I question the findings of this meta-analysis[1] and the
content of the associated editorial.[2] The meta-analysis has drawn from
available long-term data from randomised-controlled studies (RCTs) into
inhaled corticosteroids (ICS) in chronic obstructive airways disease
(COPD). The whole purpose of meta-analysis is to systematically analyse
such data to answer a question. This study seems to selectively...
I question the findings of this meta-analysis[1] and the
content of the associated editorial.[2] The meta-analysis has drawn from
available long-term data from randomised-controlled studies (RCTs) into
inhaled corticosteroids (ICS) in chronic obstructive airways disease
(COPD). The whole purpose of meta-analysis is to systematically analyse
such data to answer a question. This study seems to selectively use the
data so as to demonstrate an effect. Another recent meta-analysis, and in
my opinion properly conducted, drew on the same studies and reached the
opposite conclusion.[3] The fact of the matter is that four long-term,
adequately powered, RCTs have examined the effect of ICS. All of these
studies showed no effect of ICS on the primary outcome measure of FEV1
decline. There may be a subset of people where exacerbation rate is
reduced, a secondary outcome in some of these studies.
In any case, as the authors point out, an annual difference of 7.7-
9.9 mls in FEV1 decline, compared to placebo, is of "debatable clinical
importance".[1] It is hardly something to shout about, as occurred
following this publication (probably egged on by the editorial), which was
quoted in the GP press as suggesting that current widespread ICS use
(albeit “off-label”) was now clinically justified.[5]
Another major problem with this study is that it does not analyse
harm. For example, the largest RCT showed a significant reduction in bone-
mineral density of the lumbar spine and femur in patients receiving
inhaled triamcinolone.[4] People with COPD likely to receive ICS are frail
and have poor mobility, so this finding raises particular concern as they
are more likely to fall and falls could result in fracture. Even if
inhaled triamcinolone is not used in the UK, fluticasone is. Fluticasone
has been the subject of particular cautionary advice because of its
ability to cause systemic effect at high dose.[6] If there is indeed a
marginal clinical benefit from using these drugs I think these people
deserve a better assessment of risk and benefit than presented in this
meta-analysis and the accompanying editorial.[2] This editorial claimed
that it is no longer ethical to do more long-term trials: surely the
conclusion is the opposite? We need better data to justify widespread use
of ICS in COPD.
References
(1) Sutherland ER, Allmers H, Ayas NT, Venn AJ, and Martin RJ. Inhaled
corticosteroids reduce the progression of airflow limitation in chronic
obstructive pulmonary disease: a meta-analysis. Thorax 2003; 58: 937-941.
(2) Burge PS and Lewis SA. So inhaled steroids slow the rate of
decline of FEV1 in patients with COPD after all? Thorax 2003; 58(11): 911
- 913.
(3) Highland KB. Strange C, Heffner JE. Long-term effects of inhaled
corticosteroids on FEV1 in patients with chronic obstructive pulmonary
disease. A meta-analysis. Ann Intern Med 2003;138:969-73.
(4) The Lung Health Study Research Group. Effect of inhaled
triamcinolone on the decline in pulmonary function in chronic obstructive
pulmonary disease. N Engl J Med 2000;343:1902–9.
(5) News: NICE steroids advice for COPD thrown into doubt. Pulse 3rd
November 2003.
(6) CSM/MCA. Reminder: Fluticasone propionate (Flixotide): use of high
doses (>500micrograms/twice daily). Current Problems in
Pharmacovigilance, August 2001.
Just a casual letter from a layman here, but it would seem clear that
the NOx higher levels correlating with higher lung cancer would be as a
result simply of higher exposure to diesel exhaust. Looking on the Web I
see worker exposure studies to older diesels show higher lung cancer rates
as well. When I was in Norway visiting my wife's relatives in 1992 I was
stunned by the unhealthy stench of diesel even...
Just a casual letter from a layman here, but it would seem clear that
the NOx higher levels correlating with higher lung cancer would be as a
result simply of higher exposure to diesel exhaust. Looking on the Web I
see worker exposure studies to older diesels show higher lung cancer rates
as well. When I was in Norway visiting my wife's relatives in 1992 I was
stunned by the unhealthy stench of diesel even in Bergen in places. The
US, which has its own air pollution problems of course, managed through
sheer luck to avoid having many diesel autos due to cheap gas and some
poorly designed diesel engines which soured the US auto buyers on diesels.
Perhaps Norway should tax diesel fuel at higher rate than gasoline rather
than a lower rate as it does now. I would guess the health cost and human
suffering from the air pollution per mile driven is higher with diesel but
the fuels are currently taxed per liter used. Someday I hope to sit by the
fountain in beautiful Bergen and smell only the flowers and the fountain,
not diesel exhaust.
I read with great interest the Roberts et al. Thorax article [1] and the accompanying
editorial by Rudolf.[2]
The study
highlights important variation in the outcomes of patients with a common
chronic disease and once more illustrates that doctor: patient ratios may
be an important contributor to variation. It is also likely that some of
the observed variation may arise because of varia...
I read with great interest the Roberts et al. Thorax article [1] and the accompanying
editorial by Rudolf.[2]
The study
highlights important variation in the outcomes of patients with a common
chronic disease and once more illustrates that doctor: patient ratios may
be an important contributor to variation. It is also likely that some of
the observed variation may arise because of variations in individual
clinicians decision-making. A recent study carried out in the eight
hospitals of the Heart of England Critical care network interviewed 98
clinicians who made end of life decisions for patients with COPD.[3]
Clinicians had made a median of 10 end of life decisions for COPD patients
in the previous 12 months. Clinicians showed marked variability in
critical care admitting decisions for identical patients with clinicians
who choose not to admit patients to critical care forming very pessimistic
predictions of outcome compared to clinicians who would admit. It seems
possible that poor outcomes for COPD patients may not simply reflect a
lack of resources, but also therapeutic nihilism that may have grown up
over the years in response to the cognitive dissonance that arose when
beds on critical care could not be found for COPD patients in extremis. It
seems likely that reversing variations in outcome will require both
changes in resources and changes in clinicians’ expectations. In this
respect the GMC guidance on Withholding and Withdrawing life-prolonging
treatments [4] may well be helpful in that section 20 recommends that where:
"there is a reasonable degree of uncertainty about the appropriateness of
providing a particular treatment, treatment which may be of some benefit
to the patient should be started until a clearer assessment can be made."
In The Heart of England Critical Care network study over one third of
clinicians would not admit a 75 year old COPD patient with single organ
respiratory failure yet in a recent study of over 3700 COPD admissions to
UK Intensive Care Units in which patients had a median age of 67.8 years,
patients with single organ respiratory failure had a hospital survival of
over 70%.[5] It is important that chest physicians continue to be strident
advocates for the COPD patients admitted as emergencies and take every
opportunity to point out to general medicine and intensivist colleagues
how well COPD patients can do with both invasive and non-invasive
ventilation.
References
(1) C M Roberts, S Barnes, D Lowe and M G Pearson on behalf of the Clinical Effectiveness Evaluation Unit, Royal College of Physicians and the Audit Subcommittee of the British Thoracic Society. Evidence for a link between mortality in acute COPD and hospital type and resources.
Thorax 2003;58:947-949
(2) M Rudolf. Inpatient management of acute COPD: a cause for concern? Thorax, 2003; 58(11):914-915.
(3) Wildman MJ, O'Dea J, Kostopoulou O, Walia S, Tindall M, Khan Z.
Variation in intubation decisions for patients with chronic obstructive
pulmonary disease in one critical care network. Quarterly Journal of
Medicine 2003;96:583-591.
(4) General Medical Council. Withholding and Withdrawing Life-Prolonging
Treatments: Good practice in Decision-making. London: General Medical
Council, 2002.
(5) Wildman M, Harrison D, Brady AR, Rowan K. Unit and hospital outcomes
for 3752 admissions to 128 UK adult critical care units between 1995 and
2001. Thorax 2003;58(12: Supplement).
The reproducibility of FEV1 and FVC and their respective agreement
with a gold standard is an issue for early diagnosis and follow-up of COPD
patients in general practice.[1] Schermer et al. performed a within
subject comparison of FEV1 and FVC measured in 388 COPD-patients with a
turbine flow spirometer.[2] The values of FEV1 and FVC measured by general
practice personnel were compared with the val...
The reproducibility of FEV1 and FVC and their respective agreement
with a gold standard is an issue for early diagnosis and follow-up of COPD
patients in general practice.[1] Schermer et al. performed a within
subject comparison of FEV1 and FVC measured in 388 COPD-patients with a
turbine flow spirometer.[2] The values of FEV1 and FVC measured by general
practice personnel were compared with the values measured by certified
laboratory personnel, using the same type of turbine spirometer, as the
reference test. In spite of equivalent reproducibility the agreement
between measurement of lung function in general practices and in
laboratories was limited. Training of general practice staff is thought to
be the key for valid spirometric measurements. From a primary care
practice point of view three questions remain.
Firstly, the validity of FVC measured with a turbine spirometer
compared with the real life gold standard of an FVC measured with a
pneumotachometer, that is currently used in the lung function laboratory,
might be questioned. Godschalk et al. found that underestimation of FVC
measured with a turbine spirometer was much more excessive than the
underestimation of FEV1 when compared with the respective outcomes of FVC
and FEV1, measured with a pneumotachometer.[3] Inertia of the turbine
spirometer explains the inaccuracy of the measurements in the very low
flows at the end of the forced expiratory manoeuvre when the FVC is
completed. Schermers’ choice for a ‘fairer’ comparison conceals the
technical imperfection of the turbine spirometer compared with the gold
standard of the pneumotachometer in the lung function laboratory.
Unfortunately, flow volume curves made with turbine spirometers do not
show this error and may therefore lead to wrong assumptions by the
physician who uses a turbine spirometer. Systematic underestimation of FVC
in primary care patients might result from the study as presented by
Schermer et al. Do the authors agree with that?
Secondly, turbine spirometers are available for use in primary care
settings, without and with ‘built in prompts’, ‘real time flow volume
curves’, ‘patient instructions’ and ‘time indicators to monitor duration
of expiratory flow’ as the authors state. However, sophisticated turbine
spirometers seem to be in itself a barrier for their widespread use for
measuring FEV1 and FVC in primary care patients.[4] On the other hand,
most common faults can be detected by observation of the well-instructed
patient during his forced expiratory manoeuvre, rather than by an observer
who concentrates on the flow volume curves only.
In spite of the use of the flow volume curves by the general practice
personnel in the study of Schermer et al. the results of FEV1 and FVC were
not estimated interchangeable with the results of the laboratories,
although measured with the same type of turbine spirometer. Based on the
study of Schermer et al. the flow volume loop would appear be too
sophisticated for the primary care setting. Therefore it would be better
to encourage GPs to measure lung function in their practices,
straightforward with a simple handheld spirometer. Wouldn’t it?
Thirdly, in COPD the patients’ own base-line values provide the best
reference data.[5] The study of Schermer et al. might underpin the
relevance of frequent measurement of FEV1 and FVC. In order to promote
lung function testing in primary medical care, could Schermer et al. provide us with some more detailed data on the limits of agreement of FEV1
and FVC measured by the practices and the lung function laboratories?
References
(1) Buist AS. Guidelines for the management of chronic obstructive
pulmonary disease. Respir Med. 2002;96:S11-6.
(2) Schermer TR, Jacobs JE, Chavannes NH, Hartman J, Folgering HT, Bottema
BJ, van Weel C. Validity of spirometric testing in a general practice
population of patients with chronic obstructive pulmonary disease (COPD).
Thorax. 2003;58:861-6.
(3) Godschalk I, Brackel JCK, Peters JCK, Bogaard JM. Assessment of
accuracy and
applicability of a portable electronic diary card spirometer for asthma
treatment. Respir Med
1996;90:619-22.
(4) Ferguson GT, Enright PL, Buist SA, Higgins MW. Office spirometry for
lung health assessment in adults: a consensus statement from the national
lung health education program. Chest 2000;117:1146-61.
(5) Crapo RO. Pulmonary-Function Testing. N Eng J Med 1994;331:25-30.
I thank Dr Wolstenholme for his comments.[1] Although the 90
day mortality was very similar for both teaching hospitals
and large DGHs, the in-hospital death rate for large DGHs
was 9% compared with 4.8% for the teaching hospitals.
Whether or not hospital size and resource is indeed
significant in deciding mortality from acute COPD clearly
needs to be established, and hopefully the large nation...
I thank Dr Wolstenholme for his comments.[1] Although the 90
day mortality was very similar for both teaching hospitals
and large DGHs, the in-hospital death rate for large DGHs
was 9% compared with 4.8% for the teaching hospitals.
Whether or not hospital size and resource is indeed
significant in deciding mortality from acute COPD clearly
needs to be established, and hopefully the large national
audit that has just been conducted by the BTS and CEEU
will settle this matter for us.
Reference
(1) Wolstenholme RG. Inpatient management of acute COPD: A cause for concern? [electronic response to M Rudolf;
Inpatient management of acute COPD: a cause for concern?] thoraxjnl.com 2003http://thorax.bmjjournals.com/cgi/eletters/58/11/914#102
We read with interest the guidelines for the management of suspected
acute pulmonary embolism by the British Thoracic Society.[1] However, we
were somewhat concerned about the recommendation of administering a 50mg
intravenous bolus of alteplase for the treatment of patients with massive
PE [grade C recommendation]. We believe that this recommendation is
misleading as this advice is based on a case ser...
We read with interest the guidelines for the management of suspected
acute pulmonary embolism by the British Thoracic Society.[1] However, we
were somewhat concerned about the recommendation of administering a 50mg
intravenous bolus of alteplase for the treatment of patients with massive
PE [grade C recommendation]. We believe that this recommendation is
misleading as this advice is based on a case series of just 6 patients, of
whom 2 died.[2] There is also a paucity of data on the safety and
efficacy of bolus dose alteplase compared to placebo and to other
thrombolytic regimens.
There are only two small studies comparing bolus dose and standard
infusions of alteplase,[3,4] neither of which were large enough to detect
any significant difference in terms of thrombolytic efficacy or safety.
There was, however, a slightly higher all cause mortality rate and death
due to recurrent PE and major bleeding episodes in the bolus dose group in
one study.[3]
We have reviewed the data on the safety and efficacy of bolus dose
alteplase in comparison to standard alteplase infusions and have produced
some worrying data on thrombolytic efficacy, safety and the Number Needed
to Harm (NNH) if bolus dose alteplase is used in preference to standard
infusions.
Standard alteplase infusions produce a statistically significantly
greater rate of objectively measured thrombolysis compared to bolus dose
regimens (67% of patients vs. 33% respectively, p=0.0007) corresponding to
a NNH = 3 if practice was changed according to the BTS guidance. The
resultant death rate due to the initial PE is consequently greater in
patients receiving bolus dose alteplase (3.2% vs. 0.5%, p=0.01),
equivalent to a NNH = 37. Bolus dose alteplase is also associated with a
trend towards statistically significantly greater all cause mortality,
deaths due to major bleeding events and recurrent PE and also a worse side
effect profile (major bleeding episodes and recurrent PE).
The implications for practice from our review are that on the current
available evidence, standard alteplase infusions are more effective and
safer than bolus dose regimens. Thrombolytic treatment of massive PEs
should continue to utilise the licensed alteplase infusion regimen rather
than the bolus dose method recommended in the recent BTS guidance.
References
(1) British Thoracic Society Standards of Care Committee Pulmonary
Embolism Guideline Development Group. British Thoracic Society guidelines
for the management of suspected acute pulmonary embolism. Thorax 2003; 58:
470-484.
(2) Ruiz-Bailén M, Aguayo-de-Hoyos E, Seerano-Corcoles MC, et al.
Thrombolysis with recombinant tissue plasminogen activator during
cardiopulmonary resuscitation in fulminant pulmonary embolism: A case
series. Resuscitation. 2001; 51: 97-101.
(3) Goldhaber SZ, Agnelli G, Levine MN, on behalf of the Bolus
Alteplase Pulmonary Embolism Group. Reduced dose bolus alteplase versus
conventional alteplase infusion for pulmonary embolism thrombolysis: An
international multicenter randomized trial. Chest. 1994; 106: 718-724.
(4) Sors H, Pacouret G, Azarian R, et al. Hemodynamic effects of
bolus versus 2-hr infusion of alteplase in acute massive pulmonary
embolism: A randomized controlled multicenter trial. Chest. 1994; 106:
712-717.
We thank Dr Gueiros for his interest in our paper and appreciate his
comment.[1] Indeed, whooping cough should not be forgotten as an important
cause of chronic cough. Especially the emergence of B. pertussis strains
that are less sensitive to the protective effects of vaccination has
caused increased morbidity.
We mentioned pertussis in our paper several times: in the paragraph
on infections...
We thank Dr Gueiros for his interest in our paper and appreciate his
comment.[1] Indeed, whooping cough should not be forgotten as an important
cause of chronic cough. Especially the emergence of B. pertussis strains
that are less sensitive to the protective effects of vaccination has
caused increased morbidity.
We mentioned pertussis in our paper several times: in the paragraph
on infections (p. 999), in the 'diagnostic approach' section, and in
figure 1.
Thus, this important disorder was not forgotten, and should be considered in any child where chronic cough presents without evidence of a serious underlying disorder, especially (but not exclusively) in cases
where the cough has a pertussis-like nature.
We thank Dodd et al. for their letter that reflects the concerns of many clinicians that short burst oxygen must be beneficial to patients if only we could prove it. Unfortunately the evidence collected to date for short bust therapy does not support this hope and since our own publication [1] a further very similar study has reached the same conclusion.[2]
We thank Dodd et al. for their letter that reflects the concerns of many clinicians that short burst oxygen must be beneficial to patients if only we could prove it. Unfortunately the evidence collected to date for short bust therapy does not support this hope and since our own publication [1] a further very similar study has reached the same conclusion.[2]
In answer to the specific points raised in this letter we reassert that the conclusion of the study accurately reflects the results in which it is stated that "we found no increase in mean walk distance after oxygen and no improvement in mean breathlessness scores or recovery times with oxygen taken either before or after exercise" (abstract) and "Oxygen during recovery. The two walks performed by each subject in this study were comparable; there was no significant difference between the mean distances walked degree of breathlessness or arterial oxygen saturation at the end of the walks" (results). In the discussion we state:
"The outcomes of both parts of this study are clear. At rates available from domiciliary systems in the UK, neither pre-breathing oxygen before exercise nor breathing oxygen during recovery was effective in relieving dyspnoea or usefully increasing submaximal exercise tolerance in COPD patients with exercise limitation and desaturation on air". We conclude;
"In summary. Our studies do not support a useful therapeutic role for domiciliary oxygen by cylinder in COPD patients who desaturate on exercise, whether it is used before or after exercise. We suggest that current prescribing practice for this therapy in the UK be revised. If the evidence from this and previous studies is to be followed, only patients with a demonstrable objective benefit should be considered suitable for such therapy".
The argument that 28% oxygen with a flow rate of 4 litres per minute may have reduced alveolar oxygen tensions and hence increased the work of breathing is negated by the increased arterial oxygen saturations observed in the subjects who were administered oxygen. We agree that the conclusion of this study is ’the practice of prescribing 28% oxygen at 4 litres to relieve dyspnoea following exercise is inappropriate without careful assessment’ and state in our own conclusions ‘domiciliary oxygen should in future only be prescribed for such patients if they have shown objective evidence of benefit on exercise testing’. The suggestion that such patients would benefit from higher flow rates delivered from new lightweight cylinders now appearing in the UK market is an interesting one but at present is just speculation and we could not deduce such a conclusion from the results of our study. We are sure that further research in this area will be conducted.
References
(1) Nandi K, Smith AA, Crawford A et al. Thorax 2003;58:670-3.
(2) Lewis CA, Eaton TE, Young P, Kolbe J. Eur Respir J 2003;2:584-8.
The paper of Beddow et l. deal with important topics such as acute
respiratory failure following lung resection.
Postoperative mortality and
morbidity after lung resection are decreasing but remain significant. When
treated with invasive endotracheal mechanical ventilation (ETMV), acute
respiratory insufficiency after lung resection is fatal in up to 80% of
cases. In a prospective observat...
The paper of Beddow et l. deal with important topics such as acute
respiratory failure following lung resection.
Postoperative mortality and
morbidity after lung resection are decreasing but remain significant. When
treated with invasive endotracheal mechanical ventilation (ETMV), acute
respiratory insufficiency after lung resection is fatal in up to 80% of
cases. In a prospective observational study conducted after bilateral lung
transplantation, NIV was found to avoid reintubation. Furthermore
oxygenation and respiratory acidosis were improved, with a low rate of
complications and no mortality in the intensive care unit (ICU).[1] A
prospective randomized controlled study, in the ICU setting, demonstrated
that NIV was safe and effective in reducing the need for reintubation and
improving in-hospital and 3-month survival in 24 patients with hypoxemic
ARF after lung resection compared with standard medical treatment.[2]
These findings suggest that NIV may replace conventional mechanical
ventilation in some circumstances. In the paper of Beddow, the use of NIV
should have been discussed. Was mini-trachesostomy the treatment of choice
in hypoxemic respiratory failure following lung resection? Litterature
is convincing today and suggests that NPPV should be added to the
standard conservative therapy of AHRF complicating lung resection.
Finally, we agree with the authors "although not the most frequent
postoperative complication in this patient population, lung injury
produces the highest all cause mortality". In this setting Non Invasive
ventilation could reach the goal : to avoid endotracheal intubation
References
(1) Rocco M, Conti G, Antonelli M, et al. Noninvasive pressure support
ventilation in patients with acute respiratory failure after bilateral
lung transplantation. Intensive Care Med. 2001;27:1622-1626.
(2) Auriant I, Jallot A, Hervé P, et al. Noninvasive ventilation reduces
mortality in acute respiratory failure following lung resection. Am J
Respir Crit Care Med. 2001;164:1231-1235.
We thank Dr Chan for his further reponse 'error in citation' to the
recently published BTS guidelines for the management of spontaneous
pneumothorax.[1]
Dr Chan has pointed out that our statement in a previous correspondence to
him, that a 2cms rim of pneumothorax was a clear indication for use of an
intercostal chest drain, was supported by the recent ACCP Delphi consensus
document [2] is a error in...
We thank Dr Chan for his further reponse 'error in citation' to the
recently published BTS guidelines for the management of spontaneous
pneumothorax.[1]
Dr Chan has pointed out that our statement in a previous correspondence to
him, that a 2cms rim of pneumothorax was a clear indication for use of an
intercostal chest drain, was supported by the recent ACCP Delphi consensus
document [2] is a error in citation is technically correct. The evidence
for this statement is supported in the BTS document by a references also
qouted in our previous reply to him later in that paragraph and again
below. We recommended the use of the '2 cm rule' in secondary spontaneous
pneumothoraces only and not in primary pneumothoraces. As pointed out in
the previous correspondence 2 cm will usually (but not always) correspond
to a pneumothorax of >50% and these tend not to respond to simple
aspiration in patients with secondary pneumothoraces. The same evidence is
not available for primary pneumothoraces. As Dr Chan will be aware the two
sets of guidlelines quoted were arrived at by totally different means. The
delphi document was arrived at by consensus of many specialists, whereas
the BTS guidelines were arrived at by review of the published evidence and
in the absence of evidence on which to base recommendations, a consensus
of the BTS standards of care committee made recommendations. It is not
therefore surprising that there are differences between the various sets
of guidelines.
References
(1) Henry MT, Arnold T, Harvey J. BTS guidelines for the management of
spontaneous pneumothorax. Thorax 2003; 58: 39ii-52ii.
(2) Baumann MH, Strange C, Heffner JE, et al. Management of
spontaneous pneumothorax. An American College of Chest Physicians Delphi
Consensus Statement. Chest 2001; 119: 590-602.
(3) Archer GJ, Hamilton AAD, Upadhyag R, et al. Results of simple
aspiration of pneumothoraces. Br J Dis Chest 1985; 79: 177-182. III
Dear Editor
I question the findings of this meta-analysis[1] and the content of the associated editorial.[2] The meta-analysis has drawn from available long-term data from randomised-controlled studies (RCTs) into inhaled corticosteroids (ICS) in chronic obstructive airways disease (COPD). The whole purpose of meta-analysis is to systematically analyse such data to answer a question. This study seems to selectively...
Dear Editor
Just a casual letter from a layman here, but it would seem clear that the NOx higher levels correlating with higher lung cancer would be as a result simply of higher exposure to diesel exhaust. Looking on the Web I see worker exposure studies to older diesels show higher lung cancer rates as well. When I was in Norway visiting my wife's relatives in 1992 I was stunned by the unhealthy stench of diesel even...
Dear Editor
I read with great interest the Roberts et al. Thorax article [1] and the accompanying editorial by Rudolf.[2]
The study highlights important variation in the outcomes of patients with a common chronic disease and once more illustrates that doctor: patient ratios may be an important contributor to variation. It is also likely that some of the observed variation may arise because of varia...
Dear Editor
The reproducibility of FEV1 and FVC and their respective agreement with a gold standard is an issue for early diagnosis and follow-up of COPD patients in general practice.[1] Schermer et al. performed a within subject comparison of FEV1 and FVC measured in 388 COPD-patients with a turbine flow spirometer.[2] The values of FEV1 and FVC measured by general practice personnel were compared with the val...
Dear Editor
I thank Dr Wolstenholme for his comments.[1] Although the 90 day mortality was very similar for both teaching hospitals and large DGHs, the in-hospital death rate for large DGHs was 9% compared with 4.8% for the teaching hospitals.
Whether or not hospital size and resource is indeed significant in deciding mortality from acute COPD clearly needs to be established, and hopefully the large nation...
Dear Editor
We read with interest the guidelines for the management of suspected acute pulmonary embolism by the British Thoracic Society.[1] However, we were somewhat concerned about the recommendation of administering a 50mg intravenous bolus of alteplase for the treatment of patients with massive PE [grade C recommendation]. We believe that this recommendation is misleading as this advice is based on a case ser...
Dear Editor
We thank Dr Gueiros for his interest in our paper and appreciate his comment.[1] Indeed, whooping cough should not be forgotten as an important cause of chronic cough. Especially the emergence of B. pertussis strains that are less sensitive to the protective effects of vaccination has caused increased morbidity.
We mentioned pertussis in our paper several times: in the paragraph on infections...
Dear Editor
We thank Dodd et al. for their letter that reflects the concerns of many clinicians that short burst oxygen must be beneficial to patients if only we could prove it. Unfortunately the evidence collected to date for short bust therapy does not support this hope and since our own publication [1] a further very similar study has reached the same conclusion.[2]
In answer to the specific points ra...
Dear Editor
The paper of Beddow et l. deal with important topics such as acute respiratory failure following lung resection.
Postoperative mortality and morbidity after lung resection are decreasing but remain significant. When treated with invasive endotracheal mechanical ventilation (ETMV), acute respiratory insufficiency after lung resection is fatal in up to 80% of cases. In a prospective observat...
Dear Editor
We thank Dr Chan for his further reponse 'error in citation' to the recently published BTS guidelines for the management of spontaneous pneumothorax.[1] Dr Chan has pointed out that our statement in a previous correspondence to him, that a 2cms rim of pneumothorax was a clear indication for use of an intercostal chest drain, was supported by the recent ACCP Delphi consensus document [2] is a error in...
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