that dose, the sedation is consistent, lasts long enough for most procedures but may cause more vomiting. The college of emergency medicine has recently published a guideline on paediatric sedation recommending 2mg/Kg IM dose which is likely to provide inconsistent sedation needing a top-up second dose.

Ref 1. Should I Give Ketamine IV or IM? Green SM, Krauss B. Annals of Emergency Medicine 2006. 48(5):613-614.

Ref 2. A Randomized Controlled Trial of IV Versus IM Ketamine for Sedation of Pediatric Patients Receiving Emergency Department Orthopedic Procedures. Roback MG, Wathen JE, Mackenzie T, Bajaj L. Annals of Emergency Medicine 2006. 48(5):605-612.

Competing interests: None declared

Pain management and sedation for children in the emergency department
Miscellaneous points intended to help
15 November 2009
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Steven Ford,
Retired GP
Haydon Bridge. NE47 6HJ

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Re: Miscellaneous points intended to help

Editor

The authors of this piece have offered a great deal of useful information for hospital practitioners. May I be permitted to add a handful of observations from primary care?

Individual children require individual management and then there is the potentially confounding influence of parents. Much can be achieved in the first few seconds of contact or, alternatively, your best efforts and intentions can be ruined by the wrong first impressions.

If the practitioner at the instant of first contact is in the wrong frame of mind (angry, upset, apprehensive, offended, tired, careless, rushed...) the child will immediately be on guard and remain so. Take a few seconds to gather yourself before opening the door. A confident, calm and assured approach with a low pitched, relaxed tone of voice will win many children over, even when they are in pain. If the child is conscious and beyond the earliest stages of language development, always greet them by name first and give your own name - and then greet the parent. A smile will not always be appropriate; the appearance of sympathetic concern may be called for. Emotional appropriateness is recognised at an early stage of a child's development and the wrong affect can cause fear and worsen suffering.

Would anyone in pain enjoy being peered down upon by an enormous stranger in strange clothes? Get down on eye level with the child - sit or kneel by the bed.

Parents and children can enter a cycle of mutually reinforcing distress that can magnify the child's pain. Not all parents can master their own emotions and supporting them is an important part of helping the child. If the parent is in a state of great distress or anger it may help both parent and child to attempt to allow them a few moments, at least, apart. A cup of tea, a fag, a walk in the fresh air, phone relatives, an opportunity for floods of tears, loo break, form filling... A female member of staff will almost always be able to be an acceptable short term substitute - no sexism intended; this is the way the world works. Parents should be offered the choice of being present for painful procedures, give them the benefit of the doubt about whether they can cope.

Giving the child something to do can help - hold the Entonox mask, hold the cotton wool ball, put your finger on the knot, wipe those tears away, blow your nose, lift this, press that, tell me about your home/school/brother. Involving the child will build their confidence in both you and themselves.

If the child asks 'Is this going to hurt?', and it is, then do not lie. Say 'Yes' and, if necessary, add 'a little' or 'a lot'. Don't spring a surprise on a child, tell them what is happening and when and where and how and why.

Children know that sticking needles through the skin is going to hurt.

Breastfed babies who do not require a 'nil by mouth' approach can be put to the breast and will rarely notice the injection when well attached and feeding. A knuckle or dummy to suck is second best. The BMJ had a paper some years ago showing that sugared water was as effective as paracetamol - if my memory serves.

In children (and adults) injections in any part of the body can be made much less noticeable by firm local pressure or grip. Ask the child to look away or the parent to clasp the child to them in a comforting manner. In an upper arm injection (or small child's thigh), holding the entire inner upper arm (or thigh) in your free hand, leaving the injection site between your thumb and first finger, squeezing very firmly, holding the pressure and then injecting will almost always result in an unnoticed injection. My rationalisation of this is that firm hand/finger pressure is understandably 'uncomfortable' and, by comparison, the needle prick is trivial - is it distraction or is it some neurological gate mechanism controlling adjacent nociceptive stimuli?

For abdominal wall injections (heparin, LHRH implants etc) taking a firm generous handful of skin and fat in your free hand will create the distracting stimulus, an immobile target and freedom from the risk of painful rectus sheath perforation, all in one action.

Instinct, acumen and experience can eclipse the value of scoring systems, frameworks, protocols and guidelines in practical patient management at any age but in paediatrics they can make all the difference.

I pray that the numbers of grandparents who only now know how to suck eggs is minimal and I offer my apologies to those who were already familiar with the procedure.

Yours sincerely

Steve Ford

Competing interests: None declared

Pain management and sedation for children in the emergency department
Intranasal Midazolam for sedation in emergency department
12 November 2009
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Angela De Cunto,
Pediatrician
IRCCS Burlo Garofolo Via dell'Istria 65/1 34100 Trieste,
Egidio Barbi, Angela De Cunto, Patrizia Salierno

Send response to journal:
Re: Intranasal Midazolam for sedation in emergency department

To the Editor,

we greatly appreciated the paper by Atkinson et al about “Pain management and sedation for children in the emergency department .” - Even though, we believe that a major issue, which can be of significant relevance in clinical practice has not been addressed. While we are well aware of the fact that sedation without pain control is not a reasonable goal we strongly support the use of intranasal midazolam, which is not even mentioned in the paper, in many setting in the ER, in association with adequate analgesia (1).

The evidence from the literature as well as our pragmatic everyday experience suggest that intranasal midazolam via a MAD device (mucosal atomization device) offers a major opportunity for a rapid onset (compared to buccal administration which can be swallowed with a delayed onset or spitted by an uncooperative child) of adequate sedation (1). Another issue of major relevance in this setting is the one of midazolam dosage which is usually reported in most experiences to be higher of the standard dosage 0.2 mg/kg, eg for intranasal administration 0.4-0.8 mg/kg (1).

From this point of view we make an exception also to the dosage reported for oral midazolam in table 2, in which is reported a maximum dose of 5 mg up to 10 years of age (2). A 10 year old child can weight more than 30 kilograms and we believe that a weight tailored dose would be more appropriate in this setting.

1. Lane RD, Schunk JE. Atomized intranasal midazolam use for minor procedures in the pediatric emergency department. Pediatr Emerg Care. 2008 May;24(5):300-3.

2. Borland M, Esson A, Babl F, Krieser D.Procedural sedation in children in the emergency department: a PREDICT study. Emerg Med Australas. 2009 Feb;21(1):71-9.

Competing interests: None declared

Pain management and sedation for children in the emergency department
Its not always good to reassure
10 November 2009
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Liam G Mahoney,
Academic Foundation Officer Year 1
Royal Sussex County Hospital, Brighton, BN2 5BE

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Re: Its not always good to reassure

The clinical review by Atkinson, Chesters and Heinz made reference to the non-pharmacological methods of coping in paediatric pain relief in the emergency department setting.[1] Twice in the article they mention the role of reassurance in reducing pain and distress for the child, once in the context of parental behaviour and once with regards to health care professional’s behaviour. Whilst being a natural approach to a distressed child, it should be noted that many studies carried out in a number of different contexts indicate that reassurance to a child, particularly during invasive procedures, is associated with increased anxiety, distress and pain in children.[2-6] Thus, health care professionals working in paediatric settings may have to be more aware that well meant verbalisations during procedures may not encourage child coping. Whilst this might be a minor point, pain and distress is a multifactorial phenomena,[7] and therefore all methods of potentially decreasing child discomfort need to be utilised.

1. Atkinson P, Chesters A, Heinz P. Pain management and sedation for children in the emergency department. BMJ 2009;339:b4234. (30 October.)

2. Chambers CT, Craig KD, Bennett SM. The impact of maternal behavior on children’s pain experiences: An experimental analysis. Journal of Pediatric Psychology 2002;27:293-301.

3. Manimala R, Blount, RL, Cohen LL. The effects of parental reassurance versus distraction on child distress and coping during immunizations. Children’s Health Care 2000;29:161-177.

4. Schechter NL, Zempsky WT, Cohen, LL, McGrath, PJ, McMurtry, C, Bright, SN. (2007). Pain reduction during pediatric immunizations: Evidence-based review and recommendations. Pediatrics 2007;119:1184-98.

5. Spagrud LJ, von Baeyer CL, Ali K, Mpofu C, Fennell LP, Friesen F, et al. Pain, distress and adult-child interaction during venepuncture in pediatric oncology: An examination of three types of venous access. Journal of Pain and Symptom 2008;36:173-84.

6. Young KD. Pediatric procedural pain. Annals of Emergency Medicine 2005;45:160-71.

7. American Academy of Pediatrics. Committee on Psychosocial Aspects of Child and Family Health; Task Force on Pain in Infants, Children, and Adolescents. The assessment and management of acute pain in infants, children, and adolescents. Pediatrics. 2001;108:793-7.

Competing interests: None declared

RESEARCH:
Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised trial
Stiell et al. (29 October 2009) [Abstract] [Full text] [PDF]
Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised...
The existence of a previously published validated study along with restricted supervision are two confounding factors in the impact of the of Canadian C-spine rule
15 November 2009
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Vafa Rahimi-Movaghar,
Associate professor of Neurosurgery, Tehran University of Medical Sciences
Sina Trauma and Surgery Research Center, Sina Hospital, Tehran, 11365-3876, Iran,
Mohammad R. Rasouli, Alexander R. Vaccaro

Send response to journal:
Re: The existence of a previously published validated study along with restricted supervision are two confounding factors in the impact of the of Canadian C-spine rule

The recent study by Stiell et al. provides an interesting evaluation of the implementation of the Canadian C-spine rule for cervical spine clearance, however the paper had several limitations. In this study, both intervention and control hospitals had a 61.7% ± 15% and 52.8% ± 8.6% respective cervical spine imaging rate before the study period (1), while the previously published validation study had shown that the average event rate was 76% (range 63-86%)(2). This lower event rate in the present study might be due to educational role of the previous published well-known study, a study well familiar to both group hospitals (2).

The authors also claim that "imaging rates went up at all six control sites, possibly reflecting a secular trend in usage of diagnostic imaging in increasingly crowded emergency departments". This increase in the number of patients imaged was present in both intervention and control hospitals and even greater in the intervention hospitals. It seems the major reason for the increase in cervical spine imaging rate in the control hospitals was not related to overcrowding, which is less than one patient per day per 6 centers, but possibly due to the lack of continuous education and supervision; i.e. the lessons learned from the previous validated study were gradually forgotten. On the other hand, the lower cervical imaging rate in the intervention hospitals one year after the completion of the 12 month study period suggests a stabilization in the educational process following long term supervised practice. It thus appears that in reality a restriction in the supervision to implement a guideline as an intervention actually results in a decrease in imaging rate thereby muting the value of the findings of this present study.

References:

1. Stiell IG, Clement CM, Grimshaw J, Brison RJ, Rowe BH, Schull MJ, et al. Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised trial. BMJ 2009;339:b4146.

2. Stiell IG, Clement CM, McKnight RD, Brison R, Schull MJ, Rowe BH, et al. The Canadian C-Spine Rule versus the NEXUS Low-Risk Criteria in Patients with Trauma. N Engl J Med 2003;349: 2510-18.

Competing interests: None declared

Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised...
Published validated study and restricted supervision are two confounding factors in implementation of C-spine rule
12 November 2009
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Vafa Rahimi-Movaghar,
Associate Professor of Neurosurgery
Sina Trauma and Surgery Research Center,
Mohammad R. Rasouli

Send response to journal:
Re: Published validated study and restricted supervision are two confounding factors in implementation of C-spine rule

Both intervention and control hospitals had respectively 61.7% ± 15% and 52.8% ± 8.6% cervical spine imaging rate before the study period (1), while the previous validation study had shown that the average event rate of study patients was 76% (range 63-86%)(2). This lower event rate in the present study might be due to educational role of the previous published well-known study, and both group hospitals were familiar with the guideline (2).

Authors claim that “imaging rates went up at all six control sites, possibly reflecting a secular trend in usage of diagnostic imaging in increasingly crowded emergency departments”, while this increase in the number of patients were present in both intervention and control hospitals and even more in the intervention hospitals. It seems the major cause of continuous increase in cervical spine imaged rate in control hospitals is not related to the overcrowding which is less than one patient per day per 6 centers, but this increase in imaging rate might be due to the lack of continuous education and supervision; thus, they gradually forgot the validated study. On the other hand, dropping further cervical imaging rate in intervention hospitals even one year after the finished 12 month study period suggests stabilization of education following long term supervised practice. At last, it is obvious that restricted supervision to implement a guideline as an intervention decreases imaging rate. Thus, the whole study adds little to the literature.

References:

1. Stiell IG, Clement CM, Grimshaw J, Brison RJ, Rowe BH, Schull MJ, Lee JS, Brehaut J, McKnight RD, Eisenhauer MA, Dreyer J, Letovsky E, Rutledge T, MacPhail I, Ross S, Shah A, Perry JJ, Holroyd BR, Ip U, Lesiuk H, Wells GA. Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised trial. BMJ. 2009 Oct 29;339:b4146.

2. Stiell IG, Clement CM, Grimshaw J, Brison RJ, Rowe BH, Schull MJ, Lee JS, Brehaut J, McKnight RD, Eisenhauer MA, Dreyer J, Letovsky E, Rutledge T, MacPhail I, Ross S, Shah A, Perry JJ, Holroyd BR, Ip U, Lesiuk H, Wells GA.Implementation of the Canadian C-Spine Rule: prospective 12 centre cluster randomised trial. BMJ. 2009 Oct 29;339:b4146.

Competing interests: None declared

EDITOR'S CHOICE:
Gagging for it
Delamothe (29 October 2009) [Full text]
Gagging for it
Response to Tony Delamothe's Article 'Gagging for it'
17 November 2009
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Helen Gavin,
Communications Officer
Liverpool Women's NHS Foundation Trust, L8 7SS

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Re: Response to Tony Delamothe's Article 'Gagging for it'

"Tony Delamothe's snide comments about the Liverpool Women's Hospital published as the Editor's Choice on the 29th October do him, and the BMJ no credit. The hospital houses the largest maternity and gynaecological services in the UK, and is at the forefront of patient safety issues in obstetrics, gynaecology and neonatology on several different fronts, nationally and internationally. We are proud to work here as consultants.

Whatever the merits or demerits of 'gagging clauses' agreed by consultants who seek early retirement after long standing conflict with their employing organisations, we are confident that Mr Bousfield's disagreement with the Liverpool Women's Trust has little to do with patient safety, and much to do with personal conflicts. Delamothe's uncritical acceptance of a one sided article, without seeking corroboration, is poor editorial practice. We expect much better from the BMJ".

Zarko Alfirevic, Professor of Fetal & Maternal Medicine

Robert MacDonald, Consultant Gynaecologist

Shuba Mallaiah, Consultant Anaesthetist

Derek Parkinson, Consultant Gynaecologist

Gillian Fowler, Consultant Gynaecologist

Mark Turner, Consultant Neonatologist

Todd Wauchob, Consultant Anaesthetist

Robert Kingston, Consultant Gynaecologist

John Kirwan, Consultant Gynaecologist

Jonathan Herod, Consultant Gynaecologist and Clinical Director for Gynaecology

Helen Scholefield, Consultant Obstetrician and Clinical Director for Obstetrics

Jim Neilson, Professor of Obstetrics and Gynaecology

Joanne Topping, Consultant Obstetrician

Mark Clement-Jones, Consultant Obstetrician

Devender Roberts, Consultant Obstetrician

Leanne Bricker, Consultant Obstetrician

Steve Walkinshaw, Consultant Obstetrician

Philip Barclay, Consultant Anaesthetist

Nabil Aziz, Consultant Gynaecologist

Bill Yoxall, Consultant Neonatologist

Ben Shaw, Professor of Neonatology

Competing interests: None declared

NEWS:
Twenty four risk factors responsible for nearly half of annual deaths, says WHO
Zarocostas (28 October 2009) [Full text]
Twenty four risk factors responsible for nearly half of annual deaths, says WHO
Remembering Mental Illnesses
12 November 2009
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Madhavan Seshadri,
ST3 in Psychiatry
Bedfordshire and Luton NHS Trust, Calnwood Court, Luton LU40LX,
Nadeem Mazi-Kotwal, ST6 in Old Age Psychiatry, Bedfordshire and Luton NHS Trust, Calnwood Court, Luton LU40LX

Send response to journal:
Re: Remembering Mental Illnesses

This WHO report brings to our attention that the top 10 leading risk factors for mortality are modifiable physical risk factors. The WHO report also identifies mental health issues like anxiety, depression, panic symptoms related to alcohol or substance misuse, childhood sexual abuse and occupational stress as risk factors 1.

It is recognised that mental illnesses in themselves (independently) are a significant cause of morbidity and mortality 2 and in writing this letter, we aim to highlight a couple of important mental health issues which are major risk factors for mortality and morbidity.

Depression is the leading cause of disability and the 4th leading contributor to the global burden of disease (DALYs) in 2000. Currently, depression is already the 2nd cause of DALYs for people aged 15-44 and by 2020, it is projected to become 2nd for all ages in both sexes 3. However, less than 25 % of those affected have access to effective treatments. In addition to contributing to suicides, depression is also an independent risk factor for coronary heart disease. Whilst there is mounting evidence that depression causes overstimulation of the HPA axis, reduced heart-rate variability and ehanced platelet aggregation causing morbidity 4 it is also an illness that kills 5,6.

Suicide is among the top 20 leading causes of death globally for all ages with nearly a million suicides a year 7. In youth under 25 it is the fourth leading cause of death. Quite often, people committing suicide approach health care professionals in the prior week or month of attempting it, and interventions at this stage may help decrease these premature deaths.

Although depression remains a leading cause of both morbidity and mortality, it is not quoted as a direct cause of death and as such, may not make to the list of mortality causes. Similarly, at least in the majority of countries, unless there is very specific and accurate evidence, coroners usually record an open verdict instead of a suicide. These factors invariably undermine the significance of depression and suicide as leading causes of mortality and morbidity.

Identifying and treating people for mental health issues particularly depression and suicidality, at the earliest will not only reduce the disability and morbidity, but will also decrease directly and indirectly, the mortality.

Reference:
  1. The report, Global Health Risks: Mortality and Burden of Disease Attributable to Selected Major Risks, is at www.who.int.
  2. Thomas Craig; Major psychiatric disorders increase risk of mortality; Evid. Based Ment. Health 2008;11;9:
  3. http://www.who.int/mental_health/management/depression/d efinition/en
  4. Wells KB, Stewart A (1989) The functioning and well-being of depressed patients. Results from the medical outcomes study. JAMA; 262: 914–9
  5. Wulsin LR, Vaillant GE, Wells VE (1999) A systematic review of the mortality of depression. Psychosomatic Medicine; 61: 6–17
  6. Jeremy Seymour & Tony B. Benning Depression cardiac mortality and all-cause mortality; Advences in psychiattic treatment. 2009; 15; 107-113.
  7. http://www.who.int/mental_health/prevention

Competing interests: None declared

ANALYSIS:
Lessons from the past decade for future health reforms
Ham (28 October 2009) [Full text]
Lessons from the past decade for future health reforms
Is there any altruistic political leader who will take us to the 21st. century?
19 November 2009
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Layla Jader,
Consultant in Public Health Medicine
Wales

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Re: Is there any altruistic political leader who will take us to the 21st. century?

Dear Editor,

I read Chris Ham’s analysis with interest and agree with some of his conclusions but was disappointed that he started in 1997 when in reality we have been on this roller coaster since the late eighties. To answer his final statement: “whether politicians are able to learn from history” I would say unfortunately, and most definitely a resounding No! They can’t because it is too big a problem to fix in one term of office. They have to muddle through and rush to leave their ‘good legacy’ on the NHS before their term of office expires.

So I cry out loud, is there any altruistic political leader who will say enough is enough? Is there anyone who will put the benefits to his/her people before his/her benefit and that of the party? We need true leaders who will rise above the others and be prepared to protect the NHS from the stormy politics of government of the day. In my view, the only way we can stabilise and protect the NHS from continuous jolts is to run it at arms length from government . Altruism necessitates that the main political parties work together and as Chris Ham refers to the word several times in his article, ‘collaborate’ in running the NHS. We need to have an ‘NHS Parliament’ made up of around 20 elected national members that reflect the body and constituents of our society in a democratic, truly modern and mature way for governing our NHS.

This body will be answerable to a cross party parliamentary scrutiny committee for its spending so it is not a quango. Political parties decide their manifesto at elections, the country elects the party which wins power but we never elect the health minister. These jobs and those of the powerful main health advisors and senior staff are usually given to members who have shown loyalty at elections as a reward not necessarily because of their experience or skills in running such a complex health organisation. The time has come for them to democratically elect the best candidate MP or AM for a new collaborative board working along side other similarly elected politicians from other parties as well as elected health care staff and patients’ representative. A one member one vote and majority decision will be the way forward. Those who can back their aspirations with good strong evidence will be able to influence others and guide us through the maize of future hard choices of what to prioritise and what to forgo. There will be so many more ethical questions the NHS will face in the future that only a free vote will do just as it happens in parliament from time to time. I am disappointed in what Nigel Hawkes had written : “the notion that it is possible to depoliticise the NHS by floating it off as a super-quango. This has never struck me as serious, in the sense defined above. You cannot spend more than £100bn a year of public money without being answerable for it in the House of Commons. And you cannot be answerable for something you no longer control”. What I would say to him is: ‘if there is a will there is a way’. I am also disappointed by politicians who say we cannot relinquish managing the NHS because we are answerable to parliament or Assembly in Wales and if you disagree with us you can register that through the ballot box. But, we don’t vote for health ministers or for their plans to the NHS if they ever have one when elected and unfortunately we always vote based on economic reasons rather than health especially now when health plans are so similar among the main political parties. Therefore, this argument doesn’t wash with us. So my final question -do we have an altruistic political leader who will take us to the 21st century?

Dr. Layla Jader
Consultant in Public Health Medicine Wales
Layla.Jader@wales.nhs.uk

Personal view- 19/11/2009 No competing interests

Competing interests: None declared

Lessons from the past decade for future health reforms
Breaking the cycle
17 November 2009
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Stephen F Hayes,
GP
The Canute Surgery. Woolston, Southampton,
SO19 9AL

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Re: Breaking the cycle

Sir

Chris Ham makes some very good points here, especially about Labour politicians making healthcare policy 'on the hoof', and the lack of an evidence base for most NHS reorganisation. It is a pity, and slightly ironic, that he began an article about learning from the history of NHS 'reform' by writing

>>>>The National Health Service in England has been on a rollercoaster ride of reform for over a decade. The journey started in 1997 with the white paper, The New NHS, and continued through the introduction of performance targets and standards. New systems for inspection and regulation were then introduced, followed by reforms to increase patient choice and competition. <<<

The journey did not start in 1997. I don't know what Chris Ham was doing in 1990, but I was a hard working council estate GP having my world turned upside down by the disastrous Thatcher/Clarke 'reforms', which in fact were the prototype of the continuing reforms which have followed them. It was Margaret Thatcher and Kenneth Clarke who introduced a pretended consumer choice, the purchaser provider split, the costly and divisive GP fundholding, a quadrupling of management costs, and micromanagement of clinicians by making their pay dependent on achievements of targets.

So we have had 2 decades of continuing 'reform', which used to be called by its more correct name, reorganisation before the spin doctors realised this was a turn off, since most people instinctively know tht when politicians tell managers to reorganise doctors and nurses it ends badly. 'Reform' however sounds very heroic and noble.

The historic pattern of NHS 'reform' goes as follows

1) the public wish to receive more healthcare product than they are willing to pay for, and the flames of their unhappiness are fanned by the media

2) vote-hungry politicians in our adversarial and centralised system blame the other lot of politicians for mismanaging the service and offer to solve the problem by 'reform' if they get into power.

3) clinicians sign and groan 'Oh no, not again!', but have no choice and so do their best, like the faithful workhorse Boxer in George Orwell's 'Animal Farm' to 'work harder', to shoulder the burden of costly, ill- judged, top-down, ideologically driven 'reform' and make the best of it that they can for their patients and themselves

4) The money is spent, the systems fiddled with, the worst of the harmful side-effects of reform are managed by clinicians, and particularly stupid 'reforms' may even be revoked, but the public STILL want more healthcare product than they wish to pay for

5...and so, and the whole cycle inevitably begins again.

In a few months we will go through the charade of a General Election, in which we get to choose a dictator for the next 5 years from a shortlist of 2 that most of us had no choice in drawing up. Whichever one wins will repeat the cycle, again.

We need to break the cycle by taking the power away from the politicians and appointing some sort of body of technocrats and representatives (answereable to a parliamentary cross party body) who manage a ring fenced NHS budget from a hypothecated tax. Or borrow a system from another Eurpoean country that does better than us. But above all, break the connection between people who want a Rolls Royce for the price of a Mini and the politicians who promise this in return for their votes.

Competing interests: I work in the NHS

Lessons from the past decade for future health reforms
Groundhog Day
17 November 2009
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Christopher L Manning,
Director, UPstream Healthcare Ltd
Teddington, TW11 9HG

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Re: Groundhog Day

Dear Editor,

The conclusion of this article should have been that politicians do not learn from the lessons of history and WE are condemned to repeat it.

One way forward, as Prof David Nutt's direct challenge to Government demonstrates very powerfully , is to end our mindless and learned-helpless commitment to party politics and, as citizens, taxpayers and experts with evidence and experience, to press for the firewalling of health, social care, education and essential infrastructure from endlessly opinionated and frequently ego-driven politics.

The mechanisms for undertaking this task are within our whit if enough of us can adhere to the maxim "nothing is impossible if people do not need to claim the credit for doing it".

Yours Sincerely
Dr Chris Manning

Competing interests: None declared

OBSERVATIONS:
The chilling effect of English libel law
Hurley (28 October 2009) [Full text]
The chilling effect of English libel law
Video now online
12 November 2009
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Richard Hurley,
technical editor
BMJ

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Re: Video now online

A video of the event is now online
http://www.city.ac.uk/whatson/2009/10_oct/151009-scij.html

Competing interests: None declared

OBSERVATIONS:
The perversion of choice
Heath (27 October 2009) [Full text]
The perversion of choice
Why should choice drive inequality?
10 November 2009
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stephen black,
management consultant
london sw1w 9sr

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Re: Why should choice drive inequality?

I'm not driven by ideology when I suggest some use of market forces in health. My motivation is pragmatic and partially based on the observation that 50 years of central command and control have not been conspicuously successful at creating continuous improvement of clinical service, consistency of service or an NHS that always puts the patient first.

But the argument that allowing choice must injure those who do not exercise it is bizarre for several reasons.

First as long as the funding formula is not naive to the point of stupidity, it should not matter which GP patients choose: the money will follow the need.

Second, if a GP is offering poor service, forcing patients to stay is unlikely to drive improvement of that service. Do we really prefer uniform but poor service to non-uniform but improving service? If people choose to reject their local GP that sends an important signal that they need to improve. If they respond to the signal, that will improve the service for the remaining patients who didn't choose to leave.

Third, choice recognizes that not everyone wants the same mix of services from their GP. Choice allows much more flexibility in matching patient needs/wants to the actual service offered.

There is nothing at all in the idea of choice that should foster inequality.

The analogy with schools reinforces this point. Denying choice to parents about schools has not driven systemic improvement in standards and has fostered an insidious form of inequality in provision driven by which parents can afford the extra mortgage payments required to live near a good school.

Competing interests: None declared

SHORT CUTS:
All you need to read in the other general journals
(27 October 2009) [Full text]
All you need to read in the other general journals
Spironolactone is underused in people with heart failure.
12 November 2009
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Manish Ramlall,
Core Medical Trainee Year 2
York Hospital, Wigginton Road, York, YO31 8HE,
Usma Khan, Steve Hyde, and Rob Crook

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Re: Spironolactone is underused in people with heart failure.

We read with dismay the shortcut relating to the underuse of Spironolactone in American patients with heart failure (JAMA 209;302:1658- 65).

We are pleased to report that patients seen by the Heart Failure nurses in York are likely to be faring better. Our protocol states that any patient with New York Heart Association (NYHA) Class III or IV symptoms and/or severe LV dysfunction should be considered for an Aldosterone antagonist, either Spironolactone or Eplerenone, once ACE Inhibitors and Betablockers have been optimised. We have briefly reviewed the database containing information relating to 731 patients with heart failure. We found 581 patients fulfilling the criteria for an Aldosterone antagonist and, of those, 375 (64.5%) who were actually taking it. Unfortunately, the database does not formally highlight patients that have been considered for an Aldosterone antagonist but are not taking it for some reason, for example, patients with contraindications or poor tolerance. Either way, we think that we can confidently say that the majority of our patients are considered for and receive an Aldosterone antagonist where indicated.

Competing interests: None declared

RESEARCH:
Differences in atherosclerosis according to area level socioeconomic deprivation: cross sectional, population based study
Deans et al. (27 October 2009) [Abstract] [Full text] [PDF]
Differences in atherosclerosis according to area level socioeconomic deprivation:...
Atherosclerosis cannot be understood without knowledge of blood viscosity.
23 November 2009
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Les.O Simpson,
retired experimental pathologist
Dunedin New Zealand 9077

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Re: Atherosclerosis cannot be understood without knowledge of blood viscosity.

Deans et al have reported the results of a high-tech assessment of vascular changes which occur in both deprived and in non-deprived participants. It is noteworthy that although the blood levels of cholesterol and smoking history were recorded, there was no recognition of the effects of such variables on the physical properties of the blood, or on blood flow in the presence of plaques. As plaques reduce the lumenal diameter, the rate of blood flow distal to the plaque will be reduced, resulting in thixotropic amplification of blood viscosity. This is because blood is a thixotropic system in which viscosity is related directly to rate of blood flow. Blood viscosity is minimal at the highest rates of blood flow.

A PubMed search for "atherosclerosis and blood viscosity" produced 316 titles, so it is not an unresearched topic. The significance of blood viscosity is that it is a determinant of intravascular pressure. The relevance of this was explained by JE French writing on atherosclerosis in Florey's "General Pathology," 1958. French drew attention to the fact that, "There are no capillary vessels in the tunica intima of normal arteries.In general, the vasa vasorum do not penetrate further than the middle of the tunica media and the nutrition of the intima and the inner part of the media is maintained by filtration from the arterial lumen."

It seems reasonable to consider that the nature of the filtrate entering the intima will be determined by the blood pressure. If this is so then an elevation of blood pressure would produce a different filtrate possibly with larger molecules. This could explain the vascular changes seen in healthy subjects, as French had noted, "...the so-called fatty streaks may be seen in the posterior wall of the aorta in children, and by the age of 20, some evidence of atherosclerosis can always be found on careful inspection of the aorta." It is possible that such deposits represent non-metabolised substances which had been filtered from the vessel lumen.

So what do the observations of French imply for the results of the Deans et al study ? Firstly, because of the absence of any measures of blood rheology, they were unable to explain some of the similarities which linked the deprived and nondeprived data. For example, blood viscosity could be increased in both groups, but due to different mechanisms. Stress, smoking, alcohol intake and dietary factors in different mixes would increase blood viscosity in both groups.

Secondly, in circumstances where blood viscosity was increased, plaque score and intima-media thickness measurements could be good predictors of adverse events.

Thirdly, the recognition of blood viscosity as an important factor, indicates that lowering of blood viscosity could have beneficial effects. Dietary changes which lowered the intake of saturated fats, and increased the intake of oily fish would be beneficial. As 6 grams daily of fish oil has been found to be effective in hypertension, it is possible that the effects of 6 grams of fish oil daily on blood viscosity could reduce the significance of atherosclerosis.

Competing interests: None declared

FEATURE:
The price of silence
Gornall (27 October 2009) [Full text]
The price of silence
Re. ‘The price of silence’ (Vol.339 31 October)
23 November 2009
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Helen Gavin,
Communications Officer
L8 7SS

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Re: Re. ‘The price of silence’ (Vol.339 31 October)

I am writing to voice my concern regarding the way in which the article by Jonathan Gornall, originally researched back in July of this year, was eventually published and also the disgraceful editorial comment that accompanied it.

Despite earlier contact during July, the Trust was not afforded the courtesy of being informed that you intended to publish after a lapse of some three months. Had you chosen to inform us that you were going to print we could have perhaps corrected some of the factual inaccuracies in the piece. An example of this is the assertion that all of the compromise agreements entered into by the Trust were with doctors in order to ‘gag’ them. Accurately reported the article could have referred to the fact that agreements were with a range of staff who left the Trust for a variety of reasons, only two of whom were doctors. It would also have been accurate and balanced to have reported that there is a specific clause within such agreements which states that “nothing…prevents the employee making disclosures to the National Patient Safety Agency or any NHS regulatory body.”

Apart from being guilty of taking the same biased approach as the main article, the editorial is also written in the most insulting, inflammatory and unprofessional terms about an organisation that has a long track record of success and an excellent reputation locally, nationally and internationally.

The slapdash and biased treatment of what is undoubtedly a serious issue does little to further a mature debate and in the process brings the standing of the BMJ into disrepute. Fortunately your discerning readers will recognise that this was an error of judgement on the Editorial department’s part.

Yours faithfully,

Ken Morris, Chairman, Liverpool Women's NHS Foundation Trust

Competing interests: None declared

EDITORIALS:
Migraine with aura and increased risk of ischaemic stroke
Loder (27 October 2009) [Full text]
Migraine with aura and increased risk of ischaemic stroke
Progesterone or progestogen or progestin; which is it?
19 November 2009
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M Joy Spark,
Pharmacy lecturer
LaTrobe University, Bendigo Campus Vic Australia3550

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Re: Progesterone or progestogen or progestin; which is it?

This editorial refers to combination oestrogen-progestin contraceptives but in the concluding sentences implies that levonorgestrel and norethisterone are types of progesterone. Stephenson in her letter [1] refers to the etonogestrel containing implant as a progesterone implant. Progesterone appears to have been used as a synonym for progestin. The British Pharmacopeia [2] lists the action and use of progesterone and progestins such as levonorgestrel and norethisterone as progestogen. There appears to be a lot of confusion around the group name for progestational agents. In 1976 Dalton [3] argued that progesterone should not be confused with or considered the same as progestins (synthetic progestogens). Yet in 2009 it appears they are still being confused.

The confusion possibly arises because of the use of oestrogen and progesterone to represent the female sex hormones. Oestrogen is a generic term for oestrogenic agent, and there are three primary oestrogens in the human body; oestrone (E1), oestradiol (E2), and oestriol (E3). On the other hand progestogen is the generic term for a progestational agent and progesterone (P4) is a single chemical entity and the primary progestogenic hormone synthesised by the human body.[4] The term progestin can be used to refer to synthetic progestational agents.

It appears that the difference between progesterone, progestogens, and progestins is still not appreciated. Confusion associated with interpreting research findings with regard to progesterone and progestins would be reduced if a consistent name, other than progesterone, was used to represent synthetic progestogens.

1. Stephenson V. Migraine and risk of stroke: For contraception try IUDs BMJ 2009;339:b4841.

2. British Pharmacopoeia Commission. British Pharmacopoeia. London: The Stationery Office, 2009.

3. Dalton K. Progesterone or progestogens? BMJ 1976;2(6046):1257.

4. Dorland's illustrated medical dictionary. 29th ed. Philadelphia: W.B. Saunders Company, 2000.

Competing interests: None declared

Migraine with aura and increased risk of ischaemic stroke
Author's reply
15 November 2009
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Elizabeth Loder,
chief, division of headache and pain
DepartmenBrigham and Women’s/Faulkner Hospitals and Harvard Medical School, Boston, MA 02130, USA

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Re: Author's reply

My thanks to Drs. Stephenson and Rivet for reminding us that progestin- only methods are one of several alternatives to oestrogen-containing contraceptives for women who have migraine with aura. Guidance from a number of authoritative groups does recommend against the use of oestrogen -containing contraceptives in women who have aura. (1-3) For many of these women the potential harms probably do outweigh the benefits. I contend, though, that a blanket ban does not take adequate account of the spectrum of risk within this group or of the need to individualize treatment depending on an individual woman’s situation and priorities. The International Classification of Headache Disorders assigns a diagnosis of migraine with aura to anyone who has had two episodes of aura. (4) It seems unlikely that women with a remote history of aura on two occasions face the same degree of stroke risk as those for whom aura is a frequent occurrence.

Dr. Petrie is right that the absolute risk of stroke in women with aura is low, particularly in those who have no additional stroke risk factors. The cumulative lifetime incidence of migraine in women is 43%, however, so even small reductions in stroke risk at the level of the individual may translate into large benefits at a population level. (5) This is especially likely to be true for stroke in young women, which may result in many years of impairment and disability.

1. The use of hormonal contraception in women with coexisting medical conditions. ACOG Practice Bulletin No. 18. Int J Gynecol Obstet. 2001;75:93-106.

2. World Health Organization. Improving Access to Quality Care in Family Planning: Medical Eligibility Criteria for Contraceptive Use, 2nd ed. Geneva: World Health Organization; 2000.

3. International Headache Society Task Force. Recommendations on the use of oral contraceptives in women with migraine. Cephalalgia. 2000;20:155-156.

4. Headache Classification Committee of the International Headache Society. Classification and diagnostic criteria for headache disorders, cranial neuralgias and facial pain. Cephalalgia 1988;8 Suppl. 7:1–96.

5. Stewart WF, Wood C, Reed ML, Roy J, Lipton RB. Cumulative lifetime migraine incidence in women and men. Cephalalgia 2008;28:1170-78

Competing interests: EL has in the past five years consulted for and conducted studies funded by or received lecture honorariums from Merck, Allergan, GlaxoSmithKline, Johnson and Johnson, Pfizer, and Elan. She is a clinical research editor for BMJ and an associate editor of Headache and Cephalalgia.

FEATURE:
Falling foul of gagging clauses
Cassidy (27 October 2009) [Full text]
Falling foul of gagging clauses
Clarification of a clarification
16 November 2009
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Gerald Shaw,
Retired Consular worker
Nil

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Re: Clarification of a clarification

Clarification of a clarification

The GMC has no power to vary employment contracts. Employers are not registered with the GMC unlike the other party to the contract, the lucky doctors, so it is unclear how the GMC would control the issue, or in which forum or court. I cannot see what the cause of action would be.

I am even unsure that a termination agreement is an employment contract, as no employment results from it. The GMC is a 'disapproval organisation'. You can read into the President's words how he itches to get hold of any doctors involved in gagging clauses and say - 'Oh very bad doctors, strike them all off !' whereas the employers get off scot free to do it all over again with another willing party.

This episode serves much better to show that there is an inbuilt conflict between employers and the GMC, who may well have different aims and world views, and this will get worse when the great money waster Revalidation takes hold - as it is the GMC who directs and the employers who will pay for the Great Paper Run Around.

Gerald Shaw

COI who is not registered with or licensed by the GMC or in any way get-at-able, so is able to speak out on this issue.

Competing interests: None declared

Falling foul of gagging clauses
Clarification on article: 'Falling Foul of Gagging Clauses'
13 November 2009
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Prof. Peter Rubin,
Chair, GMC
NW1 3JN,
Please note, although this response has been sent by the press office, the author is Prof. Rubin

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Re: Clarification on article: 'Falling Foul of Gagging Clauses'

Dear Sir,

The article Falling Foul of Gagging Clauses (October 31) is very concerning.

I want to make clear that any doctor who wants to report genuine concerns will have nothing to fear from the GMC. The GMC emphasises the responsibility of doctors to report their concerns and this is echoed throughout our guidance. In particular Good Medical Practice (2006) states both that doctors should raise concerns about inadequate resources and that they must protect patients from risk of harm posed by a colleague's conduct, performance or health. Raising Concerns (2006) makes clear that provided doctors have been honest, raising a concern is justified even if it turns out to be groundless.

The article alleges that some Trusts are using gagging clauses to prevent doctors from speaking out. The Public Interest Disclosure Act 1998 prohibits the NHS from inserting ‘gagging’ clauses into employment contracts for doctors. Doctors should not enter into agreements or sign contracts which prevent them from fulfilling their professional obligations or complying with our guidance. Any manager who is registered with us and who is complicit in implementing a gagging clause could be subject to our fitness to practise procedures and would therefore be placing their registration at risk.

GMC guidance Management for Doctors (2006) makes clear that doctors in a management role must make sure that adequate systems are in place for complaints to be thoroughly investigated and that those who raise concerns are protected from unwarranted criticism or actions. Agreements or contracts that impede doctors raising genuine concerns with us about the conduct or competence of another doctor represent a significant risk to patient safety and would be of obvious concern to the GMC.

Competing interests: None declared

PRACTICE:
Depression in adults, including those with a chronic physical health problem: summary of NICE guidance
Pilling et al. (27 October 2009) [Full text]
Depression in adults, including those with a chronic physical health problem: summary...
Depression: its pathophysiology and treatment.
20 November 2009
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Les.O Simpson,
retired experimental pathologist
Dunedin New Zealand 9077

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Re: Depression: its pathophysiology and treatment.

The article by Pilling et al discusses treatment of depression without reference to the pathophysiology. However, there are a number of published reports which raise the possibility that depression is a consequence of impaired cerebral blood flow. Possibly such studies have been rejected because of their small size. But a PubMed search for "Depression and impaired cerebral blood flow," produced 60 titles. Even though many of such studies involve animals, they show a common thought pattern.

In 1995, Bench et al reported a study in which patients underwent brain scans while depressed, and were rescanned on remission. The report concluded, "Thus, recovery from depression is associated with increases in regional cerebral blood flow in the same area in which focal decreases in regional cerebral blood flow are described in the depressed state, in comparison with normal subjects." It is difficult to ignore such direct observations as they imply that depression has a blood flow-related cause.

While there is general acceptance that stressful events are triggers for episodes of depression, it seems not to be recognised that the stress hormones stiffen the red blood cells. The resulting reduction in cell deformability will increase blood viscosity. For example, the English translation of a paper in Italian (Psychological stress and sudden death, 2002) included the statement, "...the second mechanism acts through adverse health behaviours, such as poor diet, alcohol consumption or smoking in case of acute psychological stress, the mechanisms involved are mainly the ability to trigger myocardial ischemia, to promote arrhythmogenesis, to stimulate platelet function and to increase blood viscosity." It seemed not to be recognised that the increased blood viscosity was the primary agent. As similar statements have been made by other authors, it is not surprising that a PubMed search for "Depression and blood viscosity," should produce 83 titles. This raises the pertinent question, "Could treatments aimed at reducing blood viscosity be helpful for those suffering from depression?"

As Stoll has reported that fish oil was an excellent mood stabiliser in bipolar disorder, and 6 grams of fish oil daily has been found to be an effective treatment for hypertension, would 6 gams of fish oil daily help those suffering from major depressive disorder ?

Competing interests: None declared

Depression in adults, including those with a chronic physical health problem: summary...
Medical illnessess and depression.
20 November 2009
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Gnanie Panch,
consultant in chronic pain managment and anaesthesia
Whittington hospital London N195NF

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Re: Medical illnessess and depression.

NICE guidelines 90, 91 and 88

The nice guidelines published by Pilling et al come 14 years after the publication of the joint recommendations by the royal colleges of physicians and psychiatrists – The psychological care of medical patients, recognition of need and service provision document. It is a timely reminder at a time when the CG 88 has caused so much of controversy. It emphasizes the need for considering emotional factors as co-morbidity among patients who fail to show predictable response to treatment of physical conditions. The document emphasizes the reality - under recognition being the major problem, particularly in those suffering from physical illnesses.

The continuing acceptance in the 21st century of the Descarte’s philosophy of mind body dualism inevitably leads to an under recognition of depression in secondary care. The authors have described the consequences to patients and the wider society of continuing to ignore depression and have outlined the recommendations for the clinical assessment, screening and treatment. It is worth emphasizing that the “Two questions depression screen” is 97% sensitive and 59% specific. Therefore its use on a target group of physically ill patients whose care fails to result in expected improvement is to be highly recommended. Unfortunately the NICE GDG for the CG 88 have not included the recommendations for screening, severity scoring, monitoring or the use of pharmacological treatments for those who are diagnosed to be severely depressed.

It is clear that the CG90and 91 recommendations could be applied to chronic pain care. All clinicians, even within the limited time available, could administer screening and severity scoring questionnaires. Emotional factors being a major component in chronic pain, its improvement is worth measuring as a response to chronic pain treatments. Finally it is worth reiterating Lord Darzi’s slogan – “we can only aim to improve on what we actually measure”

Competing interests: None declared

Depression in adults, including those with a chronic physical health problem: summary...
Updates on treatment for depression: NICE in theory not always in practice.
12 November 2009
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June S. L. Brown,
Senior Lecturer
Department of Psychology (PO77), Institute of Psychiatry, De Crespigny Park, London, SE5 8AF,
Louisa Rhodes

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Re: Updates on treatment for depression: NICE in theory not always in practice.

Pilling et al (2009) have written a summary of the ‘updated’ NICE Guidelines for Depression (2009) in which they highlight the new guidance on treating patients with depression, ‘subthreshold’ symptoms of depression as well as depression in the presence of chronic physical health problems. While these are very welcome updates to the guidance as the new Guidelines are a lot more focussed, we still felt a huge sense of disappointment with NICE for providing so little guidance on treating patients with depression and complex social difficulties.

We have been given the responsibility of implementing the Guidelines in a London borough and conducted an audit to see how well the NICE Guidelines for Depression (2004 version) were being implemented. We found that, based on strict compliance with the NICE recommendations, 44% of patients treated by the secondary care Assessment and Brief Treatment (ABT) CMHT teams in our area were ‘inappropriate’ for treatment in secondary care.

However, when we examined this, we found that many of the patients who were considered to be ‘inappropriate’ for treatment in secondary care, had depression with complex social difficulties. The ABT teams in our area regularly treat patients who fall into this category because these patients are referred by GPs that feel they need the support of a multidisciplinary team to tackle their social difficulties alongside their mental health problem(s), even though their depression may be mild or moderately severe.

Despite the commonness of the problem, there was nothing in the original guidelines for Depression (2004) about this issue. We therefore requested during the Consultation, that NICE address this and hoped that the updated version would tackle this difficult topic.

We were very pleased to see that the newly updated NICE Guidelines for Depression (2009) make several references to the relationship between depression and social difficulties and recommend that clinicians consider social factors when conducting assessments with depressed patients. The guidelines also recommend ‘referral to specialist services for a programme of multiprofessional care’ for those with severe depression or moderate depression with complex problems. However, should a clinician want specific advice on how information about social difficulties should be used to guide treatment decisions, the guidelines do not actually provide this. Some questions that may arise are: should the social problems be dealt with first, or should psychological treatment be offered first, or should the two be offered in parallel? Another question is whether these patients should be referred to CMHTs at level 4 in the stepped care model or should they be referred to services lower down the stepped care model, where they can get treatment for depression and be signposted to other services for support with their social difficulties?

This is a very frustrating situation. We risk losing the interest of local clinicians who may see NICE as being unable to offer guidance on a key everyday issue in CMHTs and NICE runs the risk of losing credibility. At the very least, NICE should flag this up as a research priority so that guidance can be offered, even tentatively, on handling depression and complex social problems at the next revision.

References

NICE. (2004). CG23 Depression: Full Guideline. www.nice.org.uk/CG23

NICE (2009). CG90 Depression in adults: Full Guidelines. www.nice.org.uk/CG90

Pilling, S., Anderson, I., Goldberg, D., Meader, N. & Taylor, C. Depression in adults, including those with a chronic physical health problem: summary of NICE guidance. BMJ 2009; 339:b4108

Competing interests: None declared

CLINICAL REVIEW:
Hyperkalaemia
Nyirenda et al. (23 October 2009) [Full text]
Hyperkalaemia
Re: Salbutamol unsafe in hyperkalaemia
23 November 2009
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Moffat J Nyirenda,
MRC clinician scientist/honorary consultant physician
The Queen's Medical Research Institute, University of Edinburgh, EH16 4TJ,
Justin I. Tang, Paul L. Padfield, Jonathan R. Seckl

Send response to journal:
Re: Re: Salbutamol unsafe in hyperkalaemia

We agree with Prof Dimmitt1 that tachycardia is an adverse effect of β-agonist therapy, and we would advise that sulbutamol should be used with caution in patients with significant coronary artery disease or unstable heart rhythms. There have been no robust controlled clinical trials on management of severe hyperkalaemia, but most studies (including a recent Cochrane review)2 have shown that β-agonists are effective at lowering serum potassium levels. Unfortunately, most reports have only focused on serum potassium levels, but not on mortality or cardiac arrhythmias. Indeed, in studies cited by Prof Dimmitt, β-agonists were not used for management of hyperkalaemia, but to treat COPD in normokalaemic patients.3,4

It is true that β-agonists, like insulin, only promote intracellular potassium shift, but this is thought to be an important early temporizing measure to prevent potential adverse effects of hyperkalaemia – before definitive strategies to remove excess potassium from the body take effect. The use of resonium resins remains controversial, with some authorities not recommending their use for treatment of acute hyperkalaemia.5

1. Dimmitt SB. Salbutamol unsafe in hyperkalaemia. Bmj.com, 19 Nov 2009.

2. Mahoney BA, Smith WA, Lo DS, Tsoi K, Tonelli M, Clase CM. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev 2005;cd003235.

3. Kallergis EM, Manios EG, Kanoupakis EM, Schiza SE, Mavrakis HE, Klapsinos NK, Vardas PE. Acute electrophysiologic effects of inhaled salbutamol in humans. Chest (2005) 127:2057-2063.

4. Salpeter SR, Ormiston TM, Salpeter EE. Cardiovascular effects of β-agonists in patients with asthma and COPD. Chest (2004)125:2309- 2321.

5. Kamel KS, Wei C. Controversial issues in the treatment of hyperkalaemia. Nephrol Dial Transplant (2003) 18: 2215-2218.

Competing interests: None declared

Hyperkalaemia
Salbutamol unsafe in hyperkalaemia
19 November 2009
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Simon B Dimmitt,
Clinical Professor of Medicine
University of Western Australia,
Rukshen Weerasooriya

Send response to journal:
Re: Salbutamol unsafe in hyperkalaemia

We were concerned to see that salbutamol was recommended for the management of hyperkalaemia in the recent BMJ Clinical Review.1 Salbutamol, like insulin, only promotes intracellular redistribution of potassium. Clinical and outcome benefits with this strategy, although widely practiced, do not appear to be evidence based. Resonium resins and diuretics lower total body and plasma potassium,2 usually sufficiently given that most hyperkalaemia is subacute. The objective in lowering plasma potassium is to reduce the risk of arrhythmia, which is likely to be related to the severity of hyperkalaemia but may not be reduced simply shifting the potassium intra-cellularly. Salbutamol is potentially hazardous because of its arrhythmogenic3 and chronotropic effects.4 In systematic review, the mean increase in heart rate with a single dose of inhaled beta-2 agonist was 9 beats/minute, with a mean reduction in serum potassium of only 0.36 mmol/L.4 The risk/benefit in hyperkalaemic patients with beta-2 agonists is uncertain. Persisting with resonium and if appropriate, diuretics, in a monitored setting is probably usually the safest management.

1 Nyirenda MJ, Tang JI, Padfield PL, Seckl JR. Hyperkalaemia. BMJ 2009;339:b4114

2 Sood MM, Sood AR, Richardson R. Emergency management and commonly

encountered outpatient scenarios in patients with hyperkalaemia Mayo Clin Proc

2007;82:1553-61.

3 Kallergis EM, Manios EG, Kanoupakis EM, et al. Acute electrophysiologic effects of inhaled salbutamol in humans. Chest 2005;127:2057-63.

4 Salpeter SR, Ormiston TM, Salpeter EE. Cardiovascular effects of ƒÒ -agonists in patients

with asthma and COPD. Chest 2004;125:2309-21.

Competing interests: None declared

Hyperkalaemia
Damage to the juxta glomerular apparatus and impairment of aldosterone release.
11 November 2009
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Richard G Fiddian-Green,
FRCS, FACS
None

Send response to journal:
Re: Damage to the juxta glomerular apparatus and impairment of aldosterone release.

In this review damage to the juxta glomerular apparatus with a deficit in renin production was cited as a cause of hyperkalaemia induced by reducing the secretion of aldosterone. How might damage to the juxta glomerular apparatus be induced?

Permit me a brief review of the physiology from Wikipedia. "If the perfusion of the juxtaglomerular apparatus in the kidney's macula densa decreases, then the juxtaglomerular cells release the enzyme renin..."Renin cleaves a zymogen, an inactive peptide, called angiotensinogen, converting it into angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE) which is found mainly in lung capillaries. Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular mesangial cells, causing these cells to contract along with the blood vessels surrounding them and causes the release of aldosterone from the zona glomerulosa in the adrenal cortex".

In one of our case reports a man, with abdominal pain and weight loss, had his a gastric intramucosal acidosis reversed, his symtoms relieved and regained his lost weight after an angioplasty that restored normal pulsatile flow in the coeliac axis. One of the figures shows the before and after pulse pressures (1). This raises the possibility that it is a fall in pH in the juxta blomerular apparatus, rather than of perfusion or pulse pressure per se, that triggers the release of renin, possibly by inducing a local increase in the ionized [Ca++]. But in my rapid responses addressing H pylori I made the point, pancreatic polypeptide and insulin being examples, that an energy defict can impair the ability to synthesize new hormone and replenish hormone pools and, thereby, cause an impaired release of hormone. I have also reported that Shukri Khuri, a cardiac surgeon at Harvard, has shown that apoptosis within myocytes increases as the intramyocardial pH falls. One might presume, therefore, that the probability of autophagia and cellular necrtosis, with potasssium release, are associated with different degrees of tissue acidosis, the tissue pH providing a measure of the degree of metabolic stress present. In which case stimulation of the release of renin, and autophagia, apoptosis and necrosis of cells in the juxta glomerular apparatus might be graded responses to a progressive increase in energy deficit, potassium being released by the latter.

Angiotensin II is also a selective vasoconstrictor of the splanchnic vasculature and has been implicated in the pathogenesis of multiple organ failure, as reviewed by Bulkley in our book on splanchnic ischameia and multiple organ failure (2). How then might ACE inhibitors cause renal damage? By positive feedback on renin release and increasing the demand for ATP beyond the capacity for its timely resynthesis? That, however, is likely to cause damage to the juxta glomerular apparatus, but not the kidney unless hypovolaemia or some other cause of renal damage, such as NSAIDS, is also present. Like metformin NSAIDS are associated with an adverse effect upon mitochondria in many organs including the kidney (3). The combination of effects might then be additive but the adverse effect of ACE inhibitors in elderly subjects has been reported in those who were being treated with diuretics (4).

What of statins given that aldosterone is a product of cholesterol synthesis? Drugs that reduce aldosterone secretion are known to cause hyperkalaemia, as reported in this review. Might statins also predispose to hyperkalaemia by increasing the risk of damage to the juxta glomerular apparatus or having a direct effect upon the adrenals?

1. Fiddian-Green RG, Stanley JC, Nostrant T, Phillips D.Chronic gastric ischemia. A cause of abdominal pain or bleeding identified from the presence of gastric mucosal acidosis. J Cardiovasc Surg (Torino). 1989 Sep-Oct;30(5):852-9

2. A. Marston, G. B. Bulkley, R. G. Fiddian-Green and U. H. Haglund, Editors, Splanchnic Ischemia and Multiple System Organ Failure, London, Edward Arnold, 1989.

3. Fábio E. Mingatto, Antonio C. Santos, Ségio A. Uyemura, Maria C. Jordani and Carlos Curti . In Vitro Interaction of Nonsteroidal Anti- inflammatory Drugs on Oxidative Phosphorylation of Rat Kidney Mitochondria: Respiration and ATP Synthesis. Archives of Biochemistry and Biophysics Volume 334, Issue 2, 15 October 1996, Pages 303-308

4. Juhlin T, Björkman S, Höglund P.Cyclooxygenase inhibition causes marked impairment of renal function in elderly subjects treated with diuretics and ACE-inhibitors. Eur J Heart Fail. 2005 Oct;7(6):1049-56

Competing interests: None declared

RESEARCH:
Mortality in renal transplant recipients given erythropoietins to increase haemoglobin concentration: cohort study
Heinze et al. (23 October 2009) [Abstract] [Full text] [PDF]
Mortality in renal transplant recipients given erythropoietins to increase haemoglobin...
ESAs in Chronic Kidney Disease
12 November 2009
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Timothy J Littlewood,
Consultant Haematologist
Churchill Hospital, Oxford OX3 7LJ

Send response to journal:
Re: ESAs in Chronic Kidney Disease

Erythropoiesis stimulating agents (ESAs) have been the treatment of choice for anaemic patients with chronic kidney disease (CKD) since 1986 when Winearls published a report of 10 patients with end stage renal failure treated with recombinant erythropoietin. This pilot study was soon followed by larger trials which confirmed that treatment with ESAS increased the haemoglobin concentration, reduced transfusion need and improved quality of life.2

There has remained controversy about the optimum target haemoglobin. Two recent studies have suggested that it is harmful to correct the haemoglobin into the normal range compared to a target of around 11.0- 11.5g/dl.3,4 Heinze et al5 have reported a retrospective study in recipients of renal transplants in which 805 of 1794 patients were treated with ESAs after the transplant. Recipients of an ESA had an increase mortality compared to those who did not. The authors admit that there may well have been differences between the two populations of patients giving rise to the differing outcomes and this study, with its design flaws, does not provide good evidence about the safety of ESAs in anaemic patients post renal transplant.

Nevertheless, there is an increasing evidence base that raising the haemoglobin into the normal range using ESAs in patients with kidney disease is harmful.6 The cause of that harm is unclear. One, of many, hypotheses is that subclinical iron deficiency occurs commonly in ESA treated patients especially when they are not given intravenous iron supplements, and that the iron deficiency results in a reactive thrombocytosis.7 The increased platelet count may be responsible for the increased cardiovascular and cerebrovascular morbidity and mortality.

It would be very interesting to know whether Heinze et al have the data on platelet counts in their two groups of patients.

References.

1.Winearls C, Oliver DO, Pippard MJ et al. Effect of human erythropoietin derived from recombinant DNA on the anaemia of patients maintained by chronic haemodialysis. Lancet 1986; 2; 1175-1178

2. Canadian Erythropoietin Study Group: Association between recombinant human erythropoietin and quality of life and exercise capacity of patients receiving haemodialysis. BMJ 1990; 300; 573-578

3. Drueke TB, Locatelli F, Clyne N et al. Normalisation of haemoglobin level in patients with chronic kidney disease and anemia. NEJM 2006; 355; 2071-2084

4. Singh AK, Szczech L, Tang KL et al. Correction of anemia with epoetin alfa in chronic kideny disease. NEJM 2006; 355; 2085-2098.

5. Heinze G, Kainz, Horl WH, Operbauer R. Mortality in renal transplant recipients given erythropoietins to increase haemoglobin concentration: cohort study. BMJ 2009; 339; Oct 23;339:b4018. doi: 10.1136/bmj.b4018.

6. Phrommintikul A, Haas SJ, Elsik M, Krum H. Lancet 2007; 369; 381- 388

7. Streja E, Kovesdy CP, Greenland S et al. Am J Kidney Dis. 2008; 52; 727-736

Competing interests: Payments for lectures and sitting on advisory boards received from Amgen, Roche and Johnson and Johnson.

EDITORIALS:
Use of erythropoietins in patients with renal transplants
Treleaven and Clase (23 October 2009) [Full text]
Use of erythropoietins in patients with renal transplants
‘Normalisation of haemoglobin is hazardous, ineffective and costly.’
23 November 2009
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Eric J Will,
Retired Nephrologist
St James's University Hospital, Beckett Street, Leeds LS9 7TF

Send response to journal:
Re: ‘Normalisation of haemoglobin is hazardous, ineffective and costly.’

The editorial commentary on the paper by Heinze et al rehearsed all the solecisms that careless terminology has visited on this area of clinical research. The catch-phrase metaphors of targeting and normalisation have confused the scientific discussion to the point of utterly misleading statements, like their sub-title above. As they rather awkwardly concede, any putative mischief in Erythropoietin (ESA) treated renal anaemia relates to the intention to reach ‘normal’ haemoglobin (Hb) values (‘treated to a high haemoglobin target)’ through the application of feed-back algorithms to determine ESA dose and intervention thresholds. It should not be concluded that ‘raising haemoglobin to normal concentrations, ...., seems harmful’, since those subjects that did achieve normal values in the index studies did perfectly well (their ref 8 and 10). The Heinze paper, in which neither the criterion of the nominated ‘Haemoglobin’ nor the anticipated intentions of treating clinicians were given, serves to confuse again (their ref 5). It appears to relate outcome to achieved haemoglobin, rather than the intended, unknowable ‘target’ values, a significant change in emphasis of possible causation. The editorialists then succumb to conflate the achieved Hb results with intention by assuming that achieved values were related to ‘the effect of various haemoglobin targets’. In practice, most ‘normal’ Hb values in renal disease probably occur either in patients who do not require ESA at all or are the inadvertent consequence of poorly predictable ESA sensitivity during management. It is the failure to discriminate deliberate from incidental ‘normal’ Hb values in clinical practice that bedevil the development of sensible treatment principles. A super-structure of possible pathopysiological mechanisms is only too easy for clinician scientists to erect and repeat, which further establishes a more readily understood, mechanistic, but potentially erroneous, interpretation of the studies.

It would matter less if it were not likely that misguided attempts to avoid ‘high’ Hb levels would result in many lower values, for which there is evidence of avoidable symptomatology and adverse outcome. This sequence of events parallels the probable disbenefit of deliberately reduced haemodialysis hours after the quantification of dialysis dose in the early 1980s, both phenomena being of especial relevance to the private dialysis sector in the US.

It would be helpful for the Heinze data to be analysed to give the absolute number of events in each ‘Hb’ category. It seems more likely that any consequence of ESA treatment in transplantation is related to unknown confounding clinical factors that lead to the use of the drugs in the first place, the Hb response being a token of ESA management but in no way causative.

Because of the difficulties of ESA management in patient groups the ‘optimal target’ for Hb is an aspirational value towards which clinical effort might be directed by whatever means, in the same sense that optimal Systolic Blood Pressure is a poorly defined ‘less than XXX mmHg’ value. The ‘optimal target’ is also the desirable achieved Hb, but ‘target’ and achievement are qualitatively different components of a treatment vocabulary for which we use only the one word in discourse. So, what may be hazardous, of limited effectiveness and costly are the processes of deliberately attempting to ‘normalise’ Hb in patient cohorts, which few clinicians were anyway pursuing but which cannot be distinguished from inadvertent ESA reactions. The convenient, punchy, publication shorthand of ‘Normalisation’, like ‘tight’ control, is flattering to researchers but ultimately misleading. For the citizen it was fortunate that these semantic confusions allowed governments and payers to move in on the costs of ESA management. It is perhaps less creditable that the scientific academic community have not unpacked the issues, but then it is a Kuhnian universe and they have their own considerations. It is all rather subtle.

Competing interests: None declared

Use of erythropoietins in patients with renal transplants
Anemia and kidney function are related
18 November 2009
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Jan Gossmann,
Nephrologist
Transplant clinic, KfH Nierenzentrum, Schleusenweg 22, 60528 Frankfurt am Main, Germany

Send response to journal:
Re: Anemia and kidney function are related

Clearly it is important to know, if for kidney transplant patients the same rules apply for the treatment with erythropoieseis stimulating agents (ESA) as for dialysis patients or diabetic patients with impaired renal function. The effort by Heinze et al. may therefore be a first step to clarify this question. I see, however, a major drawback in their study. And that is that is does not take into account transplant function (serum creatinine or creatinine clearance). In table 1 are given a large number of data about their population of kidney transplant patients but creatinine is missing. In figure 4 the hazard ratios for mortality are shown against the hemoglobin concentration in patients treated or not treated with ESA. But how can the authors exclude that they are simply comparing patients with different levels of renal function. If a patients needs therapy with an ESA to reach a hemoglobin of say 13 his renal function is likely to be worse than that of a patient reaching the same hemoglobin without an ESA. It looks as if the difference between the 2 groups may not only be treatment with ESA but also different degrees of transplant function which clearly has influence on survival.

Competing interests: None declared

RESEARCH:
The PRaCTICaL study of nurse led, intensive care follow-up programmes for improving long term outcomes from critical illness: a pragmatic randomised controlled trial
Cuthbertson et al. (16 October 2009) [Abstract] [Full text] [PDF]
The PRaCTICaL study of nurse led, intensive care follow-up programmes for improving...
Cognitive Function assessment might improve the quality of life in intensive care survivors
19 November 2009
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David John Bowen Thomas,
Consultant Physician
The Hillingdon Hospital NHS Trust ,Uxbridge, Middlesex UB8 3NN

Send response to journal:
Re: Cognitive Function assessment might improve the quality of life in intensive care survivors

The number of survivors on an Intensive Care Unit has increased. However many surviving patients never return to work and close family members experience severe psychological stress. Nurse led intensive care follow up does not make a big difference to outcome up to one year after discharge.

I would like to make some additional comments, because I was admitted to Intensive care following a severe Road Traffic Accident and had subsequent rehabilitative care for six months.

It is now recognised that many patients discharged from intensive have Cognitive Dysfunction which may limit their full potential for recovery. If I might briefly recount some of my experiences. For example, I had forgotten how to play golf and jog, so I could not get fit. I could not remember any of my family. An insight into how I would need to relearn how to do this helped me to evolve a strategy to combat these deficiencies and much else. I would never have gained the insight into my defective cognitive function without the input of a psychologist and therapists. I feel that the all patients discharged from ITU should have the opportunity for psychological assessment, which might help to improve their recovery further.

1 Chapman R, Brett SJ, Cognitive function in intensive care survivors.

Br J Hosp Med 2007;68(9):467-9

2 Thomas DJB. The journey back to effective cognitive function after

injury. A patient perspective. Internationl Journal of Therapy and

Rehabilitation. 2009;16:497-500

Competing interests: None declared

OBSERVATIONS:
The unpalatable truth about ethics committees
Sokol (14 October 2009) [Full text]
The unpalatable truth about ethics committees
The need for evidence based ethics
10 November 2009
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Simon Hatcher,
Senior Lecturer in Psychiatry
University of Auckland, Private Bag 92109, Auckland 1142, New Zealand

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Re: The need for evidence based ethics

Dear Sir

Maybe the reason that ethics review bodies are not used is that they are not seen as particularly useful1. Medical Ethicists justify their role by making claims that knowledge of ethics will help with making difficult decisions. However there are also clinical (what is possible and what is likely to happen) and legal (what society allows you to do) aspects of making difficult decisions. Ethical aspects are often only part of the consideration which goes into making hard decisions. Furthermore I know of no evidence that clinicians make different decisions if they have knowledge of ethics than those who have not had any ethical instruction.

My anecdotal experience of teaching on ethics courses is that clinicians make the same decisions at the start of the course and the end of the course. The difference being that at the end of the course they have a slightly different language to describe the problem. So before we are all subjected to an obscure dialogue on Greek ancients in the name of ethics teaching let’s see some evidence that this knowledge actually makes a difference.

Yours

Dr. Simon Hatcher
Senior Lecturer in Psychiatry, The University of Auckland s.hatcher@auckland.ac.nz

1. Sokol, D. The unpalatable truth about ethics committees. BMJ 2009; 339:b4179 (17 October)

Competing interests: None declared

RESEARCH:
Rate of undesirable events at beginning of academic year: retrospective cohort study
Haller et al. (13 October 2009) [Abstract] [Full text] [PDF]
Rate of undesirable events at beginning of academic year: retrospective cohort study
Doctors’ transitions: critically intensive learning periods
11 November 2009
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Sue Kilminster,
Principal Research Fellow
University of Leeds, leeds LS2 9NL,
Miriam Zukas, and Trudie E. Roberts.

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Re: Doctors’ transitions: critically intensive learning periods

Doctors’ transitions: critically intensive learning periods

Sue Kilminster, Miriam Zukas and Trudie E. Roberts.

In view of recent UK media reporting about the issue of increased incidents occurring when new doctors start their F1 year in August, we were interested to read this paper which demonstrates that there is an increase in undesirable events at the beginning of a transition, regardless of the level of clinical experience (1). This confirms our findings from a recent qualitative study which demonstrated the importance of teams and local environments for doctors’ performance in transitions (2). Hitherto this has been implicitly, but not explicitly, recognised.

We have suggested that every transition involves a critically intense learning period (CILP) in which doctors engage with the specific setting and establish working relationships with doctors and other professionals working in that setting. This CILP can only happen in actual practice; therefore doctors can never be fully prepared in advance of a transition. This conflicts with current ideas about ‘preparedness’ which are dominant in medical education and training. The extent to which the specific learning cultures of the clinical workplace (at ward and at institutional levels) recognise transitions as CILPs contributes to or inhibits the performance of new doctors. This has important implications for the regulation and management of doctors’ performance as they move from one ward to another, from one hospital to another, and from one level of responsibility to another. Understanding and working with the idea of CILPs also has implications for policy, practice and research about doctors’ transitions.

References

1. Haller G, Myles PS, Taffé P, Perneger TV, Wu CL. Rate of undesirable events at beginning of academic year: retrospective cohort study. BMJ 2009;339:b3974. (13 October.)

2. Learning responsibility? Exploring doctors’ transitions to new levels of medical performance (ESRC RES-153-25-0084)

Competing interests: None declared

RESEARCH:
Effect of a multimodal high intensity exercise intervention in cancer patients undergoing chemotherapy: randomised controlled trial
Adamsen et al. (20 October 2009) [Abstract] [Full text] [PDF]
Effect of a multimodal high intensity exercise intervention in cancer patients undergoing...
Why extended follow-up periods are important in non-pharmacological RCT's
11 November 2009
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Niels Henrik Hjollund,
MD, associate professor
Department of Clinical Epidemiology, Aarhus University Hospital, DK-8200 Aarhus N, Denmark,
Karin Biering, and Anne Louise Winther Pape

Send response to journal:
Re: Why extended follow-up periods are important in non-pharmacological RCT's

Adamsen and colleagues reported findings from a non-pharmacological randomised intervention study on cancer related fatigue (1). The intervention consisted of six weeks of supervised physical training. Outcomes were measured both by self administered questionnaires and by physiological measures. All outcomes were recorded just after termination of the intervention. At this point patients in the non-intervention arm were offered the same program. Compared with the randomised controls, patients in the intervention arm showed greater improvement in the areas of fatigue, physically functioning, mental health, and physical capacity. There were no later assessments of outcome, reportedly because nearly 60% of the control group subsequently entered a similar program, terminating its role as a reference group.

A recently updated review from the Cochrane collaboration included nine papers on exercise intervention among breast cancer patients (2). None of the studies followed patients beyond the end of intervention. Another review of 57 randomized trials of exercise and psychological interventions among cancer patients indicated that post-intervention measurements occurred in only 13 studies. None collected follow-up data on physical training (3).

Why is a longer follow-up period important?

This issue is germane for two reasons. First, research on disease- related fatigue, which has increased rapidly during the last decades, suggests that the condition is long-lasting in some individuals (4). However longer-term prognosis remains poorly described. If the aim is to understand the course of fatigue over the long term, sufficient repeat measurements are needed. Second, the nature of self-report and the inability to blind allocation status could produce a significant non-specific placebo effect. This is supported by the review conducted by Kangas et al (3), which reported only slight differences between various exercise or psychological interventions. If this finding is based on a placebo or Hawthorne effect, it is likely to be temporary. Repeat measurements conducted over an adequate time span could resolve this question.

Adamsen et al. argue convincingly that they had to offer all controls the same intervention. We agree. However, extended longitudinal analysis is still warranted in the intervention group, and a separate non- randomised group could be monitored to follow the spontaneous course of symptoms.

A final question concerns why studies of patients suffering from symptoms that are only measurable by self-report include shorter follow-up than studies utilizing classical clinical endpoints. Use of self- administered questionnaires renders an extended follow-up period inexpensive, particularly compared to the resources spent on the intervention itself.

(1) Adamsen L, Quist M, Andersen C, Moller T, Herrstedt J, Kronborg D et al. Effect of a multimodal high intensity exercise intervention in cancer patients undergoing chemotherapy: randomised controlled trial. BMJ 2009; 339:b3410.

(2) Markes M, Brockow T, Resch KL. Exercise for women receiving adjuvant therapy for breast cancer. Cochrane Database Syst Rev 2006;(4):CD005001.

(3) Kangas M, Bovbjerg DH, Montgomery GH. Cancer-related fatigue: a systematic and meta-analytic review of non-pharmacological therapies for cancer patients. Psychol Bull 2008; 134(5):700-741.

(4) Hjollund NH, Andersen JH, Bech P. Assessment of fatigue in chronic disease: a bibliographic study of fatigue measurement scales. Health Qual Life Outcomes 2007; 5:12.

Competing interests: None declared

LETTERS:
Paper or patient safety?
Sandler et al. (12 October 2009) [Full text]
Paper or patient safety?
Effective audit improves patient safety
11 November 2009
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Elizabeth A. Edwards,
FY2 doctor
Eastbourne District General Hospital BN21 2UD,
Dr Luke Hodgson, Dr David Maxwell

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Re: Effective audit improves patient safety

Recently, our department conducted an audit to establish the proportion of acute medical admissions offered appropriate thromboprophylaxis and whether a simple intervention could improve uptake. We looked prospectively at compliance with Government guidelines for acute medical patients. Control and intervention groups were used. The intervention was a sticker attached to drug cards reminding clinicians to prescribe thromboprophylaxis. This audit demonstrated that a simple intervention increased the number of patients given thromboprophylaxis by 6-fold (12% pre-intervention, 71% post-intervention p<0.0001). We aim to change regional drug charts to incorporate the intervention on a permanent basis. Our results show that when conducted effectively, audit can directly enhance patient safety. The writer has made the case that audit work may deflect from time spent with patients. We would argue that Clinical Governance including Audit should be a central pillar of healthcare delivered by medical professionals.

Competing interests: None declared

PRACTICE:
Chest radiographs in pregnancy
O’Connor et al. (9 October 2009) [Full text]
Chest radiographs in pregnancy
Chest Radiographs in Pregnancy - why not?
17 November 2009
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B D McCann,
Consultant Emergency Medicine
Waterford Regional Hospital, Ireland,
Aidan Grufferty, Rabinder Gill

Send response to journal:
Re: Chest Radiographs in Pregnancy - why not?

I read O Connor et al's lesson of the week regarding the importance of doing chest X-rays in pregnancy. They advise: "do not hesitate to perform chest radiography in pregnant patients if they fulfil the criteria". However, in the piece that follows, they fail to mention what these criteria are - unless they intend that the discussion between the referring clinician and the radiologist (as per the Royal College of Radiology - making the best use of clinical radiology services)represents a criterion for imaging? They do point out in the article, that there is no evidence of any risk to mother or baby from the levels of radiation required to achieve a chest film. This begs the following questions:

1. Why is a discussion with a radiologist required?

2. Why does the "decision" to irradiate need to be documented?

3. Why does the patient need to be "fully informed" in particular in this context?

Addressing these questions may serve to continue to promote the "common misconception that pregnant patients should not undergo a chest radiograph". Would it not have been more evidence-based, to advise that with respect to chest X-rays, pregnant women should be assessed and imaged as if they were "non-pregnant".

Competing interests: None declared

OBSERVATIONS:
Live and let die
McLean (7 October 2009) [Full text]
Live and let die
Clear Guidance on Capacity Assessment is Urgently Required
10 November 2009
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Joseph El-Khoury,
Specialty Trainee 6 in Adult Psychiatry
Amersham Hospital, Buckinghamshire, HP7 0JD,
Nicholas Woodthorpe ST6 in Old Age Psychiatry

Send response to journal:
Re: Clear Guidance on Capacity Assessment is Urgently Required

We found Prof McLean’s reflections [1] on the ethical and legal framework that justifies the course of action taken by the doctors involved in the Kerrie Wooltorton case very enlightening. As trainee psychiatrists, we are frequently the first port of call for medical teams or A&E officers confronted with patients objecting to treatment following an act of self harm. These situations are notorious for raising everyone’s anxiety, but as far as we recall tend to resolve themselves through a combination of patience, negotiation and assertiveness on the part of those involved. According to Prof McLean the advance directive is a red herring in the Wooltorton case, and it is the presence or absence of contemporaneous capacity to refuse treatment which deserves scrutiny.

In our view the result of the inquest has wide ranging practical implications. The Mental Capacity Act 2005 states that the assumption of capacity is universal unless proven otherwise. In other words, the purpose of a capacity assessment is to prove incapacity. There are four essential components to this assessment [2]:

1-A person should be able to understand the information relevant to the decision.

2-A person should be able to retain the information relevant to the decision.

3-A person should be able weigh that information as part of the process of making that decision.

4-A person should be able to communicate their decision.

It is the third point that can be mostly contentious and subject to interpretation, specifically in the context of a mental illness and following an act of self harm. Prof McLean recognises the difficulties involved in considering the impact of a ‘depression’ on one’s capacity to ‘weigh’ information objectively. One could argue that depression or an emotional instability, as part of a personality disorder or more acutely following adverse events (receiving bad news , the breakup of a relationship, the effect of an overdose) are states of mind that prevent a rational assessment of the pros and cons of one’s decision. This is only one example of the uncomfortable interface between the Mental Capacity Act 2005 and the Mental Health Act 2007 [3].

The choice faced by the treating physicians in the Wooltorton case is not unusual. Their decision not to treat seems to have derived from a rather narrow interpretation of the third point mentioned above, backed by the coroner and by Prof McLean as apparent in her article. In practice, the majority of doctors would tend to apply the definition in its broadest sense and treat when in doubt, since the consequences of saving a life are at least reversible. The other option would be for Emergency staff but more worryingly for Mental Health Professionals to accept at face value the wish of someone to end their life without challenge, impacting no doubt on the number of completed suicides.

A genuine debate is needed on this issue, and merely falling back on the ethical justification is of limited use in the pressured environment of emergency medicine. We might need to move to a position whereby we accept that an act of suicide can be the fruit of a rational process, but that can only follow from an in-depth review of the philosophy behind our suicide prevention strategy and the resources deployed by mental health services to prevent acts of self harm in the absence of a diagnosable severe and enduring mental illness. As doctors we want to save lives where possible. The dilemna faced by the clinical team involved in the Wooltorton case was undoubtedly an unenviable experience. The conclusions from the inquest do not offer a satisfactory template to be routinely applied by clinicians. In fact it complicates matters further and clear guidance is needed sooner rather than later.

1. British Medical Journal 2009;339:b4112

2. Section 3(1) of the Mental Capacity Act 2005

3. British Medical Journal 2009;339:b4400

Dr Joseph El-Khoury MRCPsych, ST6 in Adult Psychiatry
Dr Nicholas Woodthorpe MRCPsych, ST6 in Old Age Psychiatry

Oxfordshire & Buckinghamshire Mental Health Foundation NHS Trust

Competing interests: None declared

RESEARCH METHODS & REPORTING:
The tyranny of power: is there a better way to calculate sample size?
Bland (6 October 2009) [Full text]
The tyranny of power: is there a better way to calculate sample size?
A different test ?
20 November 2009
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Peter H FITTON,
GP
Lepton surgery, Highgate Lane,Huddersfield HD8 0HH

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Re: A different test ?

Has anyone noticed that this article is exceptionally well written? Not only is is well organised, structured,and argued ; with exactly the right examples in precisely the right places: but the prose is lucid, simple and spare. It is in fact quite beautiful

This may not make it right, but it does make it unusual!

Competing interests: Martin taught me statistics nearly thirty years ago

The tyranny of power: is there a better way to calculate sample size?
Unintended consequences of a boot-strap exercise?
18 November 2009
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Tony H. Reinhardt-Rutland,
Reader in Psychology
University of Ulster, Coleraine BT52 1SA

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Re: Unintended consequences of a boot-strap exercise?

I am an experimental psychologist, so my background will be different to those of most of BMJ's readership. Nonetheless, all researchers in the health/medical areas must know something about statistical power and its relationship with estimating sample size in the process of obtaining project approval.

Estimating sample size no matter what techniques are deemed appropriate is essentially a boot-strap exercise: intending researchers identify published research that is broadly similar to that which they propose to undertake and make the assumption that their proposals will be sufficiently similar to make the estimates meaningful. I have some questions:

(1) Is the exercise meaningful for unexplored research topics with a meagre publication base?

(2) It the answer is no, has there been a bias on the part of assessors and researchers towards well-charted topics?

(3) Have young researchers been unduly channelled towards established areas and perhaps into the large, unwieldy groups that characterise much modern research?

Competing interests: None declared

The tyranny of power: is there a better way to calculate sample size?
Stopping power calculation? Yes, but not at any price.
14 November 2009
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Pierre Charles,
Specialist registrar in Internal Medicine
40 rue Worth, 92150 Suresnes,
Agnes Dechartres

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Re: Stopping power calculation? Yes, but not at any price.

In his article, Bland questions the way sample size is currently determined in clinical trials. Actual clinical trials with a priori determination of an adequate sample size are designed to allow sufficient power to reach significant results. This way of driving clinical research may limit interpretation of trials with potentially valuable treatments which could be rejected because of lack of significance. This conservative attitude could lead to keep on using less effective or potentially harmful treatments.

Moreover, in a recent study[1], we outlined that sample-size calculations in RCTs are inadequately reported, often erroneous, and based on assumptions that are frequently inaccurate. These results let think that neither investigators nor reviewers take the reporting of power calculation very seriously. This situation challenges the scientific credibility of trials in which the sample size calculation is poorly reported and make the methodologists doubtful about sample size determination as currently performed.

We join Bland in his wish to change the way sample size is determined and we agree that using confidence intervals could be one solution. This was already proposed by Goodman in 1994[2] but this has never been used probably because it raises a major issue. Stopping a priori determination of a single primary endpoint could lead to the multiplication of endpoints with selective reporting of the endpoints for which the most favorable results were obtained. We wonder what would be the consequences of commercializing new drugs according to a posteriori selected endpoints.

In conclusion we also claim for stopping power calculation but we think that the price to pay using confidence intervals is too high: if investigators stop reporting a single primary endpoint, the temptation of data dredging will be important.

1. Charles P, Giraudeau B, Dechartres A, Baron G, Ravaud P : Reporting of sample size calculation in randomised controlled trials: review. Bmj 2009; 338 b1732

2. Goodman SN, Berlin JA: The use of predicted confidence intervals when planning experiments and the misuse of power when interpreting results. Ann Intern Med 1994; 121(3): 200-6.

Competing interests: None declared

RESEARCH:
Partial protection of seasonal trivalent inactivated vaccine against novel pandemic influenza A/H1N1 2009: case-control study in Mexico City
Garcia-Garcia et al. (6 October 2009) [Abstract] [Full text] [PDF]
Partial protection of seasonal trivalent inactivated vaccine against novel pandemic...
Authors’ response to Skowronski and colleagues
10 November 2009
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Jose Luis Valdespino-Gómez,
epidemiologist
Laboratorios de Biológicos y Reactivos de México (BIRMEX), Amores 1240, CP 03100, D.F., Mexico,
Lourdes Garcia-Garcia

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Re: Authors’ response to Skowronski and colleagues

Authors’ response to Skowronski and colleagues

The letter by Skowronski and colleagues[1] questions the effectiveness of seasonal vaccine against pandemic A/H1N1 influenza that we observed in our study. As we mentioned in the article the estimates for vaccine effectiveness could be inflated owing to a high prevalence of chronic conditions and vaccination in our control population. The vaccine effectiveness against laboratory confirmed cases of influenza A/H1N1 described in our study was of 73% (95% confidence interval 34% to 89%). Confidence intervals are wide and similar to confidence intervals of effectiveness that has been described when seasonal influenza vaccine strains are not antigenically well matched to circulating endemic strains: [50% (95% CI 27% to 65%)] among healthy adults and [36% (95% CI 24% to 46%)] among healthy children.[2,3] Available information regarding effectiveness provided by seasonal vaccines for pandemic strains indicates some level of protection against antigenically differing influenza strains occurring in epidemics.[4-6] Therefore we consider it is highly probable that the effectiveness we observed in our study is real.

We do not agree with the comment of Skowronski and colleagues that cases and controls emerged from different source populations. Both cases and controls came from the population that is served by the study hospital and we ensured that our study group resided in the same geographical area (Mexico City and the State of Mexico) which had the majority of notifications for influenza during the study period. Therefore the controls had the same probability of being exposed to infective individuals as cases. Both cases and controls were patients who requested medical care during the study period. Although the study hospital is a specialty hospital, a considerable proportion of its patient population is not referred as the referral system is poor. Differences between cases and controls regarding underlying chronic diseases are explained by the characteristics of the patient population that requests clinical care at the study hospital that includes both patients with acute (many of which occur among previously healthy individuals) and chronic respiratory diseases.

Figures for vaccine coverage are limited nationwide. National estimates for vaccination coverage are only available for certain age groups (6-35 months, children aged 3-9 years, and adults older than 50) and not for young people and adults aged 10-49.[7] This is the reason that led us to model the association between vaccine status and influenza A/H1N1 for each age group. Therefore we do not agree with the comparison between observed prevalence of seasonal vaccination among influenza cases occurring in a specialty hospital in Mexico City in our study and the estimation of national coverage made by Skowronski and colleagues.

Regarding timing of recruitment in relation to immunization, for both cases and controls we investigated trivalent inactivated influenza vaccination for the 2008-9 winter season (October 2008 through February 2009). If the vaccine was administered before or after this season, we considered that he/she had not been vaccinated during the 2008-9 winter season. We agree with Skowronski and colleagues that one of the limitations of the study was that we investigated seasonal vaccination by face to face or telephone interview of the patients or close relatives. Trained staff used a standardised format to reduce the bias associated with vaccine status. We differentiated if the interviewed person was informed or not regarding vaccine status.

We agree that age is an important confounder. Thus we frequency matched our study by age and socioeconomic status (as an indicator of access to health services). We re-analyzed our results by unconditional logistic regression including the matching variables in the model. Adjusted odds ratio (aOR) and estimation of effectiveness did not differ from those published: aOR of 0.26 (95% CI 0.10 to 0.65) and effectiveness of 74% (95% CI 35% to 90%) by unconditional logistic regression as compared to 0.27 (0.11 to 0.66) and vaccine effectiveness of 73% (95% CI 34% to 89%) in our published study.

We consider that although our study provides preliminary evidence of a protective effect of seasonal vaccination against influenza A/H1N1 virus, it is prone to limitations due to small sample size and the retrospective study design. Therefore, similar studies in other settings are needed to confirm or refute our results.

Submitted by Lourdes Garcia-Garcia, MD, DrSc Instituto Nacional de Salud Pública, Cuernavaca, Mor, Mexico

Jose Luis Valdespino-Gómez, MD, MPH Laboratorios de Biológicos y Reactivos de México (BIRMEX), Distrito Federal, Mexico

References

1. Janjua N, Skowronski D, Hottes T, Serres G, Crowcroft N. Conspicuous selection bias is the likeliest explanation for findings of seasonal vaccine protection against pandemic H1N1 in Mexico City. British Medical Journal 2009;339:b3928.

2. Demicheli V, Di Pietrantonj C, Jefferson T, Rivetti A, Rivetti D. Vaccines for preventing influenza in healthy adults. Cochrane Database of Systematic Reviews 2007, Issue 2. Art. No.: CD001269. DOI: 10.1002/14651858.CD001269.pub3.

3. Jefferson T, Rivetti A, Harnden A, Di Pietrantonj C, Demicheli V. Vaccines for preventing influenza in healthy children. Cochrane Database of Systematic Reviews 2008, Issue 2. Art. No.: CD004879. DOI: 10.1002/14651858.CD004879.pub3.

4. Mogabgab WJ, Leiderman E. Immunogenicity of 1967 polyvalent and 1968 Hong Kong influenza vaccines. Jama 1970;211:1672-6.

5. Tumpey TM, Garcia-Sastre A, Taubenberger JK, Palese P, Swayne DE, Basler CF. Pathogenicity and immunogenicity of influenza viruses with genes from the 1918 pandemic virus. Proc Natl Acad Sci U S A 2004;101:3166 -71.

6. Serum cross-reactive antibody response to a novel influenza A (H1N1) virus after vaccination with seasonal influenza vaccine. MMWR Morb Mortal Wkly Rep 2009;58:521-4.

7. Centro Nacional para la Salud de la Infancia y la Adolescencia. Logro de metas del Programa de vacunación anti-influenza 2008-2009. Centro Nacional para la Salud de la Infancia y la Adolescencia. Secretaría de Salud. México.

Competing interests: JLV-G is employed by Laboratorios de Biológicos y Reactivos de México (BIRMEX)

EDITOR'S CHOICE:
The power of stories
Groves (20 November 2009) [Full text]
The power of stories
If thought corrupts language, language can also corrupt thought.
20 November 2009
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BM Hegde,
Editor in Chief, Journal of the Science of Healing Outcomes
Mangalore-575004

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Re: If thought corrupts language, language can also corrupt thought.

Dear Trish Groves,

Robert McKee, the world renowned writer and the author of the famous book “Story”, who runs one of the most successful story telling seminars in the world, writing on the power of story telling, has this to say. “As children we were naturally good at telling stories about events or topics that mattered and learning from others via their stories, but as we became older we were taught that serious people relied only on presenting information and "the facts." Accurate information, sound logic, and the facts are necessary, of course, but truly effective leaders in any field — including technical ones — know how to tell "the story" of their particular research endeavor, technological quest, or marketing plan, etc.

There are very few people talking about the importance of storytelling these days. I am happy that BMJ started it for adults and serious doctors! Good luck. If we want the readers to enjoy medical research we better find a story telling method in place of the usual statistical IMRAD (introduction, materials, results and discussion). More doctors will then enjoy reading the BMJ to improve their standard of patient care.

Yours ever, bmhegde

Competing interests: None declared

NEWS:
Poor care in hospital is delaying discharge of patients with dementia, charity says
Kmietowicz (18 November 2009) [Full text]
Poor care in hospital is delaying discharge of patients with dementia, charity says
Sound findings but confusing statistics
20 November 2009
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David E Stewart,
FY2 Public Health
NHS Walsall Public Health Department, Jubilee House, Bloxwich Lane, Walsall WS2 7JL

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Re: Sound findings but confusing statistics

Dear Editor,

I read with interest the Alzheimer's society report regarding dementia. While its premise and conclusions seem sound, its use of statistics seems confusing.

The Executive Summary states that "Over a third of people with dementia who go into hospital from living in their own homes are discharged to a care home setting". From the data provided, this figure could be closer to a sixth.

In the full report, Table 5 shows a reduction in those in their own home from a pre-hosptial 60%, to post-hospital 36%, giving us "over a third". However, we see that a total of 33% of patients admitted to hospital come from a care home, and on discharge 42% now reside there - an increase of just 9% residing in a care home overall, representing a sixth of those previously in their own homes. A total of 6% return to “other” and 9% “not applicable”, with the latter group consisting of those who have not been discharged, or have died while an inpatient. A number of those previously in a care home would fall into these categories, however it does not seem likely to fully explain the discrepancy.

Competing interests: None declared

Poor care in hospital is delaying discharge of patients with dementia, charity says
Caring for patients with Dementia
19 November 2009
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Reza Aghamohammadzadeh,
Clinical Research Fellow
Cardiovascular Research Group, Core Technology Facility, Manchester, M13 9NT

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Re: Caring for patients with Dementia

Dear Editor,

The Alzheimer Society’s report has documented what all clinicians, nurses and allied healthcare professionals have known for years.

During my years as a junior doctor, I have looked after many patients with dementia and have witnessed some of the difficulties in caring for their medical and nursing needs. This is understandable to a certain degree as some of it is the unavoidable consequence of the patients’ less- than-optimal co-operation with hospital staff.

Hospital clinicians have always strived to offer the best quality of care under the watchful eyes of hospital bed managers. I can think of two ways in which the care of patients with dementia has improved (in my experience):

a) The report suggests a lot of the admissions are with fractures after falls. These patients are transferred to orthopaedic wards under the care of surgeons. They are likely to have a variety of medical problems (similar to other patients in the same age group). In severe dementia, the patients are unable to communicate their issues effectively. Despite the surgeons’ best efforts, there exists a real need for a general medical doctor or a Geriatrician to address the medical issues of the patients and to help expedite their successful discharge. The models where regular medical ward rounds take place on orthopaedic wards are the obvious solution. There are also units where the orthopaedic patients are admitted under the medical team and the orthopaedic surgeons only deal with the fracture which in my opinion is in the patients’ best interests.
b) Many Geriatricians regularly visit nursing homes and review patients before they deteriorate to a level that would require extended hospital admissions. Extending this service across the country would go a long way to improve the care of patients with dementia, but it has its own cost and logistical implications.

The suggestion of a clinician (Geriatrician) to take the leading role of organising the care for patients with dementia (rather than a non- medical manager) would, in my opinion, be in the patients’ best interest.

Competing interests: None declared

Poor care in hospital is delaying discharge of patients with dementia, charity says
Poor care of patients with dementia: Root Causes
19 November 2009
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Bamidele Omotosho,
CMT1
Queen Elizabeth Hospital, King's Lynn. PE30 4ET

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Re: Poor care of patients with dementia: Root Causes

It is so easy to say that the care of patients with dementia is suboptimal. Even with the increased media focus on this patient group over the last few years, it is amazing how very little has changed. There are some fundamental issues that need to be addressed before any significant progress can be made.

The care of patient with dementia is undoubtedly very challenging and it also very variable depending on the severity of dementia.

The staffing levels on most elderly care wards are poor. We need to be honest with ourselves. Most junior doctors witness this everyday for example a nurse covering two or three bays, waiting for tests requested weeks before and the list goes on. Nurses are stretched to the limit most of the time, so it is almost impossible to deliver the patient centred care that these patients require. I am not saying more staff necessarily equates to better care but it is usually a step in the right direction for some hospitals.

The introduction of the EWTD has made things worse. Doctors have to do more cross cover and hand-overs due to the new EWTD compatible rotas. With more hand-overs, likelihood of delay in discharge is greater. Given that the number of patients with dementia will double over the next 20 years, the government really needs to reconsider EWTD.

I agree that we need improved training of health care staff (hospital and community), definitive care pathway and introduction of specialist liaison teams. Even with all these in place, it still will not solve the problem.

The uncomfortable truth is that the government can not solve all problems. With all the media hype about care in hospitals, there is very little mention about the crucial role for family members. I personally think this is the single most important factor that people should focus on.

Health care staff are not miracle workers. To place such an expectation on doctors and nurses in the current NHS system is not fair. Family members should be more involved in the care of their relatives. One thing I have observed throughout my medical training is how lonely and poorly supported patients with dementia are (both in hospital and community). The mental health of patients with dementia significantly impacts their rehabilitation potential, family members have a huge role to play here. It is not just up doctors and nurses.

Competing interests: None declared

EDITORIALS:
Is primary care research a lost cause?
Mar (18 November 2009) [Full text]
Is primary care research a lost cause?
Neglected virgin areas in primary health care basic and applied research.
20 November 2009
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Rodolfo J. Stusser,
Freelance PHC GFM Research Consultant (Retired from MINSAP), International Member of AAFP & NAPCRG.
Primary Care e-Research Collaboration Center http://havanacenter.familydoctors.net Havana, Cuba.

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Re: Neglected virgin areas in primary health care basic and applied research.

I agree with Del Mar's crucial and valiant editorial that primary health care (PHC) researchers need to know what to research in general family medicine (GFM),[1] when in the last 64 years all the classified diseases have progressively become handled and focused in depth by vertical hospital and lab specialists.

Coming from cardiovascular and cancer research centers to PHC, I have been working, studying and reflecting in my last 20 years on a GFM own agenda,[2] and think that on the basis of an integration philosophy of science, I can suggest some more exclusive areas for the generalist researcher.

The great influence of the specialist researcher's fragmentation philosophy on PHC GFM has meant that generalist researchers have lost focus on the possibility of research in at least three neglected virgin basic and applied areas, impossible to be approached by any specialists. These are as follows:

1) Founding a Science of Multi-System Connectedness.

2) Developing a Unified Primary Living and Health Care System.

3) Creating a Lifelong Health Maintenance Semiology-Nosology.

Strangely, recently discussed very interesting and basic science information and models--at similar top levels to those of bio-molecular labs--argue that community-oriented PHC GFM is the only horizontal specialty capable of connecting the patient parts and the wholes, going in depth in the systems hierarchy (levels of organization) or holarchy of health care, through the pyramid of healing and transcendence, prioritized care, integrated care, and fundamental health care.[3]

Hollnagel and Malterud discussed 9 years ago that Paul Backer in 1977 defined the 'health equation' as a formula weighing the balance between the patient's strains and resources. Reading the health equation, the generalist can understand why a person becomes sick when his strains are larger than his resources if he is not able to restore the balance by reducing the strains or increasing resources. According to this model, the generalist's task is to assist people in restoring the balance, not only by decreasing the negative points, but also to strengthen the positive ones.[4] Of course, the strains and resources should be both internally perceived by the patient and externally observed by the generalist.

I think that great devotion from Graunt to Cullen's classification and nosology philosophies, has stagnated the classifications family up to ICD-10, ICPC 2, and ICF, as well as the health status assessment instruments supported by WHO, WONCA and NAPCRG.[5] Most of them, still are only negative-health dependent, static-discrete, independent of positive-health resources, outside Leavell and Clark's dynamic-continuous view for GFM health promotion and disease-disability preventive levels.

Thank you.

1. Del Mar C. Is primary care research a lost cause? BMJ 2009;339:b4810. http://www.bmj.com/cgi/content/full/339/nov18_2/b4810

2. Stusser RJ. The creation of family medicine new research spaces. Havana: Plaza Community Polyclinic, 1996. http://rational.fortunecity.com/artfam2.html

3. Stange KC. A science of connectedness. Ann Fam Med 2009;7:387-395. http://www.annfammed.org/cgi/content/full/7/5/387

4. Hollnagel H, Malterud K. From risk factors to health resources in medical practice. Med Health Care Philos. 2000;3(3):257-64. http://www.springerlink.com/content/q4230jv133361x3p/

5. Salomon JA, Mathers CD, Chatterji S, Sadana R, Ustun TB, Murray CJL. Quantifying individual levels of health: definitions, concepts and measurement issues. In: Murray & Evans. eds. Health systems performance assessment: debates, methods and empiricism. Geneva: World Health Organization 2003, 301-318.

Competing interests: None declared

NEWS:
Hospitals are criticised for yielding to pressure over human rights lecture
Dyer (17 November 2009) [Full text]
Hospitals are criticised for yielding to pressure over human rights lecture
Pressures on UK medical institutions regarding coverage of Israel-Palestine
20 November 2009
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derek a summerfield,
Hon Sen Lect, Institute of Psychiatry
Maudsley Hospital, London SE5 8BB

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Re: Pressures on UK medical institutions regarding coverage of Israel-Palestine

Your report on the 2 UK hospitals sufficiently pressurised by Zionist groups into cancelling a human rights lecture by Physicians for Human Rights-Israel (PHRI), recalls my own experience, also reported in the BMJ .(1) In 2007 pro-Israel doctors threatened the Royal Society of Medicine, no less, that they would challenge the constitution of the RSM as a charity if my participation in a forthcoming conference, arranged months before, was not cancelled. At one point the RSM asked me to withdraw in order to save the conference.

I do not know if protesters were aware that the Israeli Medical Association recently declared that they were severing all ties with PHRI on the grounds that their activities were encouraging "anti-Israeli attitudes" abroad. I regard PHRI as currently unsurpassed anywhere in relation to the combination of their hands-on clinical work with their principled humanitarian witness. They have compiled a telling archive of reports about violations of the Fourth Geneva Convention and of international medical ethical codes by Israel in the Occupied Territories.

The harrassment of these 2 UK hospitals smacks of McCarthyism. Similar pressures have for years been applied to the editors of medical journals in UK regarding their coverage of Israel-Palestine. We are meant to be in the era of evidence-based medicine, yet where Israel-Palestine is concerned we encounter efforts to prevent its presentation in the first place. Indeed there is a refusal even to consider as admissible evidence which in other settings would be judged decisive and begging urgent attention: witness the reception currently being afforded the Goldstone report on war crimes during the assault on Gaza.

1 .Summerfield D. Royal Society of Medicine under attack by pro- Israel doctors. BMJ 2007;335:842.

Competing interests: 17 years involvement in human rights in Israel-Palestine

Hospitals are criticised for yielding to pressure over human rights lecture
Silencing debate is unhealthy
19 November 2009
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Nadeem Z Jilani,
Consultant Paediatrician
Pennine Acute Hospitals NHS Trust, M8 5RB

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Re: Silencing debate is unhealthy

Sir, It is a matter of great concern that healthcare professionals are stopped from discussing issues related to healthcare from around the globe due to interference from lobby groups. I was fortunate enough to attend one of the talks that went ahead at Fairfield Hospital, thanks to a principled stand taken by its Chief Executive, Mr. John Saxby. It was a well attended meeting where the lady speaker from Physicians for Human Rights Israel (PHRI) informed the audience about the pathetic health situation in the occupied territories. She gave a first hand account of the situation detailing the lack of equipments and medicines in the hospitals and hardships faced by ordinary Palestinians to get appropriate health care. She also cited many examples where right to health of Palestinians was disregarded by Israeli authorities. Her talk was supported by data, figures and references without any political overtones. I was astonished when I heard that management at Manchester Royal Infirmary and Alder Hey Children's Hospital gave in to outside interference to cancel the event at the last minute. What a shame!

Competing interests: None declared

Hospitals are criticised for yielding to pressure over human rights lecture
Hospitals are criticised for yielding to pressure over human rights lecture
19 November 2009
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Judith Emanuel,
Public Health worker
M16 9rh

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Re: Hospitals are criticised for yielding to pressure over human rights lecture

Re: Hospitals are criticised for yielding to pressure over human rights lecture

I attended the Physicians for Human Rights meeting which should have been held at Manchester Royal Infirmary. I am a public health practitioner, Jewish, not ‘anti-Israel’ but concerned about my right to be informed about global human rights issues. I see this as important as a global citizen but also professionally. Conflict has an enormous health cost and what is happening in the Middle East has a relationship with what happens here as well.

I was deeply shocked that the booked meeting venue was cancelled at short notice due to pressure from Zionist Council. In the venue where the meeting was held, there was no disturbance inside or outside the venues Miri Weingarten’s presentation was a first class, evidence based analysis of what is happening. I can understand that the Chief Executive was forced to make a rapid decision with insufficient time for this to be fully informed. I had hoped to see signs of learning (and still do) from MRI from this unfortunate incident. Otherwise, its reputation as a centre for learning will be undermined. Controversial issues are not unusual in relation to health, a world class service should be able to ensure open debate of all threats to health and health care.

Judith Emanuel In a personal capacity

Competing interests: None declared

Hospitals are criticised for yielding to pressure over human rights lecture
Paranoia about the truth
19 November 2009
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Christopher J Burns-Cox,
Consultant Physician
Southend Farm,Wotton-under-Edge,
GLOS GL12 7PB

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Re: Paranoia about the truth

You report that the Central Zionist Council led to the cancellation of two booked Lectures by Physicans For Human Rights Israel. Congratulations to those who organised and gave the lectures albeit in alternative venues.

The managers who denied the right for staff to hear the lecture in NHS Meetings rooms about healthcare in disaster areas, should be questioned about why they cancelled the lectures. This was extremely discourteous and I hope they have since apologised to the speaker.

Competing interests: None declared

Hospitals are criticised for yielding to pressure over human rights lecture
Correction
18 November 2009
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Clare Dyer,
Legal correspondent
BMJ

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Re: Correction

I should like to correct my statement that Dr Khan organised Miri Weingarten's lecture tour. He organised only the lectures at Manchester Royal Infirmary and Fairfield Hospital.

Competing interests: None declared

NEWS:
Patents on breast cancer genes are illegal and stymie research, say scientists
Lenzer (17 November 2009) [Full text]
Patents on breast cancer genes are illegal and stymie research, say scientists
Claims and uses are the real problem, not patenting
20 November 2009
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Robert M Cook-Deegan,
Research professor
Duke University

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Re: Claims and uses are the real problem, not patenting

It is great that BMJ is covering the US lawsuit over BRCA gene patents, as it is an important case no matter how it turns out.

I did want to clarify my statement. I am pretty sure Myriad did find some DNA molecules that were new, useful and not obvious, and therefore patentable. I think some of the *claims* in their patents are broader than what they had found, however, and should not have been granted in the form they were.

I also believe that many of the problems the plaintiffs in the suit raise are indeed caused by restrictive practices, and could be eliminated without litigation or change of law if Myriad merely had formal policies that permitted verification testing, basic and clinical research, clarified reimbursement and payment, and if they collaborated with some of the breast cancer constituencies they have alienated.

Competing interests: Our Duke team did analysis of how patenting and licensing affect clinical access to genetic testing for the Secretary's Advisory Committee for Genetics, Health and Society, US Department of Health and Human Services

VIEWS & REVIEWS:
Politics, science, and the White House
Smith (17 November 2009) [Full text]
Politics, science, and the White House
Harold Varmus and The Art of Politics and Science
20 November 2009
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Felix ID Konotey-Ahulu,
Kwegyir Aggrey Distinguished Professor of HumanGenetics, University of Cape Coast, Ghana
Consultant Physician Genetic Counsellor Sickle/Haemoglobinopathies, 10 Harley St, London W1G9PF

Send response to journal:
Re: Harold Varmus and The Art of Politics and Science

Harold Varmus and The Art of Politics and Science

Excellent international Editors, past and present, medical and non- medical, have a way of making much of what they write encourage people, politicians, and others to some kind of action. The action that Dr Richard Smith, immediate past editor of the British Medical Journal by his article (17 November) on Nobel Laureate Harold Varmus [1] encouraged me to take, was to rush to Amazon and buy a copy of the latter’s book [2].

FOUR THINGS THAT ATTRACTED MY ATTENTION

First, Harold Varmus is said to have “worked in a mission hospital in Uttar Pradesh as a medical student” [1]. I must read more about that. Is he a Christian I wonder? I am keen to find out. Next, he is on the WHO Commission on Macroeconomics on Health [1]. I wonder what they do. Does that mean they make sure the European Union does not put a ban on our raw materials, or/and that the USA does not dump rice at heavily subsidized prices on African markets making our farmers broke, and leading to further poverty? I am keen to know.

Thirdly, the interest in Global Health of Harold Varmus stems from “a longstanding concern about disadvantages between rich and poor” [1]. He certainly would have seen poverty in India’s Uttar Pradesh, and I am keen to read what he describes about poverty. Fourthly, and this thrills me to bits, Varmus has “a passion for open access publishing” [1]. Gone (or nearly gone) are the days when powerful Editors decide whom they will publish and whom not. If you discover something that has not been known about before, and the thing comes from your own little tribe somewhere in Africa, the powerful Editors in Europe look round their little domain for “Experts” to check on what you have offered them. Of course they find none, so they reject your paper with some very kind words like “We hope some other journal publishes it soon for you”.

No kidding, this has happened to me and not a few others. Prove me wrong by just GOOGLE-ing the words “Mid Pitch Arrest” or “Three Semitone Gap” and find whose name comes up. This discovery of mine in Tonal Linguistics with a medical dimension in Glosso-genetics was sent to the two front runners in international medical journalism, but neither was interested, only for Open Access Publishing to send it out to the world [3, 4]. To hear that Harold Varmus had something to do with this open access publishing endeavour, and that Dr Richard Smith is also ‘related’ to Public Library of Science (PLoS) gladdens my heart. I am keen to read more from the book [2].

SCIENTIFIC ADVISOR TO PRESIDENT BARACK OBAMA

Here comes the fourth reason which makes me want to read the book: For appointing this man, Harold Varmus, his “scientific advisor” [1] President Barack Obama has confirmed my very high estimation of his good judgment. New African, the widely read London based international monthly published 21 comments from all over the world in a special SOUVENIR ISSUE on the election of Senator Barack Obama as the 44th President of the United States of America. I was hugely flattered when I found my comments alongside those of President Nelson Mandela, Dr Kofi Annan, and Prime Minister Gordon Brown [5, page 22]. The last sentence of my long comment capsulated what I perceived Barack Obama was capable of – “For my part, with my enormous interest in history, placing that subject above even medical science, I make bold to say this: It is not at all hyperbolic of me to prognosticate that, God preserving him, President Obama will one day find himself the recipient of two Nobel Prizes, one for literature and the other for peace” [5, page 23]. I said that in December 2008. Within 10 months Barack Obama got one Nobel Prize, and during that time his perspicacity led him to appoint Harold Varmus his Scientific Advisor.

MY NEXT WISH IS FOR THEM TO HELP TACKLE GENETIC COUNSELLING

My next wish is for ‘Global Health’ to spare a thought for Genetic Counselling and Voluntary Family Size Limitation (GCVFSL). One in 3 of us healthy Ghanaians are walking about with a beta-globin gene trait (NORMACHE), so 1 in every 9 matings between man and wife (as in the case of my own NORMACHE parents) is a union that results in increasing the genetic disease load (ACHEACHE) thereby dragging down Global health [6]. The reason I feel none of Bill Gates Global Health money has trickled down to tackling this genetic public health time bomb is because Family Planning is an extremely sensitive subject capable of being properly handled only by the natives themselves [7, 8]. I sincerely hope Richard Smith will, please, speak to Professor Harold Varmus to, please, speak to President Barack Obama, to help us tackle in our own way, using our own methods, with all the Ethical Sensitivity required, Genetic Counseling and Voluntary Family Size Limitation (GCVFSL) both in the USA, and in Africa, not to mention the needs of hundreds of thousands of at risk families in the United Kingdom and Europe.

Felix I D Konotey-Ahulu MD(Lond) FRCP(Lond) DTMH(L’pool) FGA, Order of The Volta. Kwegyir Aggrey Distinguished Professor of Human Genetics, University of Cape Coast Ghana, and Consultant Physician Genetic Counsellor in Sickle & Other Haemoglobinopathies, 10 Harley Street, London W1G 9PF

felix@konotey-ahulu.com

Competing interests: None declared

1 Smith Richard. Politics, science, and the White House. BMJ 2009; 339: b4848 doi: 10. 1136/bmj.b4848 http://www.bmj.com/cgi/content/full/339/nov17_3/b4848

2 Varmus Harold. The Art of Politics and Science. ISBN 798- 0393061284 W W Norton & Co, 315 pages. 2009.

3 Konotey-Ahulu FID. Social pathology of cleft palate in the African: Mathematical precision of pitch gaps in tribal tonal linguistics. Ghana Medical Journal 2008; 42: 89-91. http://www.ghanamedicalassociation.org/Journal/June%202008/Social%20Pathology%20Cleft%20palate.pdf http://www.pubmedcentral.nih.gov.articlerender.fcgi?artid=2631266

4 Konotey-Ahulu FID. The Remarkable African Ear: Phenomenon of Mid Pitch Arrest in Krobo-Dangme/Gã Tonal Languages of South East Ghana. African American Museum of Philadelphia (AAMP) Award Lecture May 5 2007 http://blog.konotey-ahulu.com/blog_archives/2007/5/5/301434.html

5 Konotey-Ahulu FID. World Rejoices. New African. Dec. 2008 (No 479), pp 22-23 http://www.exacteditions.com/exact/browsePages.do?issue=4520&size=1&pageLabel=23

6 Ringelhann B, Konotey-Ahulu FID. Hemoglobinopathies and thalassemias in Mediterranean areas and in West Africa: Historical and other perspectives 1910 to 1997 – A Century Review. Atti dell’Accademia dell Science di Ferrera (Milan) 1998; 74: 267-307.

7 Konotey-Ahulu FID. Sickle Cell Disease: The Case for Family Planning. ASTAB Books, Ltd 1973; 32 pages

8 Konotey-Ahulu FID. Need for ethnic experts to tackle genetic public health. Lancet 2007; 370: 1836 doi: 10. 1016/50140-6736(07)6177- 1 http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(07)61771- 1/fulltext

Competing interests: None declared

NEWS:
Poor service provision is blamed for overuse of antipsychotics in dementia patients
Mashta (17 November 2009) [Full text]
Poor service provision is blamed for overuse of antipsychotics in dementia patients
Antipsychotic treatment for dementia may now constitute 'serious medical treatment' under the Mental Capacity Act 2005
18 November 2009
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Tim Branton,
Consultant Psychiatrist, Psychiatry of Old Age, AMD for Mental Health Legislation
The Mount, 44 Hyde Terrace Leeds LS2 9LN,
Nick Brindle Consultant Psychiatrist, Tony Zigmond, Consultant Psychiatrist

Send response to journal:
Re: Antipsychotic treatment for dementia may now constitute 'serious medical treatment' under the Mental Capacity Act 2005

We welcome Professor Sube Banerjee's recent publication of his report (1) for the Minister of State for Care Services which draws attention to the risks associated with the use of antipsychotic drugs in the management of Behavioural and Psychotic Symptoms in Dementia (BPSD).

We are surprised that the report and the Government's response(2) make no reference to the Mental Capacity Act 2005(3) and its associated Code of Practice(4) . We presume most patients with dementia who are prescribed antipsychotic medication for BPSD will have been assessed as lacking capacity to make this treatment choice. The Mental Capacity Act provides the legal authority for those who act in connection with treatment and care for those who lack capacity to make decisions about their care. In order for such treatment to be lawful, the staff responsible for its administration (the prescriber and the carer giving the medication) must have a 'reasonable belief' that they are acting in the patient's best interests. Section 4 of the Act sets out who must be consulted and what factors should be taken into account when deciding on best interests (further guidance being given in the Code).

The latest evidence suggests the prescription of anti-psychotic medication for these patients may fall within the remit of section 37 MCA Serious Medical Treatment (what is proposed is likely to have serious consequences for the patient. 'Serious consequences' are those which could have a serious impact on the patient, either from the effects of the treatment itself or its wider implications. An Independent Mental Capacity Advocate must be instructed, and then consulted, for people lacking capacity who have no-one else to support them (other than paid staff), whenever an NHS body is proposing to provide serious medical treatment.

Prescribers clearly need to adhere to a framework of assessment, consultation, prescribing and review to demonstrate that medical treatment for BPSD is in a patient's best interests and therefore lawful.

We hope that the scientific and ethical arguments, along with the legal requirements, will ensure prescribers and carers review the appropriate management of these marginalised and vulnerable patients.

1 Banerjee S (2009) The use of antipsychotic medication for people with dementia: Time for action. A report for the Minister of State for Care Services Department of Health: London

2 Department of Health (2009) Government response to Professor Sube Banerjee's report on the prescribing of anti-psychotic drugs to people with dementia. Department of Health: London

3 2005 c.9

4 Department for Constitutional Affairs (2007) Mental Capacity Act 2005 Code of Practice. London: TSO

Competing interests: None declared

Poor service provision is blamed for overuse of antipsychotics in dementia patients
Beware of antipsychotics in the elderly
18 November 2009
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Hugh Mann,
Physician
Eagle Rock, MO 65641 USA

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Re: Beware of antipsychotics in the elderly

Due to their frailty, isolation, and loneliness, the elderly have increased needs for sympathy, support, and reassurance. Sadly, it’s all too easy to disregard these needs by silencing the elderly with antipsychotics. This practice is not only unethical but also dangerous and should be stopped. Hospital administrators, medical directors, nursing supervisors, pharmacists, and family should be alert to this all-too-common scenario and intervene when necessary. The elderly need many advocates, and we can all function on their behalf.

Competing interests: None declared

NEWS:
Australia operates "closed shop" to restrict doctors from overseas, say critics
Sweet (16 November 2009) [Full text]
Australia operates "closed shop" to restrict doctors from overseas, say critics
Great Barriers
19 November 2009
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William McGuire,
Professor of Child Health
HYMS, University of York, YO10 5DD

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Re: Great Barriers

Despite being an "area of need" with doctor shortages across all specialities, Canberra may be worse than most other Australian cities with regard to practice restrictions. The Australian Capital Territory Medical Board makes no effort to support overseas trained doctors to negotiate the expensive, complex and lengthy processes to gain practice rights.

After three years working in Canberra, having been recruited from the UK to posts in shortage specialities (paediatrics and general practice), we gave up fighting the system and left. Every time we thought we'd got there, the goal posts were moved. Moving to Canberra just isn't worth the uncertainty and stress.

Yours

William McGuire, Veronica McKay

Competing interests: None declared

RESEARCH:
Concept of unbearable suffering in context of ungranted requests for euthanasia: qualitative interviews with patients and physicians
Pasman et al. (16 November 2009) [Abstract] [Full text] [PDF]
Concept of unbearable suffering in context of ungranted requests for euthanasia:...
The difficulties of subjective suffering
19 November 2009
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Emma Phillips,
FY2 doctor, Psychiatry
Wotton Lawn Hospital, Gloucester

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Re: The difficulties of subjective suffering

At last some sensible research in the never-ending and subjective debate into euthanasia and end of life care. I was pleased to see that they have considered the idea of 'unbearable suffering' in some detail.

I think that as doctors we so often focus on 'sanctity of life' above all other concepts and are sometimes keen to pursue treatements beyond all hope of cure. It is not surprising, given our training and the pervasive public view that the aim of medical treatment is to prolong life at all cost. Recent articles have talked about how poor doctors are at discussing 'do not resuscitate' decisions; we are worse yet still at promoting 'good' deaths- a comfortable end to life.

This research coming out of the Netherlands, which allows euthanasia under strict regulations, shows us how difficult it is to make these decisions appropriately. They focussed on 'unbearable suffering', probably the most subjective decision the doctors have to make when deciding whether to allow or refuse euthanasia. It was clear from their cases that patients and physicians often have quite differing views on what constituted 'unbearable suffering', with doctors quite naturally focussing on physical issues including pain, whereas patients most often considered loss of dignity, independence and 'not being needed any more' as more important than physical issues.

Medical student curricula nowadays have a much heavier weighting towards 'holistic' care and the psychosocial aspects of medicine than was previously the case, however it is apparent that doctors remain poor at actually applying many of these issues in practice.

In the UK, euthanasia remains illegal. We can however apply many of the principles of this research to end of life care for our patients with chronic illnesses, particularly those which lead to a marked loss of independence such as stroke and Parkinson's disease; at least trying to discuss these issues with them and see what can be done to alleviate any distress they may have. When we are considering patients who are 'approaching death', although far from perfect, doctors are improving at implementing end of life care pathways, which allow death free from pain. Perhaps when we start to implement these pathways, we can begin to consider issues other than pain which our patients might be experiencing and what other problems our patients might consider to constitute 'unbearable suffering'.

Competing interests: None declared

NEWS:
WHO recommends early antiviral treatment for at risk groups with suspected swine flu
Zarocostas (13 November 2009) [Full text]
WHO recommends early antiviral treatment for at risk groups with suspected swine...
Does early antiviral treatment give a false sense of protection
15 November 2009
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Dr Irugal bandara Dissanayake,
Physician Trainee
Sri Lanka 71000

Send response to journal:
Re: Does early antiviral treatment give a false sense of protection

The WHO's recommendation regarding early antiviral treatment may be commended by many. But as a matter of fact if someone asked for it what are the circumstances under which health authorities could refuse it? Prevention is better than cure may be that individual's motto!

Competing interests: None declared

VIEWS & REVIEWS:
Dr Doom
Spence (12 November 2009) [Full text]
Dr Doom
Re: Re: Re: Re: Re: This will hurt...
19 November 2009
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Des Spence,
GP
G20 9DR

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Re: Re: Re: Re: Re: Re: This will hurt...

Thank you Sam, you seem to the only person willing to debate these issues in public. I don't know which one of us is right ( although I am pretty sure I am !) You are correct, to convince me I need to see hard data ( the QOF should be able to show this ) with a knee bend change at least in recorded vascular events ( but ideally mortality )

The real issue is the treatment paradox - the millions on treatment who will never benefit , ever . Also the current risk assessment tools - I choose my words carefully - are completely flawed . Take the prospective data from WOSCOPS and look at vascular event rate for a smoking 55 year old male Glaswegian with a cholesterol of 7.1 the “real” 10 year event rate is roughly 15-20% but the calculation using the joint committee Framingham equation is nearly 30% - the simple truth is that we are overdiagnoisising and overtreating huge numbers of people and this is an indisputable fact.

Until the great and good, do get the evidence to roast me over their fire of retribution - I will continue to bleat as loudly as I can in the wilderness. Unfortunately , if I am right , then the scale our collective error will be no cause of celebration to me

Competing interests: None declared

Dr Doom
Re: Re: Re: Re: This will hurt...
18 November 2009
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L Sam Lewis,
GP
Surgery, Newport, Pembrokeshire, SA42 0TJ

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Re: Re: Re: Re: Re: This will hurt...

Dear Des,

Dear Des,

 

 

There’s always a catch… !

 

Herewith the hard mortality data , from Clarke's paper upto 2005 :- 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

What happens after 2005 is the question !  Or rather - whether QOF effected it ?  Until we can ethically construct a randomised placebo-controlled blinded allocation to QOF or non-QOF practice, you’ll always be able to say “Ah, but… “.

 

And there’s always ‘ascertainment bias’ – eg. Coding changes, and exception codes !

 

Meantime , a trend graph with knee-bend at 2005,  would be the best evidence of QOF benefit that I can hope for..  But to convince doubters such as yourself, it would have to be mortality or other outcome measures.  Process measures like HbA1c, such as these [in this window]  from http://www.bmj.com/cgi/content/full/338/may26_2/b1870/FIG2 , simply won't be enough.

 

 

References

Life expectancy in relation to cardiovascular risk factors: 38 year follow-up of 19 000 men in the Whitehall study
Clarke et al. (16 September 2009) [Abstract] [Full text] [PDF]
Melanie Calvert, Aparna Shankar, Richard J McManus, Helen Lester, and Nick Freemantle
Effect of the quality and outcomes framework on diabetes care in the United Kingdom: retrospective cohort study
BMJ 2009; 338: b1870 [Abstract] [Full text]

 

 

 

 

 

Competing interests: QOF brings substantial income, and work

Dr Doom
Re: Re: Re: This will hurt...
17 November 2009
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Des Spence,
GP
G20 9DR

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Re: Re: Re: Re: This will hurt...

We could compare quartiles , but we may not be comparing comparable populations – and it seems likely the results would be confounded by social class. We were told the QOF would address unmet need – if we all got 90% this clearly wasn’t the case and there was no need for the QOF in the first place . Also, these result were after one year of activity and a “drive” to improve care but with the statistical powering of the QOF I would expect this to be reflected in hard positive outcomes – surrogate endpoints like HbA1C are not acceptable . Also, if treatment is now optimal we should in theory see no more decline in vascular disease. The BMA/RCGP silence is interesting.

Epidemiologists please have a look at the endless reams of data from the QOF and help Sam and I out !

Competing interests: None declared

Dr Doom
Re: Re: This will hurt...
17 November 2009
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L Sam Lewis,
GP
Surgery, Newport, Pembrokeshire, SA42 0TJ

Send response to journal:
Re: Re: Re: This will hurt...

Dear Des,

Dear Des,

 

I too agree your central assertion - that its a mathematical fact that as absolute risks fall, so must NNT ( its reciprocal ) rise..  I called that a 'law of diminishing returns'.

 

Stimulated as ever by your challenges, I'm off to gather further evidence for the massive benefits ( or not, as seems more likely ) of QOF.  One immediate difficulty is that many practices had already reached the 90% mark before QOF, leaving very little margin to achieve further statistically significant improvement ( proving your first assertion ). 

 

Maybe we could compare the least improvers with the best, by quartiles ??

 

References

 

Melanie Calvert, Aparna Shankar, Richard J McManus, Helen Lester, and Nick Freemantle

Effect of the quality and outcomes framework on diabetes care in the United Kingdom: retrospective cohort study
BMJ 2009; 338: b1870 [Abstract] [Full text]

Rapid Responses published:

[Read Rapid Response]Qof provided equity for patients

Rupert A Gude   (8 June 2009)

[Read Rapid Response]Role of Pharmaceutical Care in Diabetes Management

Ajay G. Pise, Shilpa Pise, D. Sreedhar, Manthan J., Virendra L, N. Udupa   (10 June 2009)

[Read Rapid Response]Coding Changes

Gavin M Jamie   (12 June 2009)

[Read Rapid Response]Improvements in glycaemic control and cholesterol concentrations associated with the Quality and Outcomes Framework.

Christopher D Byrne, Isaac Oluwatowoju, Emmanuel Abu, Sarah H. Wild   (12 June 2009)

[Read Rapid Response]QOF Effects Across Lothian

Kieran Montgomery, Ian JB Young, Dan Pugh, Manreek Basi, Bruce T McLintock   (27 October 2009)

[Read Rapid Response]Pre-cognition

L Sam Lewis   (29 October 2009)

 

 

Competing interests: A life outside medicine

Dr Doom
Re: This will hurt...
16 November 2009
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Des Spence,
GP
G20 9DR

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Re: Re: This will hurt...

Dear Sam – As ever I am grateful that you take the time to respond to articles – I wish more of us were willing to enter this dialogue . But I have never refuted that treating risks has a limited impact on outcomes , but merely that there are other factors involved in the steady and rapid decline in vascular disease. It is very interesting that the decline from death caused by infectious diseases ( a marker for all infectious disease ) mirrors vascular disease deaths but 40 years before. Many of these infections like rheumatic fever, Dipheria had significant acute cardiac complications but could in theory have damaged the vascular tree over the longer term . The greater burden of infectios disease in the over crowded urban areas accounting for concentration of vascular disease in cities like Glasgow. This is merely an observation and would be impossible to prove a causal link .

But my central assertion remains – if the incidence has declined by 50% in 20 years the NNT based on the research have doubled . The QOF has been running for 5 years and is the biggest public funded research project of all time – this is well long enough and powered enough, to have generated concrete outcomes by now – please show me the data. I am not that conflicted !

Competing interests: None declared

Dr Doom
This will hurt...
15 November 2009
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L Sam Lewis,
GP
Surgery, Newport, Pembrokeshire, SA42 0TJ

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Re: This will hurt...

Des' admission to 'being conflicted' means that he is beginning to concede that just possibly the dramatic decline in vascular deaths may indeed be due to medical interventions. But hey, why praise ourselves, after years of self-flagellatory masochistic delight ?

His 'trading derivatives' metaphor is apposite.. Victims of our own success, we are indeed in a process of diminishing returns. Time to diversify ?

Competing interests: None declared

VIEWS & REVIEWS:
Joking about cerebral palsy
Drife (12 November 2009) [Full text]
Joking about cerebral palsy
Passionate about CP
15 November 2009
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David JR Hutchon,
Consultant Obstetrician and Gynaecologist
Darlington Memorial Hospital, Darlington. DL3 6HX

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Re: Passionate about CP

Every obstetrician worries about cerebral palsy. After reading “Joking about cerebral palsy” (1) I immediately Googled “Francesca Martinez” and watched her on Youtube. What a talented and funny young lady. It is heartening to know that at least the injury leading to cerebral palsy did not destroy the sense of humour.

The fundamental pathology of CP is brain injury associated with hypoxia and ischaemia. When this occurs is uncertain, but the effect often does not become apparent until many months after the injury to the brain has taken place. Investigation at this late stage is not easy. Any form of care which we apply routinely to women in labour needs to be reviewed as it could be responsible for the injury. Could “less medicine” sometimes be “more medicine” as suggested in the previous article by Des Spence?. (2)

Professor Drife explains that most cases of cerebral palsy have nothing to do with events in labour. Fair enough if you restrict that to only the first and second stages of labour. He tells us that cerebral palsy has never been far from his thoughts and even in retiral will remain at the back of his mind for another 25 years. I just wish cerebral palsy had been more prominent in my thoughts during my 38 years of obstetrics. Now I have become obsessional (3-48) and I expect will remain so for the next few years after my retirement!

But what about the third stage of labour? Let me explain. There is little doubt that the brain injury is due to loss of oxygen carrying blood to the brain tissue. All the monitoring and interventions put in place over the last 40 years of my obstetric practice has not reduced the incidence of cerebral palsy. Of course some of the current prevalence of cerebral palsy occurs in preterm and very preterm babies, babies who would not have survived the first few days of life when I first started obstetrics. Actually the immature brain of the fetus or the neonate is able to withstand hypoxia much better than the more mature brain. By carefully defining the conditions for intrapartum hypoxia in terms of fetal heart measurements and fetal blood measurements, intrapartum hypoxia is not considered the main cause of cerebral palsy. Unfortunately in order to prove this a sample of cord blood is required before the third stage of labour is completed!

It is recognised that loss of circulation is much more damaging than simple hypoxia alone. This is the thinking behind the recent change in CPR guidelines with the message to keep the circulation going at all cost (with cardiac compression) as oxygenation is of secondary importance. The recent Caudwell Xtreme Everest expedition demonstrated that the adult brain can function normally at very low oxygen tensions, previously thought to be too low to be compatible with life. In 1959 Professor Dawes of Oxford stated after one of his sheep experiments that “It is a matter of common knowledge that foetuses or new-born animals of many species are able to survive in the absence of oxygen for a much longer period of time than adults of the same species.” And he concluded that “The results suggest that it is the maintenance of the circulation which is of predominant importance in survival . . . “ (49)

So is there anything which occurs in the third stage of labour which interferes with the circulation in the brain? The second stage of labour ends with the delivery of the baby and the third stage involves separation and delivery of the placenta. Traditionally at some stage during this stage the cord is clamped and cut. During the first stage of labour the fetal heart rate and pattern has been the focus of attention for 30 years. It was hoped that by delivering the baby before hypoxic injury had occurred would prevent the brain injury. At birth there are critical changes which need to take place at delivery. It is generally assumed that at the moment of birth the placental circulation is instantly redundant and can be clamped off. As about 40% of the combined cardiac output is entering the umbilical arteries, clamping the vessels causes a tremendous load on the fetal heart and a marked increase in the systemic blood pressure. Since the cerebral circulation is the second greatest circulation in the fetus the increased blood pressure would be expected to have a considerable impact on this organ. Autoregulatory mechanisms in the brain may lead to constriction of the vessels to try to limit the impact on the brain. As the pulmonary circulation opens up the blood pressure will fall again, followed by a further fall in the blood pressure as the cardiac return falls. The cardiac return is reduced as the neonate has had to fill the pulmonary circulation with a volume of blood from the rest of the body. All oxygenated blood returning from the placenta to the heart is also immediately stopped.

Thus clamping the cord quickly at birth is an intervention in what would be a normal physiological transition from placental respiration to pulmonary respiration. Why is this intervention necessary? What is the evidence that this is beneficial to the newborn baby? Why is it so strongly supported by established medical opinion? (50)

How could cord clamping be responsible for some cases of cerebral palsy? Often fetal heart abnormalities are due to cord compression. Cord compression leads to a congestion of blood within the placenta and a relative hypovolaemia within the fetal compartment. In late labour, with little remaining liquor around the baby’s limbs, the cord is easily compressed against the limbs and body. The resulting hypovolaemia may present little problem to the baby at this stage as compression of its body within the birth canal acts like a compression anti-shock garment and helps to maintain the cardiac return. However as soon as the baby is born the compression is lost and the hypovolaemia becomes important. The clamp on the umbilical cord applied quickly after birth has permanently trapped the blood in the placenta. The amount of blood trapped in the placenta varies and sometimes the newborn baby shows no signs of hypovolaemia and transitions to extra-uterine life without apparent difficulty. However at other times there is a considerable volume of blood trapped in the placenta, the baby is not able to fill the newly opened pulmonary circulation adequately due to hypovolaemia, is not able to maintain normal cerebral circulation and is not able to deal with the hypoxia and acidaemia which has occurred in the last few minutes of labour. Even the attending paediatrician is not able to correct these problems quickly enough. If hypovolaemia is recognised and distinguished from hypoxia alone, it is only possible to give crystalloid or colloid fluid to compensate instead of the blood which the baby has just lost. In addition the changes in blood pressure may be too rapid for the autoregulatory systems of the cerebral circulation to react and hypoperfusion of the cerebral circulation may be present. These problems are likely to be greater in a preterm baby.

Of course there is no proof in terms of a randomised controlled trial, partly because the timing of cord clamping is routine and is never recorded. However the intervention of immediate cord clamping is unnecessary for the safety of the mother. (51-53) For the baby there is the risk of mild or severe anaemia, intraventricular haemorrhage, and late onset sepsis. (54-57) Immediate cord clamping may reduce the need for phototherapy to treat jaundice in the term baby. (57). How can we justify an intervention to reduce the need for phototherapy especially when there are other serious risks for the intervention? At least as important is the loss stem cells which are present in the cord blood in huge numbers and normally enter the neonatal circulation as the placental circulation closes down naturally. These stem cells are believed to be able to quickly repair cerebral damage. (58)

In 2006 Gaby Logan presented a TV program on FIVE about childbirth, broadcast from the maternity unit at Queen's Medical Centre in Nottingham. It looked at pregnancy, modern medical techniques, and some of the babies in the unit. It was hoped to include the first televised natural childbirth, but did a televised Caesarean birth instead as no baby arrived naturally during the period of the live two hour. The baby was very quiet after birth and those attending stated that it was not unusual for babies born by caesarean section to be sleepy. In the program it could be clearly seen that the cord was clamped 13 seconds after delivery while the baby was held above the mothers body. Holding the baby above the level of the uterus has the effect of reducing the rate of blood returning from the placenta through the umbilical vein. It has no effect on the umbilical artery flow which continues as normal.. Could this baby have been “sleepy” as a result of mild hypovolaemia? None of us would consider running a marathon after donating a pint of blood. However the neonate can sometimes lose as much as 25% of its circulating volume when the cord is clamped quickly at birth, yet is expected to smoothly transition from intra-uterine to extrauterine life.

The need for resuscitation is often used to justify cord clamping. Indeed the World Health Organization in its document on the prevention of post partum haemorrhage states that “ for the benefit of the baby the cord should not be clamped for about three minutes. Earlier clamping may be necessary when the baby needs resuscitation.” (53) Let me refer back to some work by Professor Dawes. He showed that in the fetal lamb the umbilical cord could be gently occluded leading to complete anoxia in the fetus for 40 minutes, and during this time the cerebral circulation was maintained. (49) Gradually the heart rate and blood pressure was reducing but before the circulation stopped, he unclamped the cord and restored the placental circulation. The fetal condition immediately improved and after a short time there were signs that the cerebral activity was normal. These lambs recovered with the help of the restored placental circulation alone. Breathing was prevented. It makes no sense to close down the placental circulation before pulmonary circulation is functional. In natural birth there are well recognized physiological mechanisms which result in constriction of the umbilical artery after the lungs become functional. In the words of Charles White of Manchester in 1773, "Can it possibly be supposed that this important event, this great change which takes place in the lungs, the heart, and the liver, from the state of a foetus, kept alive by the umbilical cord, to that state when life cannot be carried on without respiration, whereby the lungs must be fully expanded with air, and the whole mass of blood instead of one fourth part be circulated through them, the ductus venosus, foramen ovale, ductus arteriosus, and the umbilical arteries and vein must all be closed, and the mode of circulation in the principal vessels entirely altered - Is it possible that this wonderful alteration in the human machine should be properly brought about in one instant of time, and at the will of a by-stander?" (59)

In a baby who fails to breath at birth, or in whom we are concerned has been hypoxic in labour, the logical measure is to establish functioning lungs before disconnecting the placental system. If these babies are given the chance they may well start breathing themselves but if not we need to be able to initiate ventilation before disconnecting the placenta. This ensures the best chance of a continued cerebral circulation without any sudden changes in pressure or flow. It is a radical change in the approach to resuscitation but one which is easily made given a little preparation and forethought. It is supported in principle. (60) The authors point out that there is sparse data behind the use of any medication at birth and poor outcome data is available. They go on to state “ The appropriate decline in the indiscriminate use of volume expansion is considered and balanced by the increasing evidence in favour of delayed clamping of the umbilical cord.” emphasising the importance of avoiding relative hypovolaemia during resuscitation.

Earlier I mentioned “fetal” blood measurements being an important part of the definition of fetal hypoxia in labour. I put fetal in inverted commas because it is in fact the moment of birth when this measurement is taken. Immediate clamping to isolate a section of cord to measure the blood gases has been recommended as part of audit and risk management. A normal cord pH generally relieves the carers of the responsibility for cerebral palsy should that develop in the months or years ahead. A normal pH shows that there was insufficient evidence of hypoxia in the later part of labour to account for cerebral injury. However it is possible, as explained above, that the very act of clamping has caused changes in the circulation which subsequently lead to the condition of cerebral palsy to occur. No consent from the parents is ever taken for this test. An abnormal result is rarely of any importance in the immediate management of the baby. It is clear that the pH of the cord blood changes after birth if the circulation is allowed to continue. The pH of the cord blood steadily falls during the first 90 seconds after birth. (61) This is thought to be largely the result of lactic acid released from parts of the fetal circulation which had closed down and the tissues had continued to generate lactic acid.

In preterm babies there is a particular challenge. (62) Bell answered his question about “When to transfuse preterm babies,” that it is “at birth.” He went on to explain.” Delaying the umbilical cord clamping for 30 to 120 seconds in the preterm infant increases the infant’s blood volume, improves circulatory and respiratory function, reduces the need for blood transfusion, and reduces the risk of intraventricular haemorrhage.and necrotising enterocolitis. Studies to date suggest that this practice is beneficial, and no adverse effects have been identified consistently except higher peak serum bilirubin concentration. The impact of delayed cord clamping on neurodevelopmental outcome has not yet been reported.”(66)

This is not new and it is very hard to explain why there is so little evidence and why what evidence there is has been largely ignored until now. Almost 70 years ago Windle stated "... The rather common practice of promptly clamping the cord at birth should be condemned. Of course, this will make it imposible to salvage placental blood for 'blood banks.' However, the collection of usable quantities of placental blood robs the newborn infant of blood which belongs to him and which he retrieves under natural conditions... Immediate clamping of the cord is comparable to submitting the infant to a rather severe hemorrhage." (63) The haemorrhage continues today (64) based on unfounded objections. (65)

References
1. James Owen Drife In and Out of Hospital. Joking about cerebral palsy
2. Des Spence From the Frontline. Dr Doom
3. David J R Hutchon Inappropriate referencing by NICE http://bmj.com/cgi/eletters/339/jul20_3/b2049#217562, 24 Jul 2009
4. David JR Hutchon Anticipate the need for physiological transition in extremely preterm babies http://bmj.com/cgi/eletters/338/jun22_2/b2325#216640, 10 Jul 2009
5. David J R Hutchon Unforeseen long-term consequences? http://bmj.com/cgi/eletters/338/may12_2/b1144#214244, 24 May 2009
6. David J R Hutchon Physiological transition at birth and Physiolgical growth http://bmj.com/cgi/eletters/338/may08_1/b1892#213547, 11 May 2009
7. David JR Hutchon Evidence from the archive http://bmj.com/cgi/eletters/338/apr29_1/b1744#213157, 3 May 2009
8. David JR Hutchon Physiology and neonatal transition http://bmj.com/cgi/eletters/338/mar05_2/b195#210263, 8 Mar 2009
9. David JR Hutchon Sound Medical Principle http://bmj.com/cgi/eletters/338/feb19_3/b707#209298, 23 Feb 2009
10. David J R Hutchon Keep to nature if possible http://bmj.com/cgi/eletters/338/jan30_1/a2657#208737, 13 Feb 2009
11. David J R Hutchon Darwin's 200year message http://bmj.com/cgi/eletters/337/dec30_1/a3015#208697, 12 Feb 2009
12. David JR Hutchon Pulse oximetry at birth http://bmj.com/cgi/eletters/338/jan08_2/a3037#207034, 13 Jan 2009
13. David JR Hutchon Hypovolaemia at birth - Endgame for some http://bmj.com/cgi/eletters/337/oct22_2/a1940#203688, 24 Oct 2008
14. David JR Hutchon Blood pressure in neonates? http://bmj.com/cgi/eletters/336/7657/1321#197137, 14 Jun 2008
15. David JR Hutchon Blood donation risk for teenagers - short cut http://bmj.com/cgi/eletters/336/7655/1212#196447, 31 May 2008
16. David JR Hutchon Regulate for safety of the baby http://bmj.com/cgi/eletters/336/7651/981#194748, 3 May 2008
17. David J R Hutchon When I read physiology http://bmj.com/cgi/eletters/336/7649/895-a#193914, 18 Apr 2008
18. David JR Hutchon Cord clamping and cord blood banking http://bmj.com/cgi/eletters/336/7645/642#192444, 21 Mar 2008
19. David J R Hutchon Look to physiology and nature http://bmj.com/cgi/eletters/336/7635/85#186939, 10 Jan 2008
20. David J R Hutchon Paediatricians and Obstetricians views http://bmj.com/cgi/eletters/335/7615/312#186280, 7 Jan 2008
21. David JR Hutchon References for paediatricans and obstetricians view http://bmj.com/cgi/eletters/335/7615/312#186300, 7 Jan 2008
22. David JR Hutchon Nature's data http://bmj.com/cgi/eletters/336/7634/23#185972, 4 Jan 2008
23. David JR Hutchon Avoid interfering with physiology when possible http://bmj.com/cgi/eletters/335/7628/1025#178949, 2 Nov 2007
24. David JR Hutchon Without intervention http://bmj.com/cgi/eletters/335/7621/667#177340, 28 Sep 2007
25. David JR Hutchon Document timing of cord clamping http://bmj.com/cgi/eletters/335/7615/312#175508, 29 Aug 2007
26. David JR Hutchon Evidence conclusive enough http://bmj.com/cgi/eletters/335/7615/312#175262, 26 Aug 2007
27. David JR Hutchon How immediate cord clamping causes intraventicular haemorrhage http://bmj.com/cgi/eletters/335/7615/312#174932, 20 Aug 2007
28. David JR Hutchon Resuscitation with the cord intact http://bmj.com/cgi/eletters/335/7615/312#174948, 20 Aug 2007
29. David JR Hutchon Immediate cord clamping may cause neonatal deaths http://bmj.com/cgi/eletters/324/7340/761#169489, 22 Jun 2007
30. David JR Hutchon Consent for cord blood gases http://bmj.com/cgi/eletters/334/7607/1281#169386, 21 Jun 2007
31. David JR Hutchon Immediate cord clamping must stop - no excuses! http://bmj.com/cgi/eletters/334/7602/1027-f#166259, 20 May 2007
32. David J R Hutchon NICE is encouraging artificial intervention BMJ Mar 2007; 334: 651; doi:10.1136/bmj.39164.428843.1F
33. David J R Hutchon Delayed cord clamping may also be beneficial in rich settings BMJ Nov 2006; 333: 1073; doi:10.1136/bmj.39030.733715.3A
34. David JR Hutchon Re: cord clamping in uk http://bmj.com/cgi/eletters/333/7575/954#147299, 4 Nov 2006
35. David J R Hutchon Commercial cord blood banking: Immediate cord clamping is not safe BMJ Oct 2006; 333: 919; doi:10.1136/bmj.333.7574.919-a
36. David J R Hutchon Unethical umbilical cord blood? http://bmj.com/cgi/eletters/330/7497/973#125011, 29 Dec 2005
37. David J R Hutchon A trial of physiological delivery at Caesarean http://bmj.com/cgi/eletters/331/7518/662#124145, 17 Dec 2005
38. David J R Hutchon Informed consent for cord clamping? http://bmj.com/cgi/eletters/331/7518/662#123663, 12 Dec 2005 David JR Hutchon Neonatal CPR http://bmj.com/cgi/eletters/331/7528/1281#122782, 1 Dec 2005
39. David J R Hutchon A physiological approach to reducing neonatal morbidity in elective Caesarean Section http://bmj.com/cgi/eletters/331/7518/662#115256, 24 Aug 2005
40. David J R Hutchon Immediate cord clamping does increase intraventricular haemorrhage http://bmj.com/cgi/eletters/329/7477/1287-a#87455, 28 Nov 2004
41. David J R Hutchon Epidemiology of preterm birth: Delayed cord clamping used to be taught and practised BMJ Nov 2004; 329: 1287; doi:10.1136/bmj.329.7477.1287
42. David JR Hutchon Delayed cord clamping 30 -120 seconds http://bmj.com/cgi/eletters/329/7474/1087#84071, 5 Nov 2004
43. David JR Hutchon Delayed cord clamping? http://bmj.com/cgi/eletters/329/7467/675#74799, 17 Sep 2004
44. D J R Hutchon and I Thakur Resuscitate with the placental circulation intact Arch. Dis. Child., May 2008; 93: 451.
45. David J R Hutchon Have bag - will travel http://adc.bmj.com/cgi/eletters/93/5/451-a#7654, 4 May 2008
46. David Hutchon Support transition by keeping the placental circulation intact . http://fn.bmj.com/cgi/eletters/adc.2007.128827#2774, 17 Nov 2008
47. David Hutchon Views and counter views A view on why immediate cord clamping must cease in routine obstetric delivery The Obstetrician & Gynaecologist 2008;10:2:112-116
48. David J R Hutchon Physiological fetal to neonatal transition is safer. http://heart.bmj.com/cgi/eletters/91/7/871#8372, 26 Aug 2008
49. Dawes G S, Mott JC, Shelley HJ. The importance of cardiac glycogen for the maintenance of life in fetal lambs and new-born animals during anoxia. J Physiol (1959) 146 516-538
50. NICE Intrapartum care guideline. http://www.nice.org.uk/nicemedia/pdf/CG55FullGuideline.pdf accessed 14/11/2009
51. Stergios K. Doumouchtsis, Sabaratnam Arulkumaran Chapter 7. Postpartum haemorrhage: changing practices In Recent Advances in Obstetrics and Gynaecology 24 (2008)
52. Mukherjee S, Arulkumaran S. Post-partum haemorrhage. Obstetrics, Gynaecology and Reproductive Medicine (2009) . 19, 5, 121-126
53. WHO Recommendations for the Prevention of Postpartum Haemorrhage. October 2006.page 15
54. H, Reynolds G, Diaz-Rossello J. A systematic review and meta-analysis of a brief delay in clamping the umbilical cord of preterm infants. Neonatology 2008;93:138-44.
55. Rabe H, Reynolds G, Diaz-Rossello J. Early versus delayed umbilical cord clamping in preterm infants. Cochrane Database Syst Rev 2004;(4):CD003248.
56. Strauss RG, Mock DM, Johnson KJ, et al. A randomized clinical trial comparing immediate versus delayed clamping of the umbilical cord in preterm infants: short-term clinical and laboratory endpoints. Transfusion 2008;48:658-65.
57. McDonald SJ, Middleton P. "Effect of timing of umbilical cord clamping of term infants on maternal and neonatal outcomes (Review)." Cochrane Database of Systematic Reviews 2008, Issue 2.
58. Autologous Cord Blood Cells for Hypoxic Ischemic Encephalopathy Study Duke University NCT00593242 http://clinicaltrials.gov/ct2/show/NCT00593242 Accessed 6/7/2008.
59. Charles White (1728-1813) White C (1773) A Treatise on the Management of Pregnant and Lying-In Women. Canton, MA: Science History Publications, 1987, p 45
60. Wylie J, Niermeyer S. The role of resuscitation drugs and placental transfusion in the delivery room management of newborn infants . Seminars in Fetal and Neonatal Medicine. (2008) 13;6: 416 - 423
61. Wiberg N, Kallen K, Olofsson P. Delayed umbilical cord clamping at birth has effects on arterial and venous blood gases and lactate concentrations. BJOG
2008;115:697–703. 62. . Reynolds GJ. Beyond sweetness and warmth: transition of the preterm infant. Arch Dis Child Fetal Neonatal Ed 2008;93:F2-3.
63. Windle WF Development of respiration, circulation, and creation of blood cells Round table discussion on anemias of infancy (from the proceedings of the tenth annual meeting of the American Academy of Pediatrics) Journal of Pediatrics (1940) 18:538-547.
64. Ononeze ABO & Hutchon DJR Attitude of obstetricians towards delayed cord clamping: A questionnaire-based study Journal of Obstetrics & Gynaecology 2009, Vol. 29, No. 3, Pages 223-224
65. Hutchon DJR & Ononeze B Delayed cord clamping and objections BJOG (2007) Volume 114, Issue 7, Pages 909-909
66. E F Bell Archives of Disease in Childhood - Fetal and Neonatal Edition 2008;93:F469-F473 When to transfuse preterm babies

Competing interests: None declared

VIEWS & REVIEWS:
Learning to teach
Jackson (12 November 2009) [Full text]
Learning to teach
Practical Teaching Tips
20 November 2009
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Avtar Singh,
4th year medical student
College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT

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Re: Practical Teaching Tips

Jackson’s article (1), highlighting the difficulties in teaching from the junior doctor’s perspective, certainly made for an interesting read. Perhaps ironic then that this reply comes from a student (especially one located around the corner at Birmingham Medical School!).

We can all recall personal examples of outstanding medical teaching that we have received in a variety of different clinical settings; from the patient’s bedside on a ward round to standing next to the surgeon in theatre, and from the outpatient clinic to primary care. So, as Jackson mentions, one could utilise the knowledge gained from these past experiences to guide us in our own teaching roles (1).

However, applying educational theory in the clinical arena is often easier said than done. Outlined below are some practical tips that may assist the newly qualified junior doctor in helping his students get the most out of their teaching session:

• Time devoted to clinical educational activity in hospitals is often variable or even absent, ranging from 0 – 25% of students’ time spent on the wards (2). So junior doctors would greatly improve the learning experiences of their students simply by trying to find more time to teach them. However, if not all the material can be covered in a time-constraint teaching session, providing a summary handout or pointing to areas of further reading is also useful.

• Failure to utilise the assets of the clinical environment is commonplace. Many doctors revert towards didactic impartment of factual knowledge best left in the lecture theatre or seminar room, thereby losing the clinical context for teaching skills of history taking and examination. This is reflected in a study on teaching rounds, where only 11% of the time was spent at the patient’s bedside, the rest of the time being spent in the conference room or discussing in hallways (3). This is particularly surprising when bedside teaching and medical clerking are considered the most valuable teaching methods amongst both students and practicing doctors (4).

• Interruptions on the ward (e.g. being bleeped when on-call, restricted times for patients at mealtimes and during visiting hours) should be taken into account so as to minimise the disruption to bedside teaching arrangements.

• Be prepared to be opportunistic in clinical teaching, since cases never occur in a logical order.

• Set clear learning goals. Discuss objectives with learners to avoid covering topics they have already met; especially since medical students, even within the same medical school, will have had completely different learning experiences (5). This also enables learners to point out areas of weakness and to help them focus on the salient points of the lesson. At the end, review the aims, clarify any misunderstandings and summarise the key information.

• The motivation of learners can be difficult to maintain at times. Simple ways of achieving this include varying the teaching stimulus (e.g. mixing up the teaching of practical skills with recall of medical knowledge) and utilising tasks that are more engaging and interactive (e.g. bedside detective work and games for teaching physical examination (6)). Moreover, it has been shown that one of the features of good clinical teaching is enabling the student to be an active participant (7); so a good teacher would involve the students on the ward round by getting them to write in the patient notes, take a patient’s blood and getting them to listen to the heart sounds before the consultant does.

• A good teacher would frequently ask relevant open questions, avoid answering his own questions, and question the answers of his students (8).

• Giving personal feedback is an important factor in student satisfaction (9). So spend time supervising their physical examinations and reviewing their histories.

Medicine is different to other professions, in that teaching, whether it be to students, fellow doctors or other healthcare professionals, is an expectation. Furthermore, the General Medical Council state that those involved in teaching should “develop the skills, attitudes and practices of a competent teacher” (10). However, few doctors have had any formal training in educational method, though many express an interest in receiving it (11). Thus, there is a need for recognised training on how to teach within the medical curriculum. This has been acknowledged in recent years with some medical schools offering Special Study Modules in teaching, as well as assessing medical students on a given teaching performance to peers. Postgraduate qualifications in medical education and teacher training courses also exist for those wishing to further their skills; however, only 6% of actively teaching doctors have ever attended masters or other short courses on teaching (12).

Patient-centred medicine to student-centred teaching seems a simple enough transition to make, but many find it a daunting prospect. So adequate training in educational methods should be in place for anyone who takes a keen interest in their teaching roles. However, being a good clinical teacher often goes beyond the theoretical teaching methods, and is characterised by being enthusiastic, inspiring and supportive (13).

References:

(1) Jackson P. Learning to Teach. BMJ 2009;339:b4554

(2) Jolly B, Rees L. Medical education in the millennium. Oxford: Oxford Medical Publications; 1998

(3) Miller M, Johnson B, Greene HL, Baier M, Nowlin S. An observational study of attending rounds. J Gen Intern Med 1992;7:646-8

(4) Ward B, Moody G, Mayberry JF. The views of medical students and junior doctors on pre-graduate clinical teaching. Postgrad Med J 1997;73:723-5

(5) Kowlowitz V, Curtis P, Sloane PD. The procedural skills of medical students: expectations and experiences. Acad Med 1990;65:656-8

(6) Ramani S. Twelve tips for excellent physical examination teaching. Med Teach 2008;30:851-6

(7) Stritter FT, Hain JD, Grimes MD. Clinical teaching re-examined. J Med Educ 1975;50:876-82

(8) Spencer J. Learning and teaching in the clinical environment. BMJ 2003;326:591-4

(9) Chesser A, Brett M. Clinical teaching in context: a factor analysis of student ratings. Research in Medical Education, Proceedings of the twenty-eighth annual conference. Washington: Association of American Medical Colleges; 1989. p49-54

(10) General Medical Council. Good Medical Practice [online]. 2006 [cited 2009 Nov 18]. Available from URL: http://www.gmc- uk.org/guidance/good_medical_practice/index.asp

(11) Wilson DH. Education and training of preregistration house officers: the consultants’ viewpoint. BMJ 1993;306:194-6

(12) Lawson M, Seabrook M, Jolly BC, Pettingale KW. Teachers at King’s: who teaches and how? Paper presented at the annual conference of the Association for the Study of Medical Education. Med Educ 1996;30:71-2

(13) Sutkin G, Wagner E, Harris I, Schiffer R. What makes a good clinical teacher in medicine? A review of the literature. Acad Med 2008;83:452-66

Competing interests: None declared

Learning to teach
Being an effective clinical teacher
15 November 2009
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Asif M Bachlani,
StR 5 General Adult Psychiatry, Hampshire Partnership Foundation NHS Trust
College Keep CMHT, 4 - 12 Terminus Terrace, Southampton, SO14 2DT

Send response to journal:
Re: Being an effective clinical teacher

I read with interest the article by Jackson (1) about teaching as a junior doctor. Her account represents many junior doctor’s difficulties with teaching (which included myself). We go from being ‘learners’ as medical students straight to teachers when we get our MBBS. Most of us had very didactic ‘product model’ of teaching (2) which sees knowledge residing in the teacher, teacher as expert and puts the learner in the passive role. How do junior doctors then teach medical students when they themselves are still early in their training and learning on the job? It is obvious to all that their knowledge can never be the same as a senior clinician.

The answer is two-fold – one to have a more collaborative way of teaching which sees ‘education as a process’ (2) where the teacher promotes the learner to gain the knowledge themselves and ideally puts the teacher role as facilitator. This encourages the learner to take more responsibility for their learning and to be more involved. Secondly being a doctor is not just about learning set knowledge and skills but is about professional practice (3) which focuses on attitudes, values and beliefs. This wider view of medical education aids the junior doctor’s role as teacher where one can role model being a professional which includes understanding individual patient context when making clinical decisions, how one’s own perceptions and attitude affect clinical judgment and how to adapt what’s learnt in the textbook to clinical practice.

This in itself is not easy and requires experience and training which goes back to the question the author asks about the necessity of formal training. I believe that some formal training in learning how to teach is important. Most deaneries I would imagine offer some learning to teach programme which I would encourage junior doctors to attend. This would start the journey on learning more skills and tools on how to teach as a doctor with more confidence. This arguably would be a minimal requirement and if one is enthusiastic could then be followed up by a postgraduate qualification.

Teaching is a fundamental part of being a doctor and the GMC is quite clear about the role of doctors as teachers and states as “doctors we have a professional obligation to contribute to the education and training” (4). It goes on to say we are responsible for the acquisition of these skills. One wouldn’t expect a junior doctor to carry out a procedure without training, and I believe the same argument could and should be said of teaching. We are don’t forget teaching the doctors of the future.

References

1. Jackson, P. Learning to Teach. BMJ 2009;339:b4554 (14th November 2009)

2. Fish, D and Coles, C (2005) Medical Education: Developing a Curriculum for Practice. Maidenhead: Open University Press

3. Fish, D and Coles, C (1998) Developing Professional Judgment in Health Care – Learning through the critical appreciation of practice. Oxford, Butterworth Heinemann

4. GMC (1999) Doctor as Teacher [Online] available at http://www.gmc- uk.org/education/postgraduate/archive/doctor_as_teacher.asp [last accessed on 14th November 2009]

Competing interests: Medical Education Fellow Wessex Deanery, and currently studying a Diploma of Education: Professional Enquiry at the University of Winchester

PRACTICE:
Investigating recurrent respiratory infections in primary care
Wood and Peckham (12 November 2009) [Full text]
Investigating recurrent respiratory infections in primary care
HIV is a very relevant cause of recurrent respiratory bacterial infection and should be excluded
18 November 2009
Previous Rapid Response Next Rapid Response Top
Paul Collini,
Clinical Lecturer in Infectious Diseases
University of Sheffield, Royal Hallamshire Hospital, Sheffield S10 2JF,
Julia Greig, Consultant in Infectious Diseases, Royal Hallamshire Hospital, Sheffield

Send response to journal:
Re: HIV is a very relevant cause of recurrent respiratory bacterial infection and should be excluded

Dear Editor, Philip Wood’s and Daniel Peckham’s article [1] provides useful advice for the investigation of underlying primary and secondary immunodeficiency in those presenting to primary care with recurrent respiratory tract infections. However, while its emphasis on primary and secondary hypogammaglobulinaemia is interesting, their article appears to suggest that HIV as an underlying cause is unlikely unless there is ‘a history of high risk sex or of misuse of intravenous drugs’. We dispute this and would like to highlight the importance of excluding HIV infection, especially in the clinical scenario used in this piece.

First, bacterial pneumonia, in particular pneumococcal pneumonia, has a markedly increased incidence in HIV, even with preserved CD4 counts, suggesting more than ‘immunodeficiency involving cellular immunity’ [2] [3]. This is recognised in the UK National Guidelines for HIV Testing 2008 which make clear that ‘HIV testing should be also routinely offered and recommended to the following patients: 1. all patients presenting for healthcare where HIV, including primary HIV infection, enters the differential diagnosis ...including bacterial pneumonia (adults) and (in children) recurrent and/or troublesome ear infections, recurrent bacterial pneumonia or bronchiectasis’ [4]. Given that the prevelance of HIV in the UK is 127 per 100,000 and that a third of these are unaware they have HIV, the likelihood of a patient with undiagnosed HIV attending primary care is roughly twice that of all causes of hypogammaglobulinaemia combined [5][1].

Secondly, those at risk of HIV are from a much broader pool than the article implies and an HIV test should be prompted by many other indicators beyond these historical risk factors. For example, the majority of new HIV in the UK is transmitted heterosexually. That those in primary and acute care take the opportun