I was intrigued by Mike Rudolf's editorial on Inpatient Management of
Acute COPD. He states that mortality was highest in small DGH's and
lowest in teaching hospitals. Roberts et al. article, in fact, indicated
that large DGH's had a smaller mortality than even teaching hospitals. I
would not be surprised, as stated, that small DGH's had fewest resources
but certainly working in a large DGH I ha...
I was intrigued by Mike Rudolf's editorial on Inpatient Management of
Acute COPD. He states that mortality was highest in small DGH's and
lowest in teaching hospitals. Roberts et al. article, in fact, indicated
that large DGH's had a smaller mortality than even teaching hospitals. I
would not be surprised, as stated, that small DGH's had fewest resources
but certainly working in a large DGH I have the impression that we have
significantly less resources than teaching hospitals, and yet the largest
DGH's do have marginally better results.
We read with great interest the article by Schanen[1] et al. - Asthma
and incident cardiovascular disease in which the authors have shown an
association between multivariate adjusted Hazard ratio and incident
stroke, but, not with Coronary heart disease in both model 1 and 2. One of
the most important risk factors for coronary heart disease in asthmatics
identified so far is the use of inhaled short-ac...
We read with great interest the article by Schanen[1] et al. - Asthma
and incident cardiovascular disease in which the authors have shown an
association between multivariate adjusted Hazard ratio and incident
stroke, but, not with Coronary heart disease in both model 1 and 2. One of
the most important risk factors for coronary heart disease in asthmatics
identified so far is the use of inhaled short-acting and long acting beta
2 agonists.[2]
More recently a meta analysis conducted by Shelley et al.[3]
reported that for trials lasting from 3 days to 1 year, ß2-agonist
treatment significantly increased the risk for a cardiovascular event
(relative risk [RR], 2.54; 95% CI, 1.59 to 4.05) compared to placebo.
Similar findings of increased risk of unstable angina, myocardial
infarction associated with inhaled beta- agonists were also reported by
Au et al.[4,5] It would have had tremendous clinical application if the
authors had studied the association between inhaled beta 2 agonist and
incident coronary heart disease in ever asthmatics.
Also studies have shown that rapid decline of FEV1 is an independent
risk factor for coronary heart disease.[6] Since this was a prospective
cohort study, it would be useful if the authors also analysed the
association between decline of FEV1 /Low quartiles of FEV1 and incident
coronary heart disease.
References
1. JG Schanen et al: Asthma and incident cardiovascular disease: the
Atherosclerosis Risk in Communities Study.
Thorax. 2005 Aug;60(8):633-8.
2. Suissa et al. Patterns of increasing beta-agonist use and the risk of
fatal or near-fatal asthma Eur Respir J 1994; 7: 1602-1609.
3. Shelley R. Salpeter, Thomas M. Ormiston, and Edwin E. Salpeter
Cardiovascular Effects of ß-Agonists in Patients With Asthma and COPD: A
Meta-Analysis
Chest, Jun 2004; 125: 2309 - 2321.
4. Au, DH, Curtis, JR, McDonell, MB, et al. Association between inhaled
beta-agonists and the risk of unstable angina and myocardial infarction.
Chest 2002;121,846-851.
5. Au, DH, Lemaitre, RN, Curtis, JR, et al. The risk of myocardial
infarction associated with inhaled beta-adrenoceptor agonists. Am J Respir
Crit Care Med 2000;161,827-830.
6. Tockman MS et al. A new risk factor for coronary heart disease
mortality. Am J Respir Crit Care Med 1995;151:390-398.
We thank Dr Ng for his comments on the recently published guidelines
on the management of spontaneous pneumothorax.[1] Dr Ng points out that
recurrence rates for pneumothorax after VATS preventative procedures were
lower than those quoted in the guidelines. It should be pointed out that
in the multiple drafts of this document, it was recognised that recurrence
rates after VATs were falling and that f...
We thank Dr Ng for his comments on the recently published guidelines
on the management of spontaneous pneumothorax.[1] Dr Ng points out that
recurrence rates for pneumothorax after VATS preventative procedures were
lower than those quoted in the guidelines. It should be pointed out that
in the multiple drafts of this document, it was recognised that recurrence
rates after VATs were falling and that further improvements in these
figures were likely as operator experience improved. This was recognised
within the guidlines. It is fully expected that as experience and
provision of services impprove, VATS will replace open thoracotomy for
treatment of recurrent pneumothoraces.
In response to Dr Ngs second points regarding surgical treatment of
tension pneumothoraces and hugh bullae, the guidelines obviously could not
take into account every possible clinical scenario. As far as we are aware
there is no evidence to suggest that tension pneumothoraces are more
likely to recur than 'non-tension' spontaneous pneumothoraces. This does
not mean of course that an individual physician should not decide that the
clinical risk in an individual patient either from rupture of a hugh bulla
or recurrence of a tension pneumothorax shouldn't warrent surgical
intervention.
Reference
(1). Henry MT, Arnold A, Harvey J. BTS guidelines for the management
of spontaneous pneumothorax. Thorax 2003; 58: 39ii-52ii.
My mother had a yearly chest x-ray in March 2003 which then showed a
mild kyphotic deformity in her thorax. In June 2004 she had another
yearly x-ray which showed a left hilar mass lesion. Needless to say a
week later she had a CT scan which showed that the cancer had metastized
to her adrenal glands and she also had numerous lesions on her liver. As
a physician would the kyphotic deformity be an indication to take fu...
My mother had a yearly chest x-ray in March 2003 which then showed a
mild kyphotic deformity in her thorax. In June 2004 she had another
yearly x-ray which showed a left hilar mass lesion. Needless to say a
week later she had a CT scan which showed that the cancer had metastized
to her adrenal glands and she also had numerous lesions on her liver. As
a physician would the kyphotic deformity be an indication to take further
tests seeing that my mother was a heavy smoker for 65 years? Her
diagnosis was small cell lung cancer.
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 have read with interest the paper of Battaglia et al.[1] regarding the
relationship between small airways function and molecular markers of
inflammation in exhaled air in mild asthma. They concluded that fractional
exhaled nitric oxide (FeNo) and 8-isoprostane in exhaled air reflect small
airway inflammation, and that 8-isoprostane particularly is increased in
patients with more prominent airway closure....
We have read with interest the paper of Battaglia et al.[1] regarding the
relationship between small airways function and molecular markers of
inflammation in exhaled air in mild asthma. They concluded that fractional
exhaled nitric oxide (FeNo) and 8-isoprostane in exhaled air reflect small
airway inflammation, and that 8-isoprostane particularly is increased in
patients with more prominent airway closure. However, the authors
reported levels of 8-isoprostane in EBC in the controls that were higher
(2.9-7.6 pg/ml) than in mildly asthmatic patients (1.6-2.7 pg/ml).
These results are in agreement with a previous report [2] and with
our findings. In a group of 13 asthmatic children without acute symptoms,
we found a mean concentration of 8-isoprostane in EBC of 1.09 + 1.69
pg/ml. Seven patients had a concentration lower than the detection limit
(5 pg/ml). The mean concentrations were higher in healthy controls than
in asthmatic children. These data raise several concerns regarding the
measurement of 8-isoprostane in exhaled breath condensate. In both our and
Battaglia's study the 8-isorostane values are either below or just above
the limit of the assay used to detect 8-isoprostane and so should be
viewed with the utmost caution.
Furthermore, the low levels of 8- isoprostane in the EBC of asthmatic
patients in comparison with controls raises the question whether the
detection of this molecule can be a reliable marker of the functional
status of small airways. We think that data of Battaglia et al. provide
only preliminary evidence. We suggest that these data indicate that 8-
isoprostane cannot be considered associated with airway inflammation in
asymptomatic asthmatic patients at the present time. The measurement of
exhaled breath condensate and inflammatory markers are not standardised
which makes comparison between studies also difficult. Further evaluations
by a more accurate technique, such as gas chromatography/mass spectrometry
[3], will be necessary.
References
1. Battaglia S, den Hertog H, Timmers MC et al. Small airways
function and molecular markers in exhaled air in mild asthma. Thorax 2005;
60: 639-644.
2. Van Hoydonck PG, Wuyts WA, Vanaudenaerde BM, et al.
Quantitative analysis of 8-isoprostane and hydrogen peroxide in exhaled
breath condensate. Eur Respir J 2004; 23:189-92.
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
Thanks to all concerned for putting together a very useful and long
awaited guideline. I have the following questions and comments.
1. What does "All Patient Rate" in table 3B mean and when should one
use it, if at all for UK born patients (say white) as opposed to table 3A?
Does a UK born white of 75 have a risk of 11 (Table 3A) or 4 (Table
3B - All patient rate column)?
2. I think that an arrow is missing between "Tuberculin test
unreliable" in "On Immunosuppressant" group AND "Stratify for TB Risk" box
in Figure 1.
3. I assume that patients who develop TB whilst on Anti TNF Alfa
treatment would qualify for 4 drug treatment simply by virtue of being on
immunosuppressants.
4. What is the guidance about patients who have developed TB whilst
on treatment with Anti TNF Alfa drugs and have not been able to tolerate
full treatment with 4 drugs, with regards to concomitant treatment with
Anti TNF Alfa drugs in "Normal CXR group" or time lag before treatment can
be started in "abnormal/suspicious group"? I have a couple of such
patients.
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.
I have just discharged a 28 year old male who had a pneumothorax
after a night of playing bass guitar standing in front of a large
amplifier. Although he has been playing in this band for years, this is
his first pneumothorax. As standing in front of this amp may be the
etiology, he intends to discontinue this practice and use earphones.
I appreciated your article with other similar case hist...
I have just discharged a 28 year old male who had a pneumothorax
after a night of playing bass guitar standing in front of a large
amplifier. Although he has been playing in this band for years, this is
his first pneumothorax. As standing in front of this amp may be the
etiology, he intends to discontinue this practice and use earphones.
I appreciated your article with other similar case histories.
Dear Editor
I was intrigued by Mike Rudolf's editorial on Inpatient Management of Acute COPD. He states that mortality was highest in small DGH's and lowest in teaching hospitals. Roberts et al. article, in fact, indicated that large DGH's had a smaller mortality than even teaching hospitals. I would not be surprised, as stated, that small DGH's had fewest resources but certainly working in a large DGH I ha...
Dear Editor,
We read with great interest the article by Schanen[1] et al. - Asthma and incident cardiovascular disease in which the authors have shown an association between multivariate adjusted Hazard ratio and incident stroke, but, not with Coronary heart disease in both model 1 and 2. One of the most important risk factors for coronary heart disease in asthmatics identified so far is the use of inhaled short-ac...
Dear Editor
We thank Dr Ng for his comments on the recently published guidelines on the management of spontaneous pneumothorax.[1] Dr Ng points out that recurrence rates for pneumothorax after VATS preventative procedures were lower than those quoted in the guidelines. It should be pointed out that in the multiple drafts of this document, it was recognised that recurrence rates after VATs were falling and that f...
My mother had a yearly chest x-ray in March 2003 which then showed a mild kyphotic deformity in her thorax. In June 2004 she had another yearly x-ray which showed a left hilar mass lesion. Needless to say a week later she had a CT scan which showed that the cancer had metastized to her adrenal glands and she also had numerous lesions on her liver. As a physician would the kyphotic deformity be an indication to take fu...
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 Sir,
We have read with interest the paper of Battaglia et al.[1] regarding the relationship between small airways function and molecular markers of inflammation in exhaled air in mild asthma. They concluded that fractional exhaled nitric oxide (FeNo) and 8-isoprostane in exhaled air reflect small airway inflammation, and that 8-isoprostane particularly is increased in patients with more prominent airway closure....
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...
Dear Editor,
Thanks to all concerned for putting together a very useful and long awaited guideline. I have the following questions and comments.
1. What does "All Patient Rate" in table 3B mean and when should one use it, if at all for UK born patients (say white) as opposed to table 3A?
Does a UK born white of 75 have a risk of 11 (Table 3A) or 4 (Table 3B - All patient rate column)?
2. I...
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,
I have just discharged a 28 year old male who had a pneumothorax after a night of playing bass guitar standing in front of a large amplifier. Although he has been playing in this band for years, this is his first pneumothorax. As standing in front of this amp may be the etiology, he intends to discontinue this practice and use earphones.
I appreciated your article with other similar case hist...
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