The paper by Hessel and colleagues is a valuable summary of the
somewhat conflicting literature concerning asbestos exposure and lung
cancer risk in the absence of a clinical diagnosis of asbestosis. The
authors rightly point out that the risk of lung cancer may be very
different in patients exposed to different fibre types and with different
degrees of fibrosis ranging from severe fibrosis on plain...
The paper by Hessel and colleagues is a valuable summary of the
somewhat conflicting literature concerning asbestos exposure and lung
cancer risk in the absence of a clinical diagnosis of asbestosis. The
authors rightly point out that the risk of lung cancer may be very
different in patients exposed to different fibre types and with different
degrees of fibrosis ranging from severe fibrosis on plain chest
radiographs to subtle localized fibrosis on a high resolution CT scan or
at autopsy.
However, one feature of the civil medicolegal system was not
mentioned. Civil courts make awards on the "balance of probability", not
on the basis of relative risk. For example, the study of Hillerdal
(reference 8) showed that the relative risk of lung cancer in patients
with pleural plaques was 2.3 if the patient had radiographic evidence of
asbestosis and 1.4 in the absence of asbestosis. This study involved 1596
men and provided strong evidence of an association between pleural plaques
and increased risk of lung cancer. However, on a "balance of probability
test", only those with asbestosis (relative risk above 2.0 ) would be
judged to have lung cancer that was the direct result of previous asbestos
exposure. Patients with plaques but no evidence of asbestosis may have a
40% increased risk of lung cancer compared with somebody not exposed to
asbestos but they would not be compensated because the balance of
probability in individual cases would not favour an asbestos attributable
cancer.
The negative findings of Joos et al. can be explained by the small
signal for bronchodilator reversibility,such that one would not expect to
detect any putative differences in beta-agonist response between
genotypes ,as compared to asthma where the signal is much bigger. With
repect to bronchial hyperresponsiveness (BHR), we have previously shown in
asthmatics ,that the glycine genotype is associ...
The negative findings of Joos et al. can be explained by the small
signal for bronchodilator reversibility,such that one would not expect to
detect any putative differences in beta-agonist response between
genotypes ,as compared to asthma where the signal is much bigger. With
repect to bronchial hyperresponsiveness (BHR), we have previously shown in
asthmatics ,that the glycine genotype is associated with enhanced BHR to
either direct (methacholine) or indirect (adenosine monophosphate) stimuli
,as compared to the arginine genotype.[1] Moreover the difference in BHR
was disconnected from airway caliber(as FEV1 and FEF25-75)or inhaled
steroid dose ,which did not differ between genotypes.Thus it may not be
possible to extrapolate from the effects of beta-2-receptor genotype in
asthma to what happens in COPD,where influences of altered airway geometry
are more important.
Reference
(1) Fowler SJ, Dempsey OJ, Sims EJ, Lipworth BJ. Screening for
bronchial hyperresponsiveness using methacholine and adenosine
monophosphate: relationship to asthma severity and beta-2-receptor
genotype.Am J Respir Crit Care Med 2000;162: 1318-1322.
Vestbo et al. did an interesting secondary analysis of the results of
the Tristan study in outpatients aged 40-70 years, with COPD (FEV1= 25-70%
predicted, and reversibity...
Vestbo et al. did an interesting secondary analysis of the results of
the Tristan study in outpatients aged 40-70 years, with COPD (FEV1= 25-70%
predicted, and reversibity <_10 predicted="predicted" fev1.="fev1." treatment="treatment" with="with" salmeterol="salmeterol" fluticasone="fluticasone" _50="_50" _500mcg="_500mcg" bd="bd" was="was" within="within" two="two" weeks="weeks" superior="superior" and="and" alone="alone" to="to" placebo.1="placebo.1" furthermore="furthermore" a="a" beneficial="beneficial" effect="effect" breathlessness="breathlessness" scores="scores" pefr="pefr" fev1="fev1" of="of" did="did" predict="predict" the="the" outcome="outcome" continuous="continuous" for="for" _1="_1" year="year" in="in" most="most" patients.="patients." p="p"/>These findings have implications for primary care. We have the following
questions that all regard the selection of patients in primary care that
may benefit inhaler therapy for COPD.
First, the lung function was measured as ‘clinic FEV1’. Was the flow-
volume loop used? And furthermore was the ‘clinic’ measurement of FEV1
done with an instrument equipped with a turbine system with rotating vane,
that is commonly used in primary care settings? Or, was a pneumotachometer used, which seems to be the gold standard in
the lung function laboratory? Could a difference between ‘clinic FEV1’ and
FEV1 measured in a lung function laboratory have biased the results of the
study?
Second, 746 out of the 1465 participants were current smokers. The
efficacy of inhaled corticosteroids (ICS) is diminished in smokers with
asthma.[2] An effect on symptoms of the lower airways of ICS for two weeks
was missing in smoking non-asthmatic adults who presented persistent
cough to the general practitioner.[3] This is in line with the finding of
Cox et al. that for four weeks treatment with ICS did not affect cigarette
smoke-induced inflammation in current smokers without airflow
obstruction.[4] Therefore, reanalysis of the current data while comparing
the short-term outcomes (within two weeks) in smokers vs. non-smokers
could be of interest.
Third, a further analysis by severity of COPD is needed. For it was
suggested that treatment of patients with chronic bronchitis and almost
normal lung function (mean FEV1 95% of the predicted value (SD18%)) with
fluticasone 250 mcg b.i.d does have a short term but no long term
effect.[5] Do patients with more severe COPD show a better short as well
as a better long term response to treatment with inhalers , compared with
patients with les severe COPD?
Further controlled trials of treatment in less severe COPD-patients in
primary care with ICS, long acting beta2 agonists, anticholinergic drugs,
and their combinations, could be needed. Then, symptom scores should
include not only the breathlessness scores that were used in the current
analysis, but also cough scores. Cough is a prominent symptom in the early
stages of COPD.
Fourth, patients with early stages of COPD in primary care show
intermittent or episodic symptoms: ‘exacerbations’. It is thought that
salmeterol/fluticasone combination treatment in particular induces rapid
improvement in lung function, enhances exercise tolerance and reduces the
perceived severity of exacerbations.[6] However, combination therapy did
not significantly improve exacerbation rate compared with salmeterol or
fluticasone alone. Therefore, the therapeutic regimens to be studied
should concentrate upon short term effects of treatments. Further, the
predictive value of the short term treatment effects for long term
outcomes has to be studied. The current analysis made a first move for
that.
Lastly, intermittent, symptomatic or ‘as needed’ inhaler treatments
for COPD must to be compared with continuous long term treatments as
studied by Vestbo et al. This approach is supported by the recent findings
that the outcomes of as-needed treatment with ICS in adults with mild
persistent asthma, in terms of morning PEFR or number of exacerbations,
was not different from sustained treatment for one year.[7]
Finally, we hypothesize that the potential of salmeterol/fluticasone in
COPD is in the exacerbation of non-smokers. If so, the ‘as-needed’ use of
combination inhaler therapy for COPD it may optimise the benefit/side
effects and benefit/cost ratio’s.
References
1. Vestbo J, Pauwels R, Anderson JA, Jones P, Calverley P. Early onset of
effect of salmeterol and fluticasone propionate in chronic obstructive
pulmonary disease.
Thorax. 2005;60:301-4.
2. Piipari R, Jaakkola JJ, Jaakkola N, Jaakkola MS. Smoking and asthma in
adults. Eur Respir J. 2004;24:734-9.
3. Ponsioen BP, Hop WC, Vermue NA, Dekhuijzen PN, Bohnen AM. Efficacy of
fluticasone on cough: a randomised controlled trial. Eur Respir J. 2005
;25:147-52.
4. Cox G, Whitehead L, Dolovich M, Jordana M, Gauldie J, Newhouse MT. A
randomized controlled trial on the effect of inhaled corticosteroids on
airways inflammation in adult cigarette smokers. Chest. 1999;115:1271-7.
5. van Grunsven P, Schermer T, Akkermans R, Albers M, van den Boom G, van
Schayck O, van Herwaarden C, van Weel C. Short- and long-term efficacy of
fluticasone propionate in subjects with early signs and symptoms of
chronic obstructive pulmonary disease. Results of the DIMCA study. Respir
Med. 2003;97:1303-12.
6. Calverley P, Pauwels R, Vestbo J, Jones P, Pride N, Gulsvik A, Anderson
J, Maden C; TRial of Inhaled Steroids and long-acting beta2 agonists study
group. Combined salmeterol and fluticasone in the treatment of chronic
obstructive pulmonary disease: a randomised controlled trial. Lancet.
2003;361:449-56.
7. Boushey HA, Sorkness CA, King TS, Sullivan SD et al. Daily versus as-
needed corticosteroids for mild persistent asthma. N Engl J Med.
2005;352:1519-28.
I read, with interest, the new BTS guidelines for the management of
spontaneous pneumothorax.[1] Arnold and colleagues acknowledged that the
plain radiograph was a poor method of quantifying the size of a
pneumothorax, yet then went on to use one radiographic method of
assessment to estimate the degree of lung collapse.
Under the new guidelines, the size of a pneumothorax is divided into
"...
I read, with interest, the new BTS guidelines for the management of
spontaneous pneumothorax.[1] Arnold and colleagues acknowledged that the
plain radiograph was a poor method of quantifying the size of a
pneumothorax, yet then went on to use one radiographic method of
assessment to estimate the degree of lung collapse.
Under the new guidelines, the size of a pneumothorax is divided into
"small" or "large" depending on the presence of a visible rim of "<
2cm" or "> or = 2cm" between the lung margin and the chest wall. The
authors then explained in detail how these distances could be used to
estimate the percentage of lung collapse. A schematic figure was even used
to illustrate the calculations. However, the method employed by the
authors (the method of Axel),[2] like most other methods, have been shown
to be a poor method for determining pneumothorax size under clinical
conditions.[3]
I do not see any evidence that the new classification is in any way
better than the old one. The calculations based on the distance of the rim
correlated poorly to the actual size of pneumothorax.[3] The "2 cm" used
is an arbitrary figure. It is even more confusing to have the American
guidelines use another arbitrary system of classification.[4] In
spontaneous pneumothorax, practitioners should at least agree on the same
classification system of size before they continue to debate about what is
the best option of treatment.
References
(1) Henry M, Arnold T, Harvey J, et al. BTS guidelines for the
management of spontaneous pneumothorax. Thorax 2003;58(Suppl II):ii39-ii52.
(2) Axwl L. A simple way to estimate the size of a pneumothorax. Invest Radiol 1981;16:165-166.
(3) Engdahl O, Toft T, Boe J. Chest radiograph - a poor method for
determining the size of a pneumothorax. Chest 1993;103:26-29.
(4) 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
Obstructive sleep apnea is an increasingly well recognized disease
characterized by periodic collapse of the upper airway during sleep.
Obstructive sleep apnea (OSA) is characterized by periodic complete or
partial upper airway obstruction during sleep, causing intermittent
cessations of breathing or reductions in airflow despite ongoing
respiratory effort. It’s defined by the presence of at least...
Obstructive sleep apnea is an increasingly well recognized disease
characterized by periodic collapse of the upper airway during sleep.
Obstructive sleep apnea (OSA) is characterized by periodic complete or
partial upper airway obstruction during sleep, causing intermittent
cessations of breathing or reductions in airflow despite ongoing
respiratory effort. It’s defined by the presence of at least 5 obstructive
apneas, hypopneas, or both per hour while the patient is sleeping.[1]
The goals of the treatment of OSA should be aimed at alleviating
symptoms while decreasing morbidity and mortality in a manner that
minimizes side effects, For example approximately 70% of patients with OSA
are obese. It has been shown that weight loss improves and in some cases
cures sleep-related breathing disorders and is dearly a low morbidity
treatment modality.[2,3] it also has been shown, however. That the
improvement in apnea-hypopnea index (AHI) with weight loss. Particularly
in moderate to severe sleep apnea. is only partial.[4]
Many surgical procedures have been described during the last 20
years. but of these procedures. Uvulopalatopharyngoplasty (UPPP) first
described in 1981 by Fujita et al.[5]
Determining the site of obstruction is problem for choice the
surgical procedure. accurate identification of the exact sites of
collapse should aid the surgeon in procedure selection, thereby improving
success rates. The difficulty in precisely determining the anatomic site
of obstruction in patients with OSA leads to challenges in predicting
which patients will benefit from palatal surgery in isolation.
Owing to the difficulty in predicting a single site of obstruction
with relative accuracy most surgeons currently advocate a multiphase
approach in the surgical treatment of OSA, with UPPP playing an integral
role. Increased success rates are seen when multiple procedures are med
that address various sites of obstruction.[6,7]
UPPP in the surgical management of OSA would be incomplete without
mentioning the complications of the procedure and its associated
morbidity.
The BTS guideline on chest drain management unfortunately fails to
recognise the severity of illness of patients who generally require chest
drain insertion on an intensive care unit. In our practice chest drainage
for pleural effusions only occurs in ventilated patients who require more
than 5cm H20 PEEP and still have significantly impaired oxygenation
limiting their ability to be weaned fr...
The BTS guideline on chest drain management unfortunately fails to
recognise the severity of illness of patients who generally require chest
drain insertion on an intensive care unit. In our practice chest drainage
for pleural effusions only occurs in ventilated patients who require more
than 5cm H20 PEEP and still have significantly impaired oxygenation
limiting their ability to be weaned from ventilation. In this population
of patients portable ultrasound guidance is used routinely to reduce the
risk of damaging underlying lung but the ventilator is not disconnected as
lung recruitment will be lost and hypoxia will rapidly develop.
Vestibo et al. report their surprise at the rapid effect of inhaled
fluticasone propionate (FP) on symptoms of dyspnoea and PEFR improvements
in COPD subjects.[1] A feasible explanation for their observation is
suggested by considering the effects of FP on airway vascular biology in
asthmatic and healthy individuals. The impressive work by Wanner et al.
demonstrated that FP causes acute vasoconstrict...
Vestibo et al. report their surprise at the rapid effect of inhaled
fluticasone propionate (FP) on symptoms of dyspnoea and PEFR improvements
in COPD subjects.[1] A feasible explanation for their observation is
suggested by considering the effects of FP on airway vascular biology in
asthmatic and healthy individuals. The impressive work by Wanner et al.
demonstrated that FP causes acute vasoconstriction (maximal at 30 minutes)
in the bronchial mucosa, as measured by the validated dimethyl ether
uptake technique.[2] The mechanism is believed to be glucocorticoid-
mediated enhancement of airway adrenergic and noradrenergic
neurotransmission.[3] This acute vasoconstrictor response results in
mucosal decongestion and reduced clearance of beta agonist from the
airway. Both of these effects serve to reduce airflow obstruction as
measured by patient symptoms and PEFR. The findings of Vestibo and
colleagues suggest inhaled corticosteroid produce a similar effect in the
COPD airway that may be of immediate benefit to the patient.
References
1. Vestibo J, Pauwels R, Anderson JA, et al. Early onset of effect of
salmeterol and fluticasone propionate in chronic obstructive pulmonary
disease.Thorax 2005;60:301-304.
2. Kumar SD, Brieva JL, Danta I, et al. Transient effect of inhaled
fluticasone on airway mucosal blood flow in subjects with and without
asthma. Am. J. Respir. Crit. Care Med. 2000;161:918-921.
3. Chang PC, van der Krogt JA, and van Brummelen P. Demonstration of
neuronal and extraneuronal uptake of circulating norepinephrine in the
forearm. Hypertension 1987;9:647-653.
"It is not the strongest of the species that survives, nor the most
intelligent, it is the one most adaptable to change." Charles Darwin (1809-1882)
The article "BTS guidelines for the management of spontaneous
pneumothorax" by Henry et al.[1] has recently stimulated some discussion
among our respiratory physicians and thoracic surgeons.
"It is not the strongest of the species that survives, nor the most
intelligent, it is the one most adaptable to change." Charles Darwin (1809-1882)
The article "BTS guidelines for the management of spontaneous
pneumothorax" by Henry et al.[1] has recently stimulated some discussion
among our respiratory physicians and thoracic surgeons.
We found it interesting that the authors quoted the recurrence rates
of pneumothorax after VATS (Video Assisted Thoracic Surgery) to be between
5-10%. Recently, numerous large series from around the world have shown
recurrence rates of primary spontaneous pneumothorax after VATS bullectomy
combined with surgical pleurodesis, to be in the range of 1.7-5.7%. [2,3]
Although the recurrence rates from VATS may be marginally higher than open
procedure, nevertheless, the benefit to the patient of shorter
postoperative hospital stay, less post-operative pain and better pulmonary
gas exchange in the postoperative period should be balanced. Furthermore,
we found in a study patients undergoing VATS to have significantly less
shoulder dysfunction and pain medication requirements in the early post-
operative period when compared with posterolateral thoracotomy.[4] Whether
VATS can be “established as being superior to thoracotomy” will in part be
decided by our patients and become clearer with future trials.
With the lowered morbidity and proven safety of VATS, even for
elderly and paediatric population,[2] the old surgical algorithms
developed based on the morbidity of thoracotomy should be re-evaluated.[5]
We feel there are two additional conditions that warrant inclusion in the
list for “accepted indication for operative intervention”. Firstly,
patients presenting with the life-threatening condition of tension
pneumothorax, even for the first time, should be considered for VATS
because of the potential grave consequences of its recurrence. Secondly,
presence of radiologically demonstrated huge bulla associated with
spontaneous pneumothorax should be an indication for VATS because of
increase risk of pneumothorax recurrence. In addition, the huge bulla may
continue to expand and impair lung function by causing compression of
adjacent healthy lung tissue, and can be manifestation of lung carcinoma
or a focus for recurrent infection.[2,6]
References
(1) M Henry, T Arnold and J Harvey. BTS guidelines for the management
of spontaneous pneumothorax. Thorax 2003;58:ii39
(2) Ng CSH, Wan S, Lee TW, Wan IYP, Arifi A, Yim APC. Video-assisted
thoracic surgery in spontaneous pneumothorax. Canadian Resp J 2002;9:122-
127.
(3) Yim APC, Ng CSH. Thoracoscopic management of spontaneous pneumothorax.
Curr Opin Pulm Med 2001;7:210-4.
(4) Li WWL, Lee RLM, Lee TW, Ng CSH, Sihoe ADL, Wan IYP, Arifi AA, Yim
APC. The impact of thoracic surgical access on early shoulder function:
video-assisted thoracic surgery versus posterolateral thoracotomy. Eur J
Cardiothorac Surg 2003;23:390-6
(5) Yim APC. Video assisted thoracoscopic surgery (VATS) in Asia: Its
impact and implications. Aust NZ J Med 1997;27:156-9
(6) Ng CSH, Sihoe ADL, Wan S, Lee TW, Arifi AA, Yim APC. Giant pulmonary
bulla. Can Respir J 2001;8:369-71
The combination of acute and chronic haemondynamic effects in
obstructive sleep apnea have been associated with increased risk of
myocardial infarction, cerebrovascular accidents, hypertension, and
congestive heart failure. It is necessary to provide appropriate treatment
for Obstructive sleep apnea syndrome (OSAS).
Most health care providers offer nasal continuous positive airway
pressure...
The combination of acute and chronic haemondynamic effects in
obstructive sleep apnea have been associated with increased risk of
myocardial infarction, cerebrovascular accidents, hypertension, and
congestive heart failure. It is necessary to provide appropriate treatment
for Obstructive sleep apnea syndrome (OSAS).
Most health care providers offer nasal continuous positive airway
pressure (CPAP) or oropharyngeal surgery for these patients, but neither
approach has proved to be a panacea. Although the use of nasal CPAP after
pressure titration in the sleep laboratory offers effective reversal of
the obstructive apneas, the short- and long-term compliance becomes an
issue in more than 50% of patients.[1] Because it is relatively
noninvasive, most practitioners offer CPAP as the first line of treatment.
Oropharyngeal surgery is a commonly performed alternative to nasal CPAP
for OSAS.
The most important issue to surface with positive airway pressure
therapy has been that of patient compliance. This was objectively shown by
Kribbs and colleagues using pressure-sensitive hour meters in CPAP units.
They found that CPAP was actually used by only 46% of patients for greater
than 4 hours of sleep for 70% or more of nights.[2]
Weaver et al reported that the long-term pattern of compliance was
determined within the first week of usage and implies that the earliest
experiences with CPAP may be fundamental to compliance.[3]
Proper mask fit, appropriate pressure titration, and immediate
intervention to correct patient discomfort may be the most important
interventions to improving patient compliance.[4]
Sincerely
Dr. Murat Enoz
References
1- T. Young, P.E. Peppard, D.J. Gottieb, Epidemology of obstructive
sleep apnea: a population health perspective, Am. J. Respir. Crit. Care
Med. 165 (2002) 1217-1239.
2- Kribbs NB, Pack AI, Kline LR, et al: Objective measurement of
patterns of nasal CPAP use by patients with obstructive sleep apnea.Am Rev
Respir Dis 147:887-895, 1993.
3- Weaver TE, Kribbs NB, Pack AI, et al: Night-to-night variability
in CPAP use over the first three months of treatment. Sleep 20:278-283,
1997.
4- Millman RP, Rosenberg CL, Kramer NR: Oral appliances in the
treatment of snoring and sleep apnea. Clin Chest Med 19:69-75, 1998.
I would like to express my concern about the recent British Thoracic
Society guidelines for the management of suspected acute pulmonary
embolism,[1] which suggest that “Patients with a good quality negative
CTPA do not require further investigation or treatment for PE.” [grade A
recommendation]:
1. According to a recent well designed study,[2] the negative
likelihood ratio of CTPA f...
I would like to express my concern about the recent British Thoracic
Society guidelines for the management of suspected acute pulmonary
embolism,[1] which suggest that “Patients with a good quality negative
CTPA do not require further investigation or treatment for PE.” [grade A
recommendation]:
1. According to a recent well designed study,[2] the negative
likelihood ratio of CTPA for the diagnosis of pulmonary embolism is about
0.33. If we assume a pre-test probability is 78% (Well’s high clinical
probability),[3] the probability of pulmonary embolism after a negative
CTPA is about 54%. This figure looks too high to suspend the anticoagulant
treatment.
2. The empirical evidence that supports the safety of withholding
anticoagulant treatment in patients with negative CTPA is of poor quality:
- Most of the studies (cohort restrospective studies), do not exclude
the possibility that the patients that were anticoagulated despite a
negative CTPA (and consequently excluded from the studies) were more prone
to recurrent thromboembolic events than patients in which anticoagulant
treatment was stopped.
- In some patients, the diagnostic workup included other diagnostic
tools to exclude deep venous thrombosis, besides CTPA.
- The magnitude of the loses to follow-up is often substantial, so we
cannot confidently exclude the occurrence of thromboembolic events in
these patients.
3. Probably the best evidence that supports the safety of stopping the
anticoagulation comes from the study of Swensen et al.[4], a retrospective
study based upon 1010 patients, with a low percent of loses to follow up
and a low prevalence of anticoagulated patients. However, this study is
based on a last generation multi-slice electron beam scanner, and its
results cannot be extrapolated to the typical clinical environment.
Taking these points altogether, I consider that there are sound
doubts about the safety of withholding anticoagulant treatment after
negative CTPA findings, at least in patients with a high clinical
probability of PE and with the usual radiologic environment. Probably,
these conclusions should be revised according the new technological
improvements.
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) Perrier A, Howarth N, Didier D, Loubeyre P, Unger PF, de
Moerloose P, Slosman D, Junod A, Bounameaux H. Performance of Helical
Computed Tomography in unselected outpatients with suspected pulmonary
embolism. Ann Intern Med 2001;135:88-97.
(3) Wells PS, 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.
(4) Swensen SJ, Sheedy PF, Ryu JH et al. Outcomes after withholding
anticoagulation from patients with suspected acute pulmonary embolism and
negative computed tomographic findings: a cohort study. Mayo Clin Proc
2002;77:130-138.
Dear Editor,
The paper by Hessel and colleagues is a valuable summary of the somewhat conflicting literature concerning asbestos exposure and lung cancer risk in the absence of a clinical diagnosis of asbestosis. The authors rightly point out that the risk of lung cancer may be very different in patients exposed to different fibre types and with different degrees of fibrosis ranging from severe fibrosis on plain...
Dear Editor
The negative findings of Joos et al. can be explained by the small signal for bronchodilator reversibility,such that one would not expect to detect any putative differences in beta-agonist response between genotypes ,as compared to asthma where the signal is much bigger. With repect to bronchial hyperresponsiveness (BHR), we have previously shown in asthmatics ,that the glycine genotype is associ...
Dear Editor,
Vestbo et al. did an interesting secondary analysis of the results of the Tristan study in outpatients aged 40-70 years, with COPD (FEV1= 25-70% predicted, and reversibity...
Dear Editor
I read, with interest, the new BTS guidelines for the management of spontaneous pneumothorax.[1] Arnold and colleagues acknowledged that the plain radiograph was a poor method of quantifying the size of a pneumothorax, yet then went on to use one radiographic method of assessment to estimate the degree of lung collapse.
Under the new guidelines, the size of a pneumothorax is divided into "...
Dear Editor,
Obstructive sleep apnea is an increasingly well recognized disease characterized by periodic collapse of the upper airway during sleep. Obstructive sleep apnea (OSA) is characterized by periodic complete or partial upper airway obstruction during sleep, causing intermittent cessations of breathing or reductions in airflow despite ongoing respiratory effort. It’s defined by the presence of at least...
Dear Editor
The BTS guideline on chest drain management unfortunately fails to recognise the severity of illness of patients who generally require chest drain insertion on an intensive care unit. In our practice chest drainage for pleural effusions only occurs in ventilated patients who require more than 5cm H20 PEEP and still have significantly impaired oxygenation limiting their ability to be weaned fr...
Dear Editor,
Vestibo et al. report their surprise at the rapid effect of inhaled fluticasone propionate (FP) on symptoms of dyspnoea and PEFR improvements in COPD subjects.[1] A feasible explanation for their observation is suggested by considering the effects of FP on airway vascular biology in asthmatic and healthy individuals. The impressive work by Wanner et al. demonstrated that FP causes acute vasoconstrict...
Dear Editor
"It is not the strongest of the species that survives, nor the most intelligent, it is the one most adaptable to change."
Charles Darwin (1809-1882)
The article "BTS guidelines for the management of spontaneous pneumothorax" by Henry et al.[1] has recently stimulated some discussion among our respiratory physicians and thoracic surgeons.
We found it in...
Dear Editor,
The combination of acute and chronic haemondynamic effects in obstructive sleep apnea have been associated with increased risk of myocardial infarction, cerebrovascular accidents, hypertension, and congestive heart failure. It is necessary to provide appropriate treatment for Obstructive sleep apnea syndrome (OSAS).
Most health care providers offer nasal continuous positive airway pressure...
Dear Editor
I would like to express my concern about the recent British Thoracic Society guidelines for the management of suspected acute pulmonary embolism,[1] which suggest that “Patients with a good quality negative CTPA do not require further investigation or treatment for PE.” [grade A recommendation]:
1. According to a recent well designed study,[2] the negative likelihood ratio of CTPA f...
Pages