We thank Dr Singh for his/her comments on our case report.[1] We
agree that LIP is an important differential diagnosis in this case and is
associated with pulmonary nodules and pulmonary cysts, although they are
usually perivascular.[1-3] Firstly we acknowledge an erratum in the text
which was edited and submitted without re-review by the contributing
pathologist (AR). Specifically there were numero...
We thank Dr Singh for his/her comments on our case report.[1] We
agree that LIP is an important differential diagnosis in this case and is
associated with pulmonary nodules and pulmonary cysts, although they are
usually perivascular.[1-3] Firstly we acknowledge an erratum in the text
which was edited and submitted without re-review by the contributing
pathologist (AR). Specifically there were numerous small non-necrotising
epithelioid granulomata within the lung parenchyma. These were interpreted
as possibly representing an immune reconstitution process, either to
Mycobacterial infection or even latent sarcoidosis.
Given the limits on the length of the pictorial report we did not
discuss this particular aspect but the open lung biopsies showed very mild
peribronchial chronic inflammation only, and the histological features of
LIP were not present. The phenomena of cystic change occurring in the
context of TB is in fact described previously and the point of the case
report was to demonstrate this radiological picture in the context of
having definitive histology ruling out other pathologies. [4,5]
Another possibility was that this case was smoking related Langerhans
cell histocytosis (LCH), which can also cause cystic changes in the lung
but importantly the patient had in fact stopped smoking as a result of the
admission and therefore the imaging would have been expected to improve
rather than deteriorate during the course of treatment. In addition there
were no histological features of LCH in the lung biopsies.
In summary we feel that we adequately eliminated other known causes
of pulmonary cystic disease seen in HIV disease in this case.[5]
References
1. Singh N. LIP reading is required. Thorax eletters
2. Lynch DA, Travis WD, Muller NL, Galvin JR, Hansell DM, Grenier PA,
King TE Jr Idiopathic interstitial pneumonias: CT features. Radiology
2005;236(1):10-21.
3: Ichikawa Y, Kinoshita M, Koga T, Oizumi K, Fujimoto K, Hayabuchi
N. Lung cyst formation in lymphocytic interstitial pneumonia: CT features.
Journal of Computer Assisted Tomography 1994;18(5):745-8.
PMID: 8089323
4: Takemura T, Akiyama O, Yanagawa T, Ikushima S, Ando T, Oritsu M.
Pulmonary tuberculosis with unusual cystic change in an immunocompromised
host. Pathology International 2000;50(8):672-7.
PMID: 10972868
5: Ko KS, Lee KS, Kim Y, Kim SJ, Kwon OJ, Kim JS. Reversible cystic
disease associated with pulmonary tuberculosis: radiologic findings.
Radiology 1997;204(1):165-9.
PMID: 9205240
6) Richardson D, Rubinstein L, Ross E, Rice A, Wright AR, Kon OM,
Walsh J. Cystic lung lesions as an immune reconstitution inflammatory
syndrome. Thorax 2005;60(10):884
Re: BTS guidelines for the insertion of a chest drain.
This is a wonderful article on chest drain and everything related to
it. I do understand that 1-2cm of tube should normally be left underwater
when doing an underwater seal drain. My actual site of interest is
regarding the length of the tube in the underwater seal when draining a
pleural effusion. So when it starts filling in... should we...
Re: BTS guidelines for the insertion of a chest drain.
This is a wonderful article on chest drain and everything related to
it. I do understand that 1-2cm of tube should normally be left underwater
when doing an underwater seal drain. My actual site of interest is
regarding the length of the tube in the underwater seal when draining a
pleural effusion. So when it starts filling in... should we still stick
on to 1-2 cm of the tube under the fluid or just leave the tube as it was
1-2 cm underwater not the fluid?!!
The above guidelines will prove useful to rheumatologists or
gastroenterologists who will be prescribing these revolutionary drugs for
their patients. I, however, have difficulty with algorithm of figure where
tuberculin testing comes before risk stratification. For patients with
normal chest x-rays and a low risk stratification it will not really
matter if their tuberculin test is positive or negativ...
The above guidelines will prove useful to rheumatologists or
gastroenterologists who will be prescribing these revolutionary drugs for
their patients. I, however, have difficulty with algorithm of figure where
tuberculin testing comes before risk stratification. For patients with
normal chest x-rays and a low risk stratification it will not really
matter if their tuberculin test is positive or negative. In neither
scenario will they receive chemoprophyllaxis. Section 4.4 should be
updated in the light of Chiron-Evans defection from the tuberculin reagent
market and I would suggest that tuberculin doses should abandon the
dilutional expressions of 1:10,000 etc. for clarity.
As a response to your letter 'Lets be honest', the amount of 'web
hits' guidelines receive isn't usually translated into the amount of
citations they may receive. The guidelines that the BTS produced that
feature so prominently on the Thorax 'Top ten most read articles' have
relatively low citations (ISI Web of Knowledge) - all the BTS Guidelines
published in 2003 only received a total of 16 cites...
As a response to your letter 'Lets be honest', the amount of 'web
hits' guidelines receive isn't usually translated into the amount of
citations they may receive. The guidelines that the BTS produced that
feature so prominently on the Thorax 'Top ten most read articles' have
relatively low citations (ISI Web of Knowledge) - all the BTS Guidelines
published in 2003 only received a total of 16 cites between them. To put
that into context the total number of cited Thorax papers in 2002 and 2003
was 2041. The bulk of the cites that give Thorax a high impact factor are
therefore from 'true' submissions.
I hope this clarifies the situation slightly. If you require further
details please see the ISI website.
There is paucity of data with regards to the management of primary and secondary spontaneous pneumothorax.
A study was conducted to evaluate whether patients with either primary or secondary spontaneous pneumothorax were managed according to current British Thoracic Society guidelines.
56 consecutive patients with spontaneous pneumothorax were assessed over a 12-month period. In patients with...
There is paucity of data with regards to the management of primary and secondary spontaneous pneumothorax.
A study was conducted to evaluate whether patients with either primary or secondary spontaneous pneumothorax were managed according to current British Thoracic Society guidelines.
56 consecutive patients with spontaneous pneumothorax were assessed over a 12-month period. In patients with primary spontaneous pneumothorax, 84% were inappropriately managed with intercostal drain insertion. 79% of these patients merely required simple aspiration and 5% warranted observation alone. For patients with secondary spontaneous pneumothorax, 50% were incorrectly managed with simple aspiration when intercostal drain insertion was required. Complications occurred in 32% of patients who had intercostal drain insertion. 77% and 85% of patients with primary and secondary spontaneous pneumothorax respectively were referred to a chest physician regardless of outcome. The mean hospital stay for patients with primary and secondary spontaneous pneumothorax was 4 and 22 days respectively.
The vast majority of patients with primary spontaneous pneumothorax were needlessly exposed to intercostal drain insertion. Implementation of the British Thoracic Society guidelines is crucial in order to avoid unnecessary patient discomfort and procedure related complications. It should also reduce the number of inappropriate referrals to a chest physician.
Prashant S Borade, MB, BS, MD
Catherine I D Ludwig, BChir, MB
D Anthony Promnitz, MB, BCh, FRCP
Daniel K C Lee, MB, BCh, MRCP, MD
Department of Respiratory Medicine Ipswich Hospital Heath Road Ipswich IP4 5PD Suffolk United Kingdom
Richardson and colleagues have described the case of a 33 year old
male who had coinfection with human immunodeficiency virus (HIV) and
tuberculosis (TB) and developed cystic lesions in the lung after
initiation of antiretroviral therapy.[1] The authors have explained these
findings as being part of the immune reconstitution inflammatory syndrome
(IRIS). IRIS or the paradoxical reaction is believed to...
Richardson and colleagues have described the case of a 33 year old
male who had coinfection with human immunodeficiency virus (HIV) and
tuberculosis (TB) and developed cystic lesions in the lung after
initiation of antiretroviral therapy.[1] The authors have explained these
findings as being part of the immune reconstitution inflammatory syndrome
(IRIS). IRIS or the paradoxical reaction is believed to represent an
enhanced immunologic response to mycobacterial antigens after initiation
of antiretroviral therapy (ART) that results in a stronger inflammatory
response at sites of TB infection.[2] Clinically apparent paradoxical
reactions have been reported to occur among 29–36% of patients with HIV-TB
coinfection who are initiated on antitubercular treatment followed by ART.
Alveolitis, intrathoracic lymph nodal enlargement and pleural effusions
are the most commonly described intrathoracic manifestations with
radiological deterioration being apparent in 46% of such patients.[3]
Although cavitation is well known, presence of parenchymal cysts has never
been described previously.
Lymphocytic interstitial pneumonitis (LIP) is a non-infectious
inflammatory interstitial lung disease that is known to occur in HIV
infected individuals. High resolution computerized tomographic (HRCT)
features of this entity include presence of nodules that are often
centrilobular in distribution, ground glass opacification and cysts.
Histopathological examination of lung biopsy specimens from such
individuals reveals a spectrum of lymphocytic infiltration ranging from
diffuse interstitial infiltrates of lymphocytes, plasma cells, and
histiocytes to more patchy, dense cellular infiltrates with lymphoid
follicles and germinal centres. Non-caseating granulomas as well as
formation of cysts have also been described.[4] LIP in most cases has a
favourable response to glucocorticoid therapy even in HIV infected
individuals.
Simultaneous occurrence of several inflammatory and infectious
entities is well known in HIV infected individuals and hence it is
mandatory that the diagnosis of IRIS be made only after other aetiologies
have been excluded with a thorough evaluation and work-up. In conclusion,
I feel that the presence of cysts on HRCT chest (complemented by a
lymphocytic infiltrate on lung biopsy and response to glucocorticoid
therapy) in this case may represent a common manifestation of LIP in the
setting of HIV-TB coinfection rather than an unusual feature of IRIS.
References
1. Richardson D, Rubinstein L, Ross E, Rice A, Wright AR, Kon OM, et
al. Cystic lung lesions as an immune reconstitution inflammatory syndrome
(IRIS) in HIV-TB co-infection? Thorax 2005; 60: 884.
2. de Jong BC, Israelski DM, Corbett EL and Small PM. Clinical
management of tuberculosis in the context of HIV infection. Annu Rev Med
2004; 55: 283–301.
3. Lawn SD, Bekker LG and Miller RF. Immune reconstitution disease
associated with mycobacterial infections in HIV-infected individuals
receiving antiretrovirals. Lancet Infect Dis 2005; 5: 361–373.
4. Das S and Miller RF. Lymphocytic interstitial pneumonitis in HIV
infected adults. Sex Transm Inf 2003; 79: 88-93.
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) rat...
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) ratio. We wish to reignite attention to the use of this uncomplicated measurement through presentation of an interesting clinical case.
A 57-year old lady presented to our respiratory clinic with a complaint of inspiratory stridor. She did not have any other significant respiratory symptoms. There were no overt symptoms of gastroesophageal reflux or oesophageal dysfunction. On direct questioning, she denied any symptoms consistent with collagen vascular disease or vasculitis, except Raynaud’s phenomenon. Her medications included losartan for hypertension and amitriptyline for depression. She is a never-smoker. Clinical examination was unremarkable apart from a soft inspiratory stridor, which was heard best above the suprasternal notch. Her blood biochemistry, haematology, autoimmune, and vasculitic screen were unremarkable. Spirometry showed FEV1 of 2.79L (110% predicted), forced vital capacity (FVC) of 3.57L (120% predicted), FEV1/FVC ratio of 78%, and PEF of 396L/min (105% predicted). Her calculated FEV1/PEF ratio was 7.05ml/L/min. The pattern of the expiratory flow-volume curve was normal with a slight plateau in the inspiratory flow-volume curve (Figure 1). Flexible fibre-optic bronchoscopy demonstrated a subglottic stenosis (Figure 2).
Several pioneering studies have previously determined the usefulness of the FEV1/PEF ratio in diagnosing UAO.1-3 FEV1 is defined as the volume measured during the initial 1 second of a forced expiration from full inspiration and PEF is defined as the maximum flow rate maintained for at least 10 milliseconds during a forced expiration from full inspiration. Therefore, in UAO where the embarrassment is in the pre-carina upper airway, one would intuitively expect the FEV1/PEF ratio to increase, as chronologically, PEF would be affected more than FEV1, with the former reflecting more proximal airway per se. Evidently, the FEV1/PEF ratio has been shown to be significantly higher in patients with UAO compared to patients with asthma, chronic obstructive pulmonary disease, and normal subjects.1;2 A value of above 10ml/L/min was initially thought to represent UAO,1;2 although this was subsequently found to vary between 7ml/L/min and 12ml/L/min depending on the different subgroups of UAO such as extrathoracic, fixed, and variable intrathoracic.3
Therefore, although definitive procedures such as flexible fibre-optic bronchoscopy are needed to confirm the diagnosis of UAO, straightforward practical measurements that are useful in day-to-day clinical practice such as the FEV1/PEF ratio, which is easily obtainable through simple spirometry, may aid in either prompting initial consideration or confirming clinical suspicion of such a diagnosis.
Daniel K C Lee, MB, BCh, MRCP, MD
Prashant S Borade, MB, BS, MD
Nicholas J Innes, MB, BS, FRCP
Department of Respiratory Medicine, Ipswich Hospital, Heath Road, Ipswich IP4 5PD, Suffolk, England, United Kingdom
Rotman HH, Liss HP, Weg JG. Diagnosis of upper airway obstruction by pulmonary function testing. Chest 1975; 68: 796-799.
Mellisant CF, Van Noord JA, Van de Woestijne KP, Demedts M. Comparison of dynamic lung function indices during forced and quiet breathing in upper airway obstruction, asthma, and emphysema. Chest 1990; 98: 77-83.
Figure 1
Expiratory and inspiratory flow-volume curve
Figure 2
Subglottic stenosis found on flexible fibre-optic bronchoscopy
Although I was pleased to see the rise in impact factor of Thorax but
I just looked at the list of 10 most 'read' articles in thorax.
I was surprised to see all of them were part of guidelines published
by the BTS and none were 'true' submissions to the journal.
Although impact factors do not rely on 'web hits' but this does imply
that the rise in Thorax's impact factor has more to do with BTS producing
more guidelines than from 'quality of publications/submissions'.
It would be interesting to know what would be the impact factor of
various journals (including Thorax) if guidelines/consensus statements etc
are taken out. I would like the editorial team to try and give us a 'truer
picture'.
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.
ARDS remains a major cause of death, yet factors contributing to the
syndrome have not yet been clearly identified. During its early stages, ARDS
may include high-permeability pulmonary edema, loss of alveolar epithelial
cells and neutrophil infiltration which may lead to remodelling of the
alveoli and interstitium. Experimental findings suggested that activation
of a renin-angiotensin system in the l...
ARDS remains a major cause of death, yet factors contributing to the
syndrome have not yet been clearly identified. During its early stages, ARDS
may include high-permeability pulmonary edema, loss of alveolar epithelial
cells and neutrophil infiltration which may lead to remodelling of the
alveoli and interstitium. Experimental findings suggested that activation
of a renin-angiotensin system in the lung could mediate changes in
vascular tone and permeability, fibroblast activity, and epithelial cell
survival.
Thus, variations in the renin-angiotensin system could be crucial
in ARDS aetiology. Furthermore, ARDS patients show increased pulmonary ACE
activity. Because genotypic differences can account for 45% of the variance
in plasma ACE activity, Richard P. Marshall et al. from the Centre for
Respiratory Research at Rayne Institute in London sought to relate ACE
genotype with ARDS incidence and outcome. Frequencies of the D allele and
of the DD genotype were significantly higher among ARDS patients than
among non-ARDS patients. In comparison, the II genotype was markedly rare
among ARDS patients; all patients had similar frequencies of the ID
genotype. Mortality was also increased among patients within the ARDS group
who had two D alleles i.e. with DD genotype.[1]
ACE’s putative role in ARDS
aetiology supports the notion that inhibitors of ACE activity might
effectively reduce the propensity of individuals with a DD genotype to
develop ARDS. Thus, genotyping could reveal a subpopulation who might
particularly benefit from therapy with ACE inhibitors—either as
prophylaxis in healthy individuals who are homozygous for the D allele or
to improve outcome in a genetic subpopulation of patients with lung
disease.
References
1. Marshall RP, Webb S, Bellingan GJ, et al.Angiotensin converting enzyme
insertion/deletion polymorphism is associated with susceptibility and
outcome in acute respiratory distress syndrome.Am J Respir Crit Care Med.
2002;166:646-650.
Dear Editor
We thank Dr Singh for his/her comments on our case report.[1] We agree that LIP is an important differential diagnosis in this case and is associated with pulmonary nodules and pulmonary cysts, although they are usually perivascular.[1-3] Firstly we acknowledge an erratum in the text which was edited and submitted without re-review by the contributing pathologist (AR). Specifically there were numero...
Dear Editor,
Re: BTS guidelines for the insertion of a chest drain.
This is a wonderful article on chest drain and everything related to it. I do understand that 1-2cm of tube should normally be left underwater when doing an underwater seal drain. My actual site of interest is regarding the length of the tube in the underwater seal when draining a pleural effusion. So when it starts filling in... should we...
Dear Editor,
The above guidelines will prove useful to rheumatologists or gastroenterologists who will be prescribing these revolutionary drugs for their patients. I, however, have difficulty with algorithm of figure where tuberculin testing comes before risk stratification. For patients with normal chest x-rays and a low risk stratification it will not really matter if their tuberculin test is positive or negativ...
Dear Dr Aziz,
As a response to your letter 'Lets be honest', the amount of 'web hits' guidelines receive isn't usually translated into the amount of citations they may receive. The guidelines that the BTS produced that feature so prominently on the Thorax 'Top ten most read articles' have relatively low citations (ISI Web of Knowledge) - all the BTS Guidelines published in 2003 only received a total of 16 cites...
Dear Editor,
There is paucity of data with regards to the management of primary and secondary spontaneous pneumothorax.
A study was conducted to evaluate whether patients with either primary or secondary spontaneous pneumothorax were managed according to current British Thoracic Society guidelines.
56 consecutive patients with spontaneous pneumothorax were assessed over a 12-month period. In patients with...
Dear Editor,
Richardson and colleagues have described the case of a 33 year old male who had coinfection with human immunodeficiency virus (HIV) and tuberculosis (TB) and developed cystic lesions in the lung after initiation of antiretroviral therapy.[1] The authors have explained these findings as being part of the immune reconstitution inflammatory syndrome (IRIS). IRIS or the paradoxical reaction is believed to...
Dear Editor,
Several measures exist to aid the diagnosis of upper airway obstruction (UAO). These include subjective clinical signs such as the presence of stridor and objective measures such as the pattern of the flow-volume curve. However, by far the simplest and easily measured, but yet relatively unknown and underutilised, is the forced expiratory volume in 1 second (FEV1) / peak expiratory flow (PEF) rat...
Dear Editor,
Although I was pleased to see the rise in impact factor of Thorax but I just looked at the list of 10 most 'read' articles in thorax.
I was surprised to see all of them were part of guidelines published by the BTS and none were 'true' submissions to the journal.
Although impact factors do not rely on 'web hits' but this does imply that the rise in Thorax's impact factor has more to do wi...
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...
Dear Editor,
ARDS remains a major cause of death, yet factors contributing to the syndrome have not yet been clearly identified. During its early stages, ARDS may include high-permeability pulmonary edema, loss of alveolar epithelial cells and neutrophil infiltration which may lead to remodelling of the alveoli and interstitium. Experimental findings suggested that activation of a renin-angiotensin system in the l...
Pages