We read with interest the editorial by Birring and Peake on early
diagnosis and screening of lung cancer [1]. The diagnosis of lung cancer is
often delayed by the patient themselves, although some doctors are still
guilty of adopting the laissez-faire approach towards small, particularly
calcified lesions. As clinicians, we are increasingly seeing referrals of
incidental small lung nodules on computed...
We read with interest the editorial by Birring and Peake on early
diagnosis and screening of lung cancer [1]. The diagnosis of lung cancer is
often delayed by the patient themselves, although some doctors are still
guilty of adopting the laissez-faire approach towards small, particularly
calcified lesions. As clinicians, we are increasingly seeing referrals of
incidental small lung nodules on computed tomography (CT).
The authors
clearly pointed out that even 10mm tumours with 109 cells can already
represent a late stage in lung cancer. In this modern era, we believe all
lung lesions should be investigated and histological diagnosis obtained.
Patients with a lesion too small to undergo image-guided fine needle
aspiration (FNA), typically smaller than 8mm in our institute, would be
fully counselled and be offered video-assisted thoracic surgery (VATS)
biopsy with intra-operative frozen section followed by oncological lung
resection if indicated. We have had successes with resection of tiny 1mm
lung cancer nodules using the above algorithm when assisted by immediate
pre-operative CT localization of the lesion with pig-tail hooked wire by
radiologist [2]. Whether these tiny lesions should have a separate cancer
stage, namely pre-stage Ia or Ia1, and result in better survival following
resection will be a matter for future debate and research. The optimum
strategy for the management of small lesions whether incidentally or
during screening certainly needs to be determined.
Yours sincerely,
Dr. Calvin S.H. Ng, Senior resident
Prof. Anthony P.C. Yim, Professor & Chief of Cardiothoracic Surgery
References
1. Birring SS, Peake MD. Symptoms and the early diagnosis of lung cancer.
Thorax 2005; 60:268-9.
2. Ciriaco P, Negri G, Puglisi A, Nicoletti R, Del Maschio A, Zannini P.
Video-assisted thoracoscopic surgery for pulmonary nodules: rationale for
preoperative computed tomography-guided hookwire localization. Eur J
Cardiothorac Surg 2004;25:429-33.
Whilst one must of course take into account the mortality figures
whilst treating multi-drug resistant tuberculosis,
there may be other aspects that need to be studied.
The collegues would to well perhaps to address some part of their research
to the mortality of those patients who had been prescribed for a protected
period antituberculous chemotherapy: (this can be for up to two years),
and who have been m...
Whilst one must of course take into account the mortality figures
whilst treating multi-drug resistant tuberculosis,
there may be other aspects that need to be studied.
The collegues would to well perhaps to address some part of their research
to the mortality of those patients who had been prescribed for a protected
period antituberculous chemotherapy: (this can be for up to two years),
and who have been misdiagnosed. There are understandable reasons for the
policy of treating asap. But everyone should be aware of the possibility
of unnecessarily rushing to treat.
In a recent issue of Thorax, van der Palen et al. [1] published a
study showing that a reduced
Maximal Inspiratory Pressure (MIP), a measure of diaphragmatic inspiratory
muscle strength, is a risk factor for incident myocardial infarction and
death from cardiovascular disease in a population of subjects without
previously reported cardiovascular events. We believe this result has a
strong impact on...
In a recent issue of Thorax, van der Palen et al. [1] published a
study showing that a reduced
Maximal Inspiratory Pressure (MIP), a measure of diaphragmatic inspiratory
muscle strength, is a risk factor for incident myocardial infarction and
death from cardiovascular disease in a population of subjects without
previously reported cardiovascular events. We believe this result has a
strong impact on the understanding of the increased cardiovascular risk in
persons with impaired lung function.
An "impaired lung function", as indicated by low forced vital
capacity (FVC), forced expiratory volume in 1 second (FEV1) and peak
expiratory flow (PEF), has been repeatedly associated with a higher risk
of cardiovascular morbidity and mortality, independently of visceral
obesity and smoking.[2] Insulin-resistance [3] and systemic inflammation
[4] qualify these subjects and potentially account for the
atherothrombotic risk. Moreover, several studies have proven a poor lung
function in the vast majority of patients affected by diabetes mellitus.[5]
However, the generic condition of "impaired lung function"
encompasses two particular respiratory alterations: a restrictive
dysfunction, characterised by a homogenous decrease of FVC, FEV1 and PEF
[6], and an obstructive pattern, with a predominant FEV1 fall and low
FEV1/FVC ratio, typical of chronic obstructive pulmonary disease (COPD).[7] Recent epidemiological data suggest that in restrictive subjects the
level of systemic inflammation [8] and the risk of incident death [7] are
comparable to what observed in patients with moderate COPD. Conversely,
restrictive subjects, but not COPD patients, are more likely to develop
diabetes mellitus [9,10], suggesting that undetermined metabolic
abnormalities specifically characterise patients with a restrictive
dysfunction. It is therefore likely that COPD and restrictive syndrome
predispose to vascular disease through partly different mechanism/s, that
should be further investigated.
The study of van der Palen et al. [1] is important because it focuses
on a particular aspect of respiratory pathophysiology, the reduction of
diaphragmatic inspiratory muscle strength, which may underlie the
restrictive syndrome and have metabolic origin. However, the authors did
not mention diabetes and impaired glucose tolerance (both included among
the descriptive variables) as potential confounding factors. Indeed,
because of the strong association between insulin resistance [3] and
diabetes [9,10] with the restrictive syndrome, the statistical impact of
pre-diabetes and diabetes in the relation between MIP and vascular events
should be better clarified by the authors.
References
1. van der Palen J, Rea TD, Manolio TA, et al. Respiratory muscle
strength and the risk of incident cardiovascular events. Thorax 2004; 59:
1063-67.
2. Hole DJ, Watt GC, Davey-Smith G, et al. Impaired lung function and
mortality risk in men and women: findings from the Renfrew and Paisley
prospective population study. BMJ 1996; 313: 711-5.
3. Lawlor DA, Ebrahim S, Davey-Smith G. Association of measures of lung
function with insulin resistance and type 2 diabetes: findings from the
British Women’s Heart and Health Study. Diabetologia 2004; 47: 195-203.
4. Engstrom G, Lind P, Hedblad B, et al. Lung function and cardiovascular
risk. Relationship with inflammatory-sensitive plasma protein. Circulation
2002; 106: 2555-60.
5. Lange P, Groth S, Kastrup J, et al. Diabetes mellitus, plasma glucose
and lung function in a cross-sectional population study. Eur Resp J 1989;
2:14-9.
6. Mannino DM, Buist AS, Petty TL, et al. Lung function and mortality in
the United States: data from the First National Health and Nutrition
Examination Survey follow up study. Thorax 2003; 58: 388-93.
7. National Institutes for Health. Global Initiative for Chronic
Obstructive Lung Disease (GOLD). Publication No 2701. Bethesda: National
Institutes for Health, 2001 (2004 update).
8. Mannino DM, Ford ES, Redd SC. Obstructive and restrictive lung disease
and markers of inflammation: data from the Third National Health and
Nutrition Examination. Am J Med 2003: 114: 758-762.
9. Ford ES, Mannino DM. Prospective association between lung function and
the incidence of diabetes. Findings from the National Health and Nutrition
Examination Survey Epidemiologic Follow-Up Study. Diabetes Care 2004; 27:
2966-70.
10. Fimognari FL, Scarlata S, Pastorelli R, et al. Restrictive ventilatory
dysfunction and dyspnea in elderly subjects. Am J Med 2005; November, in
press.
I am a graduate student in Hebei Medical University in China. Now I am
preparing for my trial, which is related to ec-sod. Although I have made my
greatest efforts, I cannot find how to measure the activity and concentration of the plasm ec-sod. Many related articles cited the article "Quantitative and qualitative changes of extracellular-superoxide dismutase
in patients with various diseases" Clinica Chi...
I am a graduate student in Hebei Medical University in China. Now I am
preparing for my trial, which is related to ec-sod. Although I have made my
greatest efforts, I cannot find how to measure the activity and concentration of the plasm ec-sod. Many related articles cited the article "Quantitative and qualitative changes of extracellular-superoxide dismutase
in patients with various diseases" Clinica Chimica Acta 229 123-131 in 1994. However, I cannot find the article.
So I am in great need of your help in how to measure the activity and concentration of the plasm ec-sod, anxiously hoping you reply. I will be very grateful to receive your help.
The letter from Dr Eltzschig [1] refers to their paper showing that
surgical embolectomy remains an option in severe pulmonary embolism.
Firstly, this required "a multidisciplinary evaluation team with a
widespread reputation for 24-hour availability, 7 days per week" (and over
half of their patients had surgery during the weekend); there must be very
few centres in the world who can offer such a service,...
The letter from Dr Eltzschig [1] refers to their paper showing that
surgical embolectomy remains an option in severe pulmonary embolism.
Firstly, this required "a multidisciplinary evaluation team with a
widespread reputation for 24-hour availability, 7 days per week" (and over
half of their patients had surgery during the weekend); there must be very
few centres in the world who can offer such a service, and few patients
would be able to reach them in time.
Secondly, they acknowledge that their
improved mortality was almost certainly due to including many patients
with submassive PE, a group in whom it is not even universally agreed that
thrombolysis is superior to heparin.
Thirdly, an alternative to
thrombolysis that could be more widely and readily available, and which
only requires one experienced radiologist, is catheter fragmentation (as
referenced in our guidelines).
This first-class Boston group are well
placed to consider a study in which patients are randomised to these
different treatment groups, and may find that the less invasive options
are at least as effective as well as being more applicable to non-specialist centres.
References
(1) Eltzschig HK, Rosenberger P. Surgical Pulmonary Embolectomy [electronic response to British Thoracic Society guidelines for the management of suspected acute pulmonary embolism] thoraxjnl.com 2003 http://thorax.bmjjournals.com/cgi/eletters/58/6/470#66
British Thoracic Society guidelines for the management of suspected acute pulmonary embolism
It is indeed unsatisfactory to make such recommendations in the
absence of prospective studies; three have now been published.[1-3]
Although differing in the way clinical probability was evaluated and in
the D-dimer assays used, all found that in combination many patients with
suspected pulmonary embo...
British Thoracic Society guidelines for the management of suspected acute pulmonary embolism
It is indeed unsatisfactory to make such recommendations in the
absence of prospective studies; three have now been published.[1-3]
Although differing in the way clinical probability was evaluated and in
the D-dimer assays used, all found that in combination many patients with
suspected pulmonary embolism (PE) could safely be managed without further
imaging or anticoagulation. These encouraging results suggest that the
same is true with our simpler clinical model, originally conceived by
extrapolation from the deep vein thrombosis study of Wells’s group and
subsequently corroborated by them for PE.[4,5] A multi-centre study of
patients seen by middle-grade doctors in district general hospitals is
certainly very desirable.
A similar dilemma occurs in suspected subarachnoid haemorrhage (SAH),
another potentially fatal condition with a wide differential diagnosis.
Perhaps here too all should have an urgent CT scan, but in practice
clinicians use clinical pointers to decide when this is unnecessary.
Therefore, when updating our guidelines for PE (far commoner than SAH), we
decided to continue with a promising (albeit unproven) suggestion because
the two alternatives were less satisfactory. The first is that clinicians
continue to make decisions based on either no or inadequate imaging, which
should now be considered indefensible both medically and legally. The
second is that all patients with suspected pulmonary embolism should
undergo appropriate imaging, with major resource implications in a
situation where the diagnosis will only be confirmed in 15-30% of cases.
Although not yet irrefutable, evidence is growing that being selective in
requesting such tests is possible and safe.
References
(1) M Rodger, Wells P, Makropoulos D, et al. The bedside investigation
of pulmonary embolism diagnosis (BIOPED) study. Acad Emerg Med 2003;10:502.
(2) MG Leclercq, Lutisan JG, van Marwijk Kooy M, et al. Ruling out
clinically suspected pulmonary embolism by assessment of clinical
probability and D-dimer levels: a management study. Thromb Haemost 2003;89:97-103.
(3) JA Kline, Webb WB, Jones AE, et al. Impact of a clinical decision rule
and a D-dimer plus alveolar deadspace measurement to rule out pulmonary
embolism in an urban emergency department. Acad Emerg Med 2003;10:502.
(4) P Wells, Hirsh J, Anderson D, et al. Accuracy of clinical assessment of
deep-vein thrombosis. Lancet 1995;345:1326-30.
(5) PS Wells, Ginsberg JS, Anderson DR, et al. Use of a clinical model for
safe management of patients with suspected pulmonary embolism. Ann Intern
Med 1998;129:997-1005.
Berkman and colleagues [1] put forward an impressive argument for the
use of exhaled nitric oxide (eNO) in diagnosing asthma through employment
of a cut off value of 7 parts per billion in differentiating between
asthmatics and non-asthmatics.
Although it is unquestionable that elevated levels of eNO indicate
underlying airway inflammation, it must be appreciated that the latter is
not syno...
Berkman and colleagues [1] put forward an impressive argument for the
use of exhaled nitric oxide (eNO) in diagnosing asthma through employment
of a cut off value of 7 parts per billion in differentiating between
asthmatics and non-asthmatics.
Although it is unquestionable that elevated levels of eNO indicate
underlying airway inflammation, it must be appreciated that the latter is
not synonymous with asthma. The same can be said of a positive response to
bronchial provocation, which merely signifies the presence of bronchial
hyperresponsiveness but not necessarily asthma.
I am slightly perturbed to note the presence of a clear outlier
within the asthma group as evidenced from the scatter plots in Figure
1(A). This is especially pertinent as eNO is the primary outcome variable
in a study consisting of a relatively small number of patients where any
outlier may be potentially confounding. Can the authors provide
reassurance that the results of the study still hold true when the
solitary outlier is excluded from data analysis?
eNO is at present best suited as a tool for monitoring response to
anti-inflammatory therapy in asthma. eNO can also be useful in aiding a
clinician in diagnosing asthma when considered in conjunction with other
measures of airway inflammation. However, to utilise eNO as a sole
diagnostic test for asthma may be premature without first embarking on
further definitive studies.
References
1. Berkman N, Avital A, Breuer R, et al. Exhaled nitric oxide in the
diagnosis of asthma: comparison with bronchial provocation tests. Thorax
2005;60:383-8.
These clinically important papers [1,2] by the Isolde researchers
provide excellent data questioning the rationale behind inclusion of
patients in the large COPD-studies that have been reported in past few
years. Selection of patients on the basis of absence of reversibility
means ruling out the easiest measurable variable that may correlate with
steroid response. When assessing effects of two weeks pred...
These clinically important papers [1,2] by the Isolde researchers
provide excellent data questioning the rationale behind inclusion of
patients in the large COPD-studies that have been reported in past few
years. Selection of patients on the basis of absence of reversibility
means ruling out the easiest measurable variable that may correlate with
steroid response. When assessing effects of two weeks prednisolone, or the
value of reversibility as a determinant of long-term treatment response to
inhaled steroids, one should bear in mind that the Isolde population does
not represent the typical patient with COPD that primary care physicians
encounter in daily practice. In primary care, one finds all degrees of
reversibility, both mild, moderate and indeed some severe COPD, some with
and some without significant response. Although highly relevant, the
results of the two Isolde papers represent only moderate to severe COPD in
absence of reversibility. Therefore, Gross is very right in his editorial
to state that we should be openminded about the future; the COOPT-Study
which is currently conducted in the Netherlands (Europe) consciously
dismissed reversibility as an entry criterion and recruited its population
in primary care.[3] Similar to Isolde we performed the two weeks'
pretreatment with prednisolone before randomisation and will look at
reversibility as a determinant for inhaled steroid response. Results will
be available next year, and then we can finally widen our focus to include
the field of primary care as well. Don't worry about the fat lady; she
will be back.
References
(1) Burge PS, Calverley PMA, Jones PW, et al. Prednisolone response in patients with chronic obstructive pulmonary disease: results from the
ISOLDE study. Thorax 2003;58:654–8.
(2) Calverley PMA, Burge PS, Spencer A, et al. Bronchodilator reversibility
testing in chronic obstructive pulmonary disease. Thorax 2003;58:659–64.
(3) Chavannes NH, Schermer TRJ, Wouters EF, Van Weel C, Van Schayck CP.
Treatment of COPD in general practice: the COOPT study. Eur Respir J
2001;18(Suppl 33):348S.
The study by Tomlinson and colleagues [1] stirs further debate in
relation to patients with asthma who continue to smoke. There are several
points in the study, which are pertinent to consider.
Firstly, the small but statistically significant difference of 25
l/min in morning peak expiratory flow (PEF) observed between smokers and
non-smokers following 12 weeks of low dose inhaled corticoste...
The study by Tomlinson and colleagues [1] stirs further debate in
relation to patients with asthma who continue to smoke. There are several
points in the study, which are pertinent to consider.
Firstly, the small but statistically significant difference of 25
l/min in morning peak expiratory flow (PEF) observed between smokers and
non-smokers following 12 weeks of low dose inhaled corticosteroid (ICS)
therapy may not be clinically relevant. Indeed, there was no difference
demonstrated in pre-bronchodilator forced expiratory volume in one second
(FEV1) following treatment with either low or high dose ICS therapy
between smokers and non-smokers. Moreover, the relatively high baseline
pre-bronchodilator FEV1 of more than 80% of predicted normal, further
questions the relevance of such a small difference in PEF.
Secondly, the increased exacerbation rate observed in asthmatic
smokers may be directly attributable to tobacco smoke itself rather than
corticosteroid insensitivity. This is because even with high doses of ICS,
a difference persisted in morning PEF between smokers and non-smokers,
albeit of smaller magnitude with a statistically non-significant trend.
One could therefore argue that high doses of ICS may actually mask the
negative effects of smoking.
Finally, the comment that asthmatics who continue to smoke may
require alternative or additional anti-inflammatory drug treatment should
be treated with caution. This may give the wrong impression that the
medical profession will automatically deal with tobacco addiction through
alternative pharmacological intervention. Clinicians should never forget
that the first line management of all asthmatic smokers must always be
strong encouragement to quit.
References
1. Tomlinson JE, McMahon AD, Chaudhuri R, et al. Efficacy of low and
high dose inhaled corticosteroid in smokers versus non-smokers with mild
asthma. Thorax 2005;60:282-7.
I read with interest the latest comprehensive BTS guidelines on chest
drain insertion. We would like to share with you some tips and words of
caution accumulated by experience from our institute.
During chest drain insertion, we routinely monitor oxygen saturation
continuously with or without prior sedation. Patient with secondary
pneumothorax i.e. from COAD can deteriorate during chest drai...
I read with interest the latest comprehensive BTS guidelines on chest
drain insertion. We would like to share with you some tips and words of
caution accumulated by experience from our institute.
During chest drain insertion, we routinely monitor oxygen saturation
continuously with or without prior sedation. Patient with secondary
pneumothorax i.e. from COAD can deteriorate during chest drain insertion.
Furthermore, at the start of the procedure, the nasal oxygen cannula is
sited ( but not necessarily turned on) to allow quick delivery of oxygen
in an emergency situation. This is particularly true when patients are put
in the lateral decubitus position because placing nasal cannula may be
more difficult than if the patient is sitting.
In the section on drain removal, as a reminder to junior doctors, it
is generally recommended that the suction should be turned off prior to
removing the drain because of the theoretical risk of tearing the lung.
Interestingly, there is currently no strong evidence to support
removal of chest drains during the Valsalva manoeuvre or expiration; even
though the majority of doctors follow this guideline. Physiological
understanding suggest that creating a positive intrapleural pressure
during chest drain removal may reduce the risk of air entering the pleural
cavity. However, study by Bell et al. found no difference in pneumothorax
rate whether removal was performed at end inspiration or end
expiration.[1] Our experience suggest that important factors influencing
post-removal pneumothorax rate are:
(a) speed of chest drain removal to
prevent air entering the pleural cavity through the side holes at removal,
and (b) preventing para-drain leakage by digital compression of wound site
during removal.
Finally, we have experience of the drain kinking at the point where
the tube penetrates the chest wall. The "omental tag of tape" referred by
the guidelines can help reduce this occurence. In addition, we found it
useful to roll up 2-3 pieces of gauze and place it under (rather than
over) the drain right at the point where the tube penetrates the chest
wall to bolster the tube and prevent the acute angle it can form with the
chest wall, especially with over zealous or tight dressings at that area.
Reference
(1) Bell RL, Ovadia P, Abdullah F, Spector S, Rabinovici R. Chest
tube removal: end-inspiration or end-expiration?
J Trauma 2001;50:674-7.
Dear Editor,
We read with interest the editorial by Birring and Peake on early diagnosis and screening of lung cancer [1]. The diagnosis of lung cancer is often delayed by the patient themselves, although some doctors are still guilty of adopting the laissez-faire approach towards small, particularly calcified lesions. As clinicians, we are increasingly seeing referrals of incidental small lung nodules on computed...
Dear Editor
Whilst one must of course take into account the mortality figures whilst treating multi-drug resistant tuberculosis, there may be other aspects that need to be studied. The collegues would to well perhaps to address some part of their research to the mortality of those patients who had been prescribed for a protected period antituberculous chemotherapy: (this can be for up to two years), and who have been m...
Dear Editor,
In a recent issue of Thorax, van der Palen et al. [1] published a study showing that a reduced Maximal Inspiratory Pressure (MIP), a measure of diaphragmatic inspiratory muscle strength, is a risk factor for incident myocardial infarction and death from cardiovascular disease in a population of subjects without previously reported cardiovascular events. We believe this result has a strong impact on...
Dear Editor,
I am a graduate student in Hebei Medical University in China. Now I am preparing for my trial, which is related to ec-sod. Although I have made my greatest efforts, I cannot find how to measure the activity and concentration of the plasm ec-sod. Many related articles cited the article "Quantitative and qualitative changes of extracellular-superoxide dismutase in patients with various diseases" Clinica Chi...
Dear Editor
The letter from Dr Eltzschig [1] refers to their paper showing that surgical embolectomy remains an option in severe pulmonary embolism. Firstly, this required "a multidisciplinary evaluation team with a widespread reputation for 24-hour availability, 7 days per week" (and over half of their patients had surgery during the weekend); there must be very few centres in the world who can offer such a service,...
Dear Editor
British Thoracic Society guidelines for the management of suspected acute pulmonary embolism
It is indeed unsatisfactory to make such recommendations in the absence of prospective studies; three have now been published.[1-3] Although differing in the way clinical probability was evaluated and in the D-dimer assays used, all found that in combination many patients with suspected pulmonary embo...
Dear Editor,
Berkman and colleagues [1] put forward an impressive argument for the use of exhaled nitric oxide (eNO) in diagnosing asthma through employment of a cut off value of 7 parts per billion in differentiating between asthmatics and non-asthmatics.
Although it is unquestionable that elevated levels of eNO indicate underlying airway inflammation, it must be appreciated that the latter is not syno...
Dear Editor
These clinically important papers [1,2] by the Isolde researchers provide excellent data questioning the rationale behind inclusion of patients in the large COPD-studies that have been reported in past few years. Selection of patients on the basis of absence of reversibility means ruling out the easiest measurable variable that may correlate with steroid response. When assessing effects of two weeks pred...
Dear Editor,
The study by Tomlinson and colleagues [1] stirs further debate in relation to patients with asthma who continue to smoke. There are several points in the study, which are pertinent to consider.
Firstly, the small but statistically significant difference of 25 l/min in morning peak expiratory flow (PEF) observed between smokers and non-smokers following 12 weeks of low dose inhaled corticoste...
Dear Editor
I read with interest the latest comprehensive BTS guidelines on chest drain insertion. We would like to share with you some tips and words of caution accumulated by experience from our institute.
During chest drain insertion, we routinely monitor oxygen saturation continuously with or without prior sedation. Patient with secondary pneumothorax i.e. from COAD can deteriorate during chest drai...
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