I want to highlight few points about the study.First, IgA nephropathy
is seen in nearly 40% of renal biopsy specimens of acute
glomerulonephritis patients in asia in various study.In this study it is
comprising only 8.1% of cases.Second, it is an crossectional study, taking
data from the renal biopsy report thus not showing the exact % of acute
glomerulonephritis caused by IgA nephropathy.So the finding is quite
exaggerat...
I want to highlight few points about the study.First, IgA nephropathy
is seen in nearly 40% of renal biopsy specimens of acute
glomerulonephritis patients in asia in various study.In this study it is
comprising only 8.1% of cases.Second, it is an crossectional study, taking
data from the renal biopsy report thus not showing the exact % of acute
glomerulonephritis caused by IgA nephropathy.So the finding is quite
exaggerated, though 10% of IgA nephropathy patient develop ESRD after 10
year & 20% after 20 years.
Management of special type of dyslipidemia; Low HDL-C, high TG, Type-
B size LDL-P in patients with T2DM is a big challenge for a physician. For
primary LDL-C goal, we the physician usually go for stronger statins like
atorvastatin or rosuvastatin. Addition of fenofibrate to the above statins
to reduce concomitant high TG really reduces TG level but does such
combination offer any strong role in reducing mortality in this p...
Management of special type of dyslipidemia; Low HDL-C, high TG, Type-
B size LDL-P in patients with T2DM is a big challenge for a physician. For
primary LDL-C goal, we the physician usually go for stronger statins like
atorvastatin or rosuvastatin. Addition of fenofibrate to the above statins
to reduce concomitant high TG really reduces TG level but does such
combination offer any strong role in reducing mortality in this population
[1]?
To increase HDL-C, trials with CETP inhibitors like torcetrapib or
anacetrapib failed to reduce CV mortality. Newer CETP inhibitor
evacetrapib although leading to increase HDL-C but cardiovascular
protection is still under question [2].
We were using extended release nicotinic acid along with statin (ARBITER 6
-HALTS trial) but my practice did not show any significant benefit.
Recently, after premature halting of AIM-HIGH trial, efficacy of nicotinic
acid also became under question and even increased events of ischemic
stroke in this population leading me to change my treatment strategy.
Currently no safe drug to increase HDL-C is available. More ever, drug
induced increased HDL has no CV benefit.
Lifestyle modification is still remaining the best strategy along with
statin and if necessary, n-3 to manage dyslipidemia in patients with
diabetes and other high risk population.
Ref:
1. Hyperlipidaemia and cardiovascular disease: do fibrates have a role?
Current Opinion in Lipidology:
August 2011 - Volume 22 - Issue 4 - p 270-276
doi: 10.1097/MOL.0b013e32834701c3
2. Effects of the CETP Inhibitor Evacetrapib Administered as Monotherapy
or in Combination With Statins on HDL and LDL Cholesterol.
JAMA.2011;306(19):2099-2109. doi:10.1001/jama.2011.1649
Kouzes and Posner (1) once wrote that "The domain of leaders is the
future. The leaders unique legacy is the creation of valued institutions
that survive over time. The most significant contribution leaders make is
not simply to today's bottom line; it is to the long-term development of
people and institutions so they can adapt, change, prosper, and grow."
As Warren and Carnall (2) stated, medical leadership is...
Kouzes and Posner (1) once wrote that "The domain of leaders is the
future. The leaders unique legacy is the creation of valued institutions
that survive over time. The most significant contribution leaders make is
not simply to today's bottom line; it is to the long-term development of
people and institutions so they can adapt, change, prosper, and grow."
As Warren and Carnall (2) stated, medical leadership is important for
delivering high-quality healthcare to patients and to function across
professional boundaries in an environment that is becoming increasingly
complex. Physicians are well educated academically and clinically, but
training in leadership lags somewhat behind. There also appears to be a
gap in leadership capabilities between junior and senior doctors. The
authors suggest several approaches to develop the non-technical, often
called "softer" skills in physicians, including mentoring by establishing
a relationship that will support personal and professional development,
coaching to enhance the performance in specific areas, and action learning
to solve jointly "real-world" problems that arise at work. There is also
formal and informal networking with peers and/or senior leaders, and
experiential learning through exposure to new environments, assignments,
etc., which trains the individual to work outside their comfort zone. The
authors also discuss participation in specific programs, schemes,
fellowships, and courses aimed at developing medical leadership skills.
As a scientist, I found myself in a similar situation as many
physicians: I did not receive any kind of training in management and
leadership during my education. Yet, after graduation with a Ph.D. in
microbiology, I was expected to lead a research laboratory, instruct
students in the classroom and guide them through their thesis experience,
and to professionally interact with administrative staff of the
organization as well as representatives of research funding agencies. So,
how did I do it? I essentially studied the way how others (e.g., mentors,
senior peers, and selected role models from the literature) lead people,
then "copied" certain leadership behaviors, and put a "personal touch" on
my leadership attempts. I used the principle of "trial and error." Not
surprisingly, it did not take me long to realize that this way of leading
was a superficial attempt to be effective and to "survive" in the highly
competitive field of biomedical science. Most significantly, I lacked
authenticity and did not know the tools needed for self-observation and
self-discovery. As it turned out, I was not alone in my leadership
insecurities as several of my young colleagues expressed similar soft-
skill deficiencies.
Since the science curriculum (apparently similar to the medical
curriculum) does not include management and leadership courses, I
eventually decided to enroll in business graduate programs to formally
study this subject matter. I was surprised how much I learned from books
and articles, group discussions, and case studies about interpersonal and
intercultural communication, management techniques, theories and elements
of leadership practice, strategic thinking approaches, ethics in action,
and organizational behavior, among many other topics. I realized that what
I have learned in business school I could immediately apply to many
aspects of my work in science. I greatly improved my understanding of
leadership and, I believe, it also made me a more attentive person in
private life. I know now that leadership is a process, which means a
transactional event that occurs between the leader and followers (3), thus
it is a collective activity (4), and undoubtedly a real challenge worth
taking on (1). Leadership is a universal phenomenon, it is real and not a
figment of the imagination, and it has a substantial effect on
organizational outcomes (5). Providing good leadership requires a
willingness for continuing learning (6), an understanding of the
importance of effective and efficient listening to others (7), and the
capability and opportunity for deep introspection and self-reflection (8,
9). One must understand that developing and refining leadership skills
takes time and requires from the individual passion, commitment, and
endurance.
In hindsight, I wish that I would have taken management and
leadership courses much earlier in my scientific career. In this regard, I
strongly support the notion that leadership training should become a part
of medical and science education. I believe that resources dedicated to
leadership education would pay off immediately during the time students
spend in medical and graduate school as well as prepare them well for
every stage of their professional life. Last, but not least, leadership
training can have positive effects on the development of one's personal
life.
I would like to conclude my letter with another citation from the
book by Kouzes and Posner (1): "Leadership is important not just in your
own career and within your own organization. It's important in every
sector, in every community, and in every country. We need more exemplary
leaders, and we need them more than ever. There is so much extraordinary
work to be done. We need leaders who can unite us and ignite us."
REFERENCES
1. Kouzes MJ, Posner BZ. The Leadership Challenge. 3rd edn. San
Francisco, California: Jossey-Bass, 2002.
2. Warren OJ, Carnall R. Medical leadership: why it's important, what
is required, and how we develop it. Postgrad Med J 2011;87:27-32.
3. Northouse PG. Leadership: Theory And Practice. 4th edn. Thousand
Oaks, California: Sage Publications, 2007.
4. Noonan SJ. The Elements Of Leadership: What You Should Know.
Lanham, Maryland: Scarecrow Press, 2003.
5. Bass BM, Bass R. The Bass Handbook Of Leadership: Theory,
Research, And Managerial Applications. 4th edn. New York: Free Press,
2008.
6. Preskill S, Brookfield SD. Learning As A Way Of Leading: Lessons
From The Struggle For Social Justice. San Francisco, California: Jossey-
Bass, 2009.
7. Treece M. Successful Communication For Business And The
Professions. 6th edn. Needham Heights, Massachusetts: Allyn and Bacon,
1994.
8. Cashman K. Leadership From The Inside Out: Becoming A Leader For
Life. Provo, Utah: Executive Excellence Publishing, 1998.
9. Palmer PJ. Let Your Life Speak: Listening For The Voice Of
Vocation. San Francisco, California: Jossey-Bass, 2000.
Reply to Reply
In reply to De Wets and Bowie's reply to my criticism:
De Wet and Bowie state
1. Our paper makes it very clear that this is a study of primary care
records and not of consultations, GPs or of primary care per se.
Reply
Although this is true, nowhere does the paper explicitly explain that is
looking in primary records for errors across the totality of healthcare.
This is not mentioned un...
Reply to Reply
In reply to De Wets and Bowie's reply to my criticism:
De Wet and Bowie state
1. Our paper makes it very clear that this is a study of primary care
records and not of consultations, GPs or of primary care per se.
Reply
Although this is true, nowhere does the paper explicitly explain that is
looking in primary records for errors across the totality of healthcare.
This is not mentioned until page 179 (4th page of article) and then only
in passing. The clear assumption is that this is a study of primary care
records and is looking for error and harm in primary care and this
impression is not overtly refuted in the article.
De Wet and Bowie state
3. The harm rate per number of records and consultations is provided to
make the results more meaningful for primary care clinicians who have
multiple patient contacts.
Reply
No primary care clinician I have spoken to thinks including secondary care
events makes the results more meaningful to primary care clinicians.
Primary care clinicians want to know what their own error/harm rate is.
They do not want secondary care error/harm rates added to their own
figures and inflating the 'primary care' error/harm rate.
De Wet and Bowie state
4. Johnstone suggests the harm rate should be expressed as '...47 per 2251
consultations (2.1%)...' We provided this measure i.e. 1 per 48
consultations (a ratio that equates to 2.1%). We could calculate at least
six different measures involving the following variables: error, harm,
preventability, setting, record and consultation. All provide useful but
limited information, none is superior. We focused on harm per record
because that is what we judged as most relevant to patient safety.
Reply
I have no problem with this, but it must be made explicit and this is not
the case in this paper. The paper does not explicitly state that secondary
care errors are being included. Spinal surgery errors are mentioned in
passing and on page 179 the paper mentions 'procedures in secondary care.'
The paper continually mentions primary care, using the tool to provide a
'primary care equivalent'. On page 2 the paper's aims are to 'test a
validated trigger tool for the primary-car setting'. It does not mention a
secondary care setting. This lack of clarity invalidates this paper.
De Wet and Bowie state
5. We detected harm that originated in secondary care, which concurs with
previous research. (4) We discuss the implications of this and that most
'severe' cases originated in this setting. We do not state that the harm
rate of 9.4% is "for" primary care but make it clear that it is the harm
rate found in the records, regardless of source of origin or
preventability judgements.
Reply
Although De Wet and Bowie mention secondary care once in the discussion
section on page 179, the rest of the paper talks about harm and error in
primary care. The whole paper is about using the trigger tool to detect
and quantify error and harm in primary care, not in secondary care.
De Wet and Bowie state
6. Definitions of error and adverse event are outlined in our Methods
section. Careful reading of Tables 3 and 4 shows that matching study data
are presented for each category using the NCCMERP Error Index employed
(which defines near misses, error and harm). We use harm and adverse event
interchangeably, which is accepted practice. (5)(6)(7)
Reply
I accept this, but harm is regularly used when error should be used. This
occurs in the titles of tables 3 and 4. The NCCMERP tool detects error,
not just harm, not all errors lead to harm and not all harm is due to
error. This suggestsharm is more common than it is. On page 179 is the
sentence Most cases of harm were graded as category A-E (temporary harm to
a patient requiring an intervention). This is inaccurate as only category
E is harm, categories A-D are errors with the potential for harm, but with
no actual harm occurring.
De Wet and Bowie state
7. The NCCMERP index was selected in the absence of a universally agreed
system and because it is used in hospital care. We did not adapt it to
reduce bias. We provide a rationale: "In secondary-care studies, only
categories E to I have been used, as they correlate with actual patient
harm occurring. We included all categories because we assumed that
relatively minor events may be more common in primary care". This
assumption was proved correct. We also made the following recommendation:
"It may be reasonable to use only categories E to I in future to target
patient harm rather than just error".
Reply
De Wet and Bowie have misread their own paper, on page 180 they state '
Few adverse events were in categories A-D despite the expectation of high
error incidence.' Their assumption was proven wrong not correct.
De Wet and Bowie state
8. Johnstone states that he "almost believes" that we "confuse" these
terms "on purpose". This comment is lacking in reason and evidence.
Reply
True
De Wet and Bowie state
10. Johnstone queries the category E harm example in Table 2 (refer also
to our No. 6 and 7 responses). Some harm events may arise from normal or
evidence-based care. There may be no associated error (as in this example)
or obvious error. To illustrate: a patient is appropriately prescribed an
antibiotic but develops an allergic reaction. Record review reveals a
similar prescription and outcome previously, but no allergy code was
added. Arguably, this is preventable harm.(9)
Reply
I agree, the second prescription is preventable harm, the first
prescription is unavoidable harm.
De Wet and Bowie state
11. Johnstone is factually incorrect in stating that of "...the 47 events
in primary care, 11 were in the range of possible harm rather than actual
harm". 47 records contained evidence of some harm i.e. categories E
(n=39), F (n=6) and G (n=2). We cannot make this clearer.
reply
Yet again De Wet and Bowie have misread their own paper and confused
primary and secondary care. There are 47 events in primary care and 11 are
the category A-D, therefore possible harm not actual harm. Co-incidentally
the number of events in categories E-G is also 47, but 11 of these
occurred in secondary care.
De Wet and Bowie state
12. Johnstone states that we make a "throwaway comment" in the opening
paragraph because we suggest that the evidence cited is "...likely to be
an underestimation". Based on the evidence in hospital care (10), we
hypothesised that the rate in primary care is greater than currently
suggested, which is standard research practice. Our findings support our
hypothesis.
Reply
I disagree, De Wet and Bowie's findings show that preventable harm in
primary care is 1:125 consultations, almost identical to 1:120
consultations which they thought was an underestimation.
De Wet and Bowie state
14. The issue over the "headline figure" being "inflated" from 9.4% to
9.5% (it was rounded to the nearest 0.5%) is external to the debate on the
published paper.
Reply
Point taken, I will follow this up separately.
De Wet and Bowie state
17. We did not exclude the records of the 94 patients (18.8%) who had no
contact with primary care in the 12-month study period. If we now exclude
them (which is reasonable), the actual harm rate is 47/406 (11.6%),
strongly suggesting we underestimated the 'true' level.
Reply
The rate of preventable harm in 1:125 consultations is unaffected whether
the these 94 patients are included or excluded.
De Wet and Bowie state
18. We concede that our Abstract should read "...27/64 (42%) of error and
harm events were judged preventable..." However, this issue is reported
clearly in the main paper.
De Wet and Bowie state
19. We cannot control how others interpret our findings and are always
careful to explain the scientific limitations of our study.
Reply
Fair point, but the authors can control how the authors interpret and
explain their study. This is not directly related to retracting this paper
but on 10th June Bowie gave a power-point presentation titled 'Patient
Safety and the GPST' . The presentation states 'The NES Trigger Tool...
may enable you to measure the preventable harm rate.. which you can
monitor and reduce overtime.' Although they include secondary events, it
is hard for primary care clinicians to reduce errors in secondary care, eg
pain after a spinal operation. Had De Wet and Bowie applied this sentence
to their own paper, they would have reported the preventable harm rate in
primary care as 0.8% not 9.4%
De Wet and Bowie state
Screening medical records for undetected harm events only provides a
single perspective. The process cannot capture 'acts of omission' that
lead to harm nor are findings likely to correlate with data from patients,
incident reporting systems, significant event analyses, complaints,
litigation claims and so on. (11)(12)(13) The patient safety problem is
highly likely to be greater than can be deduced from screening medical
records, even when we account for source of origin and preventability
judgements.
Reply
I agree that Patient Safety is a major issue and should be taken immensely
seriously. However I do not believe it helps anyone to portray the problem
as greater than it is. I believe this paper has inaccuracies and gives the
impression of a 9.4% harm rate in primary care when the actual figure
could be better described as preventable harm occurs in 1:125
consultations in primary care (0.8%).
Thank you for the opportunity to respond to Dr Chris Johnstone's
comments on our 2009 publication.(1)
1. Our paper makes it very clear that this is a study of primary care
records and not of consultations, GPs or of primary care per se.
2. There is no "common method of measuring rates of harm" in primary
care (2) as Johnstone states. We refer to research on medical error and
the consultation (3) in our Introduction to demonstrate evidence of a
'problem', not to indicate our intended data analysis method.
3. The harm rate per number of records and consultations is provided
to make the results more meaningful for primary care clinicians who have
multiple patient contacts.
4. Johnstone suggests the harm rate should be expressed as '...47 per
2251 consultations (2.1%)...' We provided this measure i.e. 1 per 48
consultations (a ratio that equates to 2.1%). We could calculate at
least six different measures involving the following variables: error,
harm, preventability, setting, record and consultation. All provide
useful but limited information, none is superior. We focused on harm per
record because that is what we judged as most relevant to patient safety.
5. We detected harm that originated in secondary care, which concurs
with previous research. (4) We discuss the implications of this and that
most 'severe' cases originated in this setting. We do not state that the
harm rate of 9.4% is "for" primary care but make it clear that it is the
harm rate found in the records, regardless of source of origin or
preventability judgements.
6. Definitions of error and adverse event are outlined in our Methods
section. Careful reading of Tables 3 and 4 shows that matching study data
are presented for each category using the NCCMERP Error Index employed
(which defines near misses, error and harm). We use harm and adverse
event interchangeably, which is accepted practice. (5)(6)(7)
7. The NCCMERP index was selected in the absence of a universally
agreed system and because it is used in hospital care. We did not adapt
it to reduce bias. We provide a rationale: "In secondary-care studies,
only categories E to I have been used, as they correlate with actual
patient harm occurring. We included all categories because we assumed that
relatively minor events may be more common in primary care". This
assumption was proved correct. We also made the following recommendation:
"It may be reasonable to use only categories E to I in future to target
patient harm rather than just error".
8. Johnstone states that he "almost believes" that we "confuse" these
terms "on purpose". This comment is lacking in reason and evidence.
9. Johnstone states that because most 'serious' harm originated in
secondary care he believes this is "Hardly a major problem for primary
care". There are over 300 million consultations annually in UK primary
care. (8) A hypothetical harm rate between 0.1% and 5% (even if only half
was preventable and most low impact) is of concern to patients, clinicians
and the public.
10. Johnstone queries the category E harm example in Table 2 (refer
also to our No. 6 and 7 responses). Some harm events may arise from
normal or evidence-based care. There may be no associated error (as in
this example) or obvious error. To illustrate: a patient is appropriately
prescribed an antibiotic but develops an allergic reaction. Record review
reveals a similar prescription and outcome previously, but no allergy code
was added. Arguably, this is preventable harm.(9)
11. Johnstone is factually incorrect in stating that of "...the 47
events in primary care, 11 were in the range of possible harm rather than
actual harm". 47 records contained evidence of some harm i.e. categories
E (n=39), F (n=6) and G (n=2). We cannot make this clearer.
12. Johnstone states that we make a "throwaway comment" in the
opening paragraph because we suggest that the evidence cited is "...likely
to be an underestimation". Based on the evidence in hospital care (10),
we hypothesised that the rate in primary care is greater than currently
suggested, which is standard research practice. Our findings support our
hypothesis.
13. We have no knowledge of those "who would like to demean general
practice for their own ends" or of any current or planned "...unnecessary
change on GPs..." that is being "imposed" because of our small preliminary
study. It is not an academic matter.
14. The issue over the "headline figure" being "inflated" from 9.4%
to 9.5% (it was rounded to the nearest 0.5%) is external to the debate on
the published paper.
15. At no point is it inferred, directly or indirectly, "...how awful
GPs are..."
16. Johnstone accuses us of having an "agenda" to "...inflate harm in
general practice" when we (and the six other clinical reviewers) only ever
reported harm in the medical records. No evidence to support this
statement is offered.
17. We did not exclude the records of the 94 patients (18.8%) who had
no contact with primary care in the 12-month study period. If we now
exclude them (which is reasonable), the actual harm rate is 47/406
(11.6%), strongly suggesting we underestimated the 'true' level.
18. We concede that our Abstract should read "...27/64 (42%) of error
and harm events were judged preventable..." However, this issue is
reported clearly in the main paper.
19. We cannot control how others interpret our findings and are
always careful to explain the scientific limitations of our study.
Screening medical records for undetected harm events only provides a
single perspective. The process cannot capture 'acts of omission' that
lead to harm nor are findings likely to correlate with data from patients,
incident reporting systems, significant event analyses, complaints,
litigation claims and so on. (11)(12)(13) The patient safety problem is
highly likely to be greater than can be deduced from screening medical
records, even when we account for source of origin and preventability
judgements.
Yours faithfully
Carl de Wet MBChB MRCGP MMed (Fam)
Paul Bowie PhD
References
(1) de Wet C, Bowie P. The preliminary development and testing of a global
trigger tool to detect error and patient harm in primary-care records.
Postgrad Med J 2009 Apr;85(1002):176-180.
(2) Wetzels R, Wolters R, van Weel C, et al. Mix of methods is needed to
identify adverse events in general practice: a prospective observational
study. BMC Fam Pract 2008;9:35.
(3) Sandars J, Esmail A. The frequency and nature of medical error in
primary care: understanding the diversity across studies. Fam Pract 2003
Jun;20(3):231-236.
(4) Forster AJ, Murff HJ, Peterson JF, et al. The incidence and severity
of adverse events affecting patients after discharge from the hospital.
Ann Intern Med 2003 Feb 4;138(3):161-167.
(5) Elder NC, Pallerla H, Regan S. What do family physicians consider an
error? A comparison of definitions and physician perception. BMC Fam Pract
2006;7:73.
(6) Grober ED, Bohnen JM. Defining medical error. Can J Surg 2005
Feb;48(1):39-44.
(7) Yu KH, Nation RL, Dooley MJ. Multiplicity of medication safety terms,
definitions and functional meanings: when is enough enough?. Qual Saf
Health Care 2005 Oct;14(5):358-363.
(8) Department of Health. Departmental Report 2008. Department of Health:
2008.
(9) Gurwitz JH, Field TS, Harrold LR, et al. Incidence and preventability
of adverse drug events among older persons in the ambulatory setting. JAMA
2003 Mar 5;289(9):1107-1116.
(10) Landrigan CP, Parry GJ, Bones CB, et al. Temporal trends in rates of
patient harm resulting from medical care. N Engl J Med 2010 Nov
25;363(22):2124-2134.
(11) Kuzel AJ, Woolf SH, Gilchrist VJ, et al. Patient reports of
preventable problems and harms in primary health care. Ann Fam Med 2004
Jul-Aug;2(4):333-340.
(12) Thomas EJ, Petersen LA. Measuring errors and adverse events in health
care. J Gen Intern Med 2003 Jan;18(1):61-67.
(13) Field TS, Gurwitz JH, Harrold LR, et al. Strategies for detecting
adverse drug events among older persons in the ambulatory setting. J Am
Med Inform Assoc 2004 Nov-Dec;11(6):492-498.
Dear Sir/Madam,
We read with interest a review on peripartum cardiomyopathy (PPCM) by
Pyatt and Dubey (1) that has recently been published in your journal.
Reviewing the epidemiology of PPCM, the authors conclude that, "PPCM
appears not to have a hereditary association", and this erroneous
assertion is supported by the citation of three references.(2,3,4)
However, all three of the papers cited, actually emphasise th...
Dear Sir/Madam,
We read with interest a review on peripartum cardiomyopathy (PPCM) by
Pyatt and Dubey (1) that has recently been published in your journal.
Reviewing the epidemiology of PPCM, the authors conclude that, "PPCM
appears not to have a hereditary association", and this erroneous
assertion is supported by the citation of three references.(2,3,4)
However, all three of the papers cited, actually emphasise the current
thinking that PPCM does indeed have heretidary and/or genetic
underpinnings. We have recently demonstrated in a series of South African
families with familial dilated cardiomyopathy (DCM) that PPCM can present
as part of the spectrum of familial DCM.(5) Similarly, in 90 Dutch
families with familial DCM, van Spaendonck-Zwarts and colleagues have
found that PPCM may be the initial presentation of familial DCM and
identified previously undiagnosed DCM in the families of PPCM patients who
did not show full recovery.(6) In the US, 45 cases of PPCM were identified
from 530 pedigrees of familial DCM, and in 19 PPCM cases offered molecular
genetic screening the causative mutations were isolated in 6 patients.(7)
Furthermore, familial clustering was noted in 23 (55%) of the 42 unrelated
cases of PPCM in this study. In an editorial titled 'Birthing the Genetics
of Peripartum Cardiomyopathy' Anderson and Horne argue that "PPCM may
develop as a result of a complex interaction of pregnancy associated
factors against a susceptible genetic background".(8)
We have previously reviewed the role of genetics in the
aetiopathogenesis of PPCM.(9) Genetic susceptibility may account for up to
a third of cases of PPCM. In a series of 17 PPCM patients, Pierce and
colleagues found 3 (18%) to have a definite family history of PPCM.(4)
Likewise, there have been many reports of familial clustering of PPCM, (10
-13) clearly showing that the disease can have a hereditary association.
Nevertheless, while genetic susceptibility seems to play a role in
the development of PPCM, the majority of cases of PPCM do not have a
family history of the disease, and other environmental and biological
factors have been postulated to play a role (including inflammatory,
infectious, autoimmune, metabolic, hormonal and biochemical factors).(9)
The high incidence of PPCM in certain communities, (14) suggests that a
common genetic founder mutation cannot be excluded, however. Within
populations there is scope for variable genetic susceptibility, as well as
incomplete penetrance and variable expression of the causative mutations,
as with other forms of DCM.(15) It is clearly the interaction of
pathogenic and modifier genes with pregnancy-specific environmental,
clinical and biological factors that determines the final common
expression of PPCM.
The picture painted by the family and molecular studies has
implications for the management of patients with PPCM. First, in every
patient with PPCM, the construction of a 3- to 5-generation pedigree is
essential to exclude familial DCM. Second, clinical screening of first
degree relatives is required in order to exclude cases of undiagnosed
familial DCM. Finally, the management of PPCM requires a multidisciplinary
team of physicians, obstetricians and medical geneticists in order to
achieve optimal care.
References
1. Pyatt JR, Dubey G. Peripartum cardiomyopathy: current
understanding, comprehensive management review and new developments.
Postgrad J Med 2011; 87: 34-39.
2. Pearson GD, Veille JC, Rahimtoola S, et al. Peripartum
cardiomyopathy: National Heart, Lung, Blood Institute and Office of Rare
Diseases (National Institutes of Health). Workshop recommendations and
review. JAMA 2000; 283: 1183-1188.
3. Witlin AG, Mabie WC, Sibai BM. Peripartum cardiomyopathy: an
ominous diagnosis. Am J Obstet Gynecol 1997; 176: 182-188.
4. Pierce JA, Price BD, Joyce BW. Familial occurrence of postpartal
heart failure. Arch Intern Med 1963; 111: 651-655.
5. Ntusi NBA, Wonkam A, Shaboodien G, et al. Frequency and clinical
genetics of familial dilated cardiomyopathy in Cape Town: Implications for
the evaluation of patients with unexplained cardiomyopathy. S Afr Med J
2011; 101: 394-398.
6. van Spaendonck-Zwarts KY, van Tintelen JP, van Veldhuisen DJ, et
al. Peripartum Cardiomyopathy as a Part of Familial Dilated
Cardiomyopathy. Circulation 2010; 121: 2169-2175.
7. Morales A, Painter T, Li R, et al. Rare variant mutations in
Pregnancy-Associated or Peripartum Cardiomyopathy. Circulation 2010; 121:
2176-2182.
8. Anderson JL, Horne BD. Birthing the Genetics of Peripartum
Cardiomyopathy. Circulation 2010; 121: 2157-2159.
9. Ntusi NBA, Mayosi BM. Peripartum cardiomyopathy: a systematic
review. Int J Cardiol 2009; 131: 168-179.
11. Pearl W. Familial occurrence of peripartum cardiomyopathy. Am
Heart J 1995; 129: 421-422.
12. Voss EG, Reddy CV, Detrano R, et al. Familial dilated
cardiomyopathy. Am J Cardiol 1984; 54: 456-457.
13. Fett JD, Sundstrom BJ, Etta King M et al. Mother-daughter
peripartum cardiomyopathy. Int J Cardiol 2002; 86: 331-332.
14. Ntusi NBA, Mayosi BM. Epidemiology of heart failure in sub-
Saharan Africa. Expert Rev Cardiovasc Ther 2009; 7: 169-180.
15. Sliwa K, Hilfiker-Kleiner D, Petrie MC, et al. Current state of
knowledge on aetiology, diagnosis, management, and therapy of peripartum
cardiomyopathy: a position statement from the Heart Failure Association of
the European Society of Cardiology Working Group on peripartum
cardiomyopathy. Eur J Heart Fail 2010; 12: 767-778.
Editor:
We agree with the authors of this wide and accurate review that persons
while they grow old have anatomic and physiological changes in central and
peripheral nervous systems, as well as, in cognitive domain expressing in the
interview and physical exam of the elderly. But, frequently, the doctors
have difficulties to determine where and when the physiological end and
the pathological begin in a proper older...
Editor:
We agree with the authors of this wide and accurate review that persons
while they grow old have anatomic and physiological changes in central and
peripheral nervous systems, as well as, in cognitive domain expressing in the
interview and physical exam of the elderly. But, frequently, the doctors
have difficulties to determine where and when the physiological end and
the pathological begin in a proper older adult.
We know today that neurological and cognitive changes are included in the
clinical features of frailty, conceptualized as a physiological syndrome
characterized by decreased reserve and reduced resistance to stressors,
resulting from cumulative decline across physiological systems resulting
in 'vulnerability to adverse outcomes.'(1).
These bad results are the followings: increased risk for acute diseases
(in particular, infections), falls and its consequences (damage,
fractures), hospitalization, institutionalization, disability, dependence
and death (2, 3).
Sarcopenia (loss of skeletal muscle mass) constitutes one determinant of
frailty syndrome. The observed age-related decrease in muscle cross-
sectional area seems to be the result of a decrease in the size of type 2
muscle fibers compared with that of type 1 muscle fibers and also from
loss of muscle fiber number. This process is believed to be consistent
with a progressive denervation and reinnervation process secondary to a
chronic neuropathic process (4).
Furthermore, many authors consider that cognitive impairment is one of the
most important components of frailty, and also, that mild cognitive
impairment, named as "benign forgetfulness", is not as benign as it seems,
because many older adults with this condition develop Alzheimer's Disease
in the course of years (5).
Thus, we consider that neurological and cognitive changes detected in the
elderly cannot be taken lightly, we must be aware for its further
evolution and not resignation to assume to ageing per se.
Sincerely,
Julio C. Romero, Angel J. Romero
References:
1. Ferrucci L, Guralnik JM, Studenski S, Fried LP, Cutler GB Jr, Walston
JD. Interventions on Frailty Working Group. Designing randomized,
cotrolled trials aimed at preventing or delaying functional decline and
disability in frail older persons: a consensus report. J Am Geriatr Soc
2004; 52(4): 625-34.
2. Daniels R, Van Rassum E, De Witle L, Van der Hervel W. Frailty in older
age: concepts and relevance for occupational and physical therapy. Phys
Occup Ther Geriatr 2008; 27(2): 81-95.
3. Romero AJ. Frailty: and emerging geriatric syndrome. Medisur 2010;
8(6): 81-90.
4. Thomas DR. Sarcopenia. Clin Geriatr Med 2010; 26: 331-346.
5. Mayeux R. Early Alzheimer Disease. N Engl J Med 2010; 362: 2194-201.
In the first few weeks of my medical internship, one intern was in
the habit of writing "DOA" in his admitting histories and physicals. He
was eventually confronted by the senior resident who asked for an
explanation. It was quite simple. DOA, after all, stood for "day of
admission". Didn't everyone know this? I still chuckle at the memory.
In the first few weeks of my medical internship, one intern was in
the habit of writing "DOA" in his admitting histories and physicals. He
was eventually confronted by the senior resident who asked for an
explanation. It was quite simple. DOA, after all, stood for "day of
admission". Didn't everyone know this? I still chuckle at the memory.
The Editor
Postgraduate Medical Journal, BMA House, Tavistock House, London WC1H 9JR
30 June 2011
Dear Editor,
A 2009 paper by de Wet and Bowie in the Postgraduate Medical Journal(1) has recently been used by its authors' employer to suggest that, "A recent pilot study reviewing a random selection of primary care electronic medical records found a harm rate of 9.5%".(2) Not only is this
interpretation of...
The Editor
Postgraduate Medical Journal, BMA House, Tavistock House, London WC1H 9JR
30 June 2011
Dear Editor,
A 2009 paper by de Wet and Bowie in the Postgraduate Medical Journal(1) has recently been used by its authors' employer to suggest that, "A recent pilot study reviewing a random selection of primary care electronic medical records found a harm rate of 9.5%".(2) Not only is this
interpretation of the paper inaccurate, there are errors contained within the paper which require scrutiny.
The de Wet and Bowie paper was designed to 'develop and test a trigger tool to detect patient harm'. The paper frequently confuses records and consultations. There were 500 records and 2,251 consultations included in the study. The 9.4% (not 9.5% as quotedii) harm rate comes from 47
episodes per record, and not per consultation (the more common method of measuring rates of harm and used by the authors in their opening paragraph). Avoiding this confusion would mean the rate of harm is 47 per
2,251 consultations (2.1%).
The authors appear to have difficulty differentiating between primary and secondary care. The trigger tool is designed to detect errors and harm in primary care records. The authors interpret these as errors and harm
resultant from primary care, however the tool actually detects errors in both primary and secondary care. Of the 64 episodes of error, adverse event and/or harm discovered in the 2,251 primary care consultations, 17 occurred in secondary care. Thus, the error, adverse event and/or harm
rate would more accurately be reported as 47 per 2,251 primary care consultations (or one episode per 47.8 consultations - 2.1% compared to the headline figure of 9.4%).
The authors also frequently confuse harm, error and adverse event. They use the NCCMERP index for categorizing harm. However the first four categories, A,B,C and D only represent potential harm, not actual harm. This is not made clear in the titles of Tables 3 and 4, both of which
mention harm, but not error or adverse event, suggesting all the episodes were of harm, not just errors or adverse events which did not lead to harm. This confusion between error, adverse event and harm is so common in the paper one could almost believe it was on purpose. Incidentally, the paper itself points out that all but 8 episodes of harm were of the lowest level and of this 8, 5 were in secondary care. The only 'severe' episode of harm also occurred in secondary care. Hardly a major problem for
primary care, but not clearly explained in the headline figure of 9.4%.
So returning to the 47 events in primary care, 11 were in the range of possible harm rather than actual harm. There were only 36 events which actually led to harm, 36/2,251 consultations, or one per 62.5 consultations in primary care (1.6%). Table 4 points out that 27 episodes of harm were preventable. Eighteen of these occurred in primary care and nine in secondary care. Therefore, of the 36 events in primary care which led to actual harm, only 18 were preventable and cannot be described as an error (e.g. a patient reasonably given a statin for heart disease who develops abnormal LFTs is described as an episode of unavoidable harm). So the error rate in primary care
which led to harm is more accurately 18 per 2,251 primary care consultations, or one per 125 primary care consultations (0.8%). Interestingly, this is very similar to the 1 per 120 consultations mentioned in the article's opening paragraph, but which the authors seem to think 'is likely to be an underestimation'. The authors do not give
their reasoning behind this throwaway comment and they fail to mention that their very own paper supports the complete opposite view.
In addition to the blatant misrepresentation of the data described above, the paper also contains a mistake in the opening Results section. It says "...an adverse event was found in 47 records... Of these, 27 were judged to be preventable (42%)". In fact 27/47 is 57.4% and not 42%. I think that authors mean 27 of all 64 episodes were preventable but they appear to have confused records with consultations, again.
I think I have shown that the paper has inaccuracies, is confused about records and consultations, primary and secondary care, error, harm and adverse event and the difference between unavoidable and preventable. The
headline figure of 9.4% has already been inflated to 9.5% by a respected organisation and the employers of the original paper.(2) This figure is being used and repeated in conversations with politicians, managers and a variety of organisations who would like to demean general practice for their own ends. It is possible, using the same data, to say that avoidable harm only occurs in 1 in 125 consultations. I believe the authors have an agenda to inflate harm in general practice as substantiated by their
comment at the end of the first paragraph.
I am a hardworking GP and I do not need to be told how awful GPs are, especially when it is based on erroneous, biased articles. I do not want to go to meetings to hear this 9.4% figure used to impose further unnecessary change on GPs. The paper is not worthy of your publication. Therefore I would be grateful if you would withdraw this paper at the earliest opportunity.
Yours sincerely,
Chris Johnstone
A really pissed off GP
The Barony Practice, Northcroft St, Paisley, PA3 4AD
References
1. de Wet C, Bowie P. The preliminary development and testing of a global
trigger tool to detect error and patient harm in primary-care records.
Postgraduate.Medical Journal 2009; 85(1002): 176-180.
2. An introduction to Safety Climate [accessed at
http://www.knowledge.scot.nhs.uk/media/CLT/ResourceUploads/23626/SC%20overview%20for%20practices%20MASTERCOPY.pdf
on 30th June 2011].
Conflict of Interest:
I am a GP in the West of Scotland. I am paid sessional work by NHS Education Scotland. I am not sure if these count.
The identification of leadership as a key skill for doctors is a
positive step, however have we undervalued the medical community's assets
when considering the development of medical leadership?
Green Templeton College is a graduate college in Oxford, specialising
in subjects relating to human welfare and social, economic and
environmental well-being in the 21st century. GTC has taken a more local
approach to ma...
The identification of leadership as a key skill for doctors is a
positive step, however have we undervalued the medical community's assets
when considering the development of medical leadership?
Green Templeton College is a graduate college in Oxford, specialising
in subjects relating to human welfare and social, economic and
environmental well-being in the 21st century. GTC has taken a more local
approach to management and leadership, making use of the diverse college
community to provide a middle road between a broad compulsory training and
intensive course for the high flyers.
We have launched a programme for doctors in training who are interested in
developing their management and leadership skills. Optional Saturday
morning workshops are provided free of charge; informal talks,
participative workshops and facilitated case studies are steered by
doctors and managers linked with the college, aiding the sharing of skills
and knowledge among those interested.
Feedback has been positive, creating a wish-list remarkably similar
to that described by Warren and Carnall, including "softer skills", career
planning events, case studies, formation of a case book, opportunities for
shadowing, mentoring and extended projects or management electives. We
plan to expand this programme to regular monthly workshops, demonstrating
that this demand can be met within an existing community.
The explosion of the leadership culture through the medical world has
brought many valuable strategies from the sphere of management, but should
we take a step back and value what we have already? Commercial leadership
courses, action learning and coaching have their role, however it might be
worth recognising what we already do well and to focus on sharing the mix
of skills, so often found in medical communities, more effectively.
I want to highlight few points about the study.First, IgA nephropathy is seen in nearly 40% of renal biopsy specimens of acute glomerulonephritis patients in asia in various study.In this study it is comprising only 8.1% of cases.Second, it is an crossectional study, taking data from the renal biopsy report thus not showing the exact % of acute glomerulonephritis caused by IgA nephropathy.So the finding is quite exaggerat...
Management of special type of dyslipidemia; Low HDL-C, high TG, Type- B size LDL-P in patients with T2DM is a big challenge for a physician. For primary LDL-C goal, we the physician usually go for stronger statins like atorvastatin or rosuvastatin. Addition of fenofibrate to the above statins to reduce concomitant high TG really reduces TG level but does such combination offer any strong role in reducing mortality in this p...
Kouzes and Posner (1) once wrote that "The domain of leaders is the future. The leaders unique legacy is the creation of valued institutions that survive over time. The most significant contribution leaders make is not simply to today's bottom line; it is to the long-term development of people and institutions so they can adapt, change, prosper, and grow."
As Warren and Carnall (2) stated, medical leadership is...
Reply to Reply In reply to De Wets and Bowie's reply to my criticism:
De Wet and Bowie state 1. Our paper makes it very clear that this is a study of primary care records and not of consultations, GPs or of primary care per se.
Reply Although this is true, nowhere does the paper explicitly explain that is looking in primary records for errors across the totality of healthcare. This is not mentioned un...
Dear Editor
Thank you for the opportunity to respond to Dr Chris Johnstone's comments on our 2009 publication.(1)
1. Our paper makes it very clear that this is a study of primary care records and not of consultations, GPs or of primary care per se.
2. There is no "common method of measuring rates of harm" in primary care (2) as Johnstone states. We refer to research on medical error and t...
Dear Sir/Madam,
We read with interest a review on peripartum cardiomyopathy (PPCM) by Pyatt and Dubey (1) that has recently been published in your journal. Reviewing the epidemiology of PPCM, the authors conclude that, "PPCM appears not to have a hereditary association", and this erroneous assertion is supported by the citation of three references.(2,3,4) However, all three of the papers cited, actually emphasise th...
Editor:
We agree with the authors of this wide and accurate review that persons while they grow old have anatomic and physiological changes in central and peripheral nervous systems, as well as, in cognitive domain expressing in the interview and physical exam of the elderly. But, frequently, the doctors have difficulties to determine where and when the physiological end and the pathological begin in a proper older...
In the first few weeks of my medical internship, one intern was in the habit of writing "DOA" in his admitting histories and physicals. He was eventually confronted by the senior resident who asked for an explanation. It was quite simple. DOA, after all, stood for "day of admission". Didn't everyone know this? I still chuckle at the memory.
Conflict of Interest:
None declared...
The Editor
Postgraduate Medical Journal, BMA House, Tavistock House, London WC1H 9JR
30 June 2011
Dear Editor,
A 2009 paper by de Wet and Bowie in the Postgraduate Medical Journal(1) has recently been used by its authors' employer to suggest that, "A recent pilot study reviewing a random selection of primary care electronic medical records found a harm rate of 9.5%".(2) Not only is this interpretation of...
The identification of leadership as a key skill for doctors is a positive step, however have we undervalued the medical community's assets when considering the development of medical leadership?
Green Templeton College is a graduate college in Oxford, specialising in subjects relating to human welfare and social, economic and environmental well-being in the 21st century. GTC has taken a more local approach to ma...
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