Science topic

Pulmonary Medicine - Science topic

A subspecialty of internal medicine concerned with the study of the RESPIRATORY SYSTEM. It is especially concerned with diagnosis and treatment of diseases and defects of the lungs and bronchial tree.
Questions related to Pulmonary Medicine
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I am looking for data related to breathing exercises that can be safely prescribed in case of spontaneous pneumothorax with / without bronchopleural fistula ; managed by inserting an intercostal drainage tube.
Can incentive spirometer be given to these patients ?
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I think that Expiratory exercise will increase the Transpleural pressure this will help to make the pressure at the point to prevent atelectasis
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 I’ll  describe what I postulate  provides the explanation of  the CAP microarousal episodes during  sleep.The information has been
based entirely on the conclusions of documented studies. Admittedly, and inasmuch as  each conclusion individually is not new information per se. nevertheless, by combining and preferentially  sequencing  them,
it becomes possible to arrange a set of contingent propositions which facilitates the creation of new awareness.
The concept can be tested  non-invasively during Cycle 1 of descending NREM sleep in a perfectly healthy individual. Additionally, it  would provide support  for the statement that “ ...several lines of evidence
suggest that the pulmonary circulation both has minimal neural regulation and is unresponsive to
changes in sleep state. and  is both significantly important and key to understanding that peripheral
mechanisms cannot be excluded”. @  http://jap.physiology.org/content/88/3/1084
 
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I am now working on similar topic.
Have you solved automatic detection for CAP arousal?
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Endosonography: Do you routinely use combined EBUS-TBNA and EUS-B-FNA approach in staging lung cancer?
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no
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In my view the cause of lung damage during modern mechanical ventilation is due to the positive pressure. Positive pressure ventilation causes atelectasis, and subsequently all the other problems if mechanical ventilation is maintained for a long time.
Negative pressure (expanding the thorax and getting air to flow in by under-pressure e.g. by a quirass sytem, or natural breathing) takes away the atelectatis very rapidly. That is why in every manual of the Anesthesiogists it says: directly after surgery, when the patient is awake again, ask him/her to take e few deep sighs.
My question: is it possible by your thechnique to prove the development of atelectasis by positive pressure and removal of the atelectasis by negative pressure vetilation?
This is very important, because patients with severe lung problems should not be ventilated by positive pressure systems. The life of a category of patients will be saved by negative pressure ventilation, because of the above reasons. So, please show the world what is going on, for most of the ventilators still believe the "law" (spoken out as a proposition around 1900) that there can be no difference between negative and positive pressure; they claim that everything is determined only by the pressure difference. They claim this is just physics. But this is only true in a static situation. During dynamic pressure variation this is absolutely not true.
Jan van Egmond.
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If the respiratory system is modeled as a single compartment model (R and C) then of course there is no difference between "positive pressure ventilation" and "negative pressure ventilation" because all assisted ventilation is by means of a positive change in trans-respiratory pressure difference (pressure at airway opening minus pressure on the body surface). But of course the respiratory system is made up of millions of resistances and compliances in complex series and parallel combinations. Hence the paradoxical views expressed in the other comments.
To the extent that negative pressure ventilation attempts to mimic normal breathing, I would suggest that the issue is even more complicated than we think.
For example in a recent paper by Yoshida et al (Am J Respir Crit Care Med. 2013 Dec 15;188(12):1420-7. doi: 10.1164/rccm.201303-0539OC.Spontaneous effort causes occult pendelluft during mechanical ventilation. Yoshida T, Torsani V, Gomes S, De Santis RR, Beraldo MA, Costa EL, Tucci MR, Zin WA, Kavanagh BP, Amato MB.)
The conclusion was: "Spontaneous breathing effort during mechanical ventilation causes unsuspected overstretch of dependent lung during early inflation (associated with reciprocal deflation of nondependent lung). Even when not increasing tidal volume, strong spontaneous effort may potentially enhance lung damage."
See also
Am J Respir Crit Care Med. 2016 Oct 27. [Epub ahead of print]. Spontaneous Breathing During Mechanical Ventilation - Risks, Mechanisms & Management.Yoshida T, Fujino Y, Amato MB3, Kavanagh BP.
Concluding that: "Notwithstanding the central place of spontaneous breathing in mechanical ventilation, accumulating evidence indicates that this may cause -or worsen acute lung injury, especially if ARDS is severe."
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In respiratory research a breathing apparatus consisting of mouthpiece, filter, Pneumotachometer, and non-rebreathing valves plus some connectors are usually used. Although a non-rebreathing valve is used to reduce dead space, each of these devices has its own dead space. Though small, adding together they build a relatively large dead space sometimes. What is the max acceptable dead space in a breathing apparatus, for a study including healthy adults?
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I fully agree with the first answer. I would however like to suggest using two pneumotachographs, one in the inspiratory limb, one in the expiratory limb. The sum of flow rates of both gives you the total flow rate. This way, the pneumotachographs do not contribute to dead space. You may consider this principle also for filters etc.
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If treated, which agent is preferred agent? NOAC or vitamin K antagonist?
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I would not!
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A case of 58 years old male PINK Puffer with very limited performance status. Pulmonary function Tests can not be done. They are going to do CABG 3 Vessels for him. They are wondering if he can benefit from lung volume reduction surgery.
 Patient had only 3 months treatment with anti TB.    Pulmonologists stratified him as a high risk for CABG alone.  Is he going to benefit from Lung Volume reduction surgery simultaneous with CABG?
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I suggest first percutaneous chest drainage of major bullae, then perform pleurodesis. In the case of procedure failure, Surgical thoracoscopic bullectomy can be done.
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Dear All,
I observed a 58 yo female patient in deep pain and was diagnosed as having a left-sided atypical chest pain. And she was sent for a chest X-Ray. It was found that she has a 1.0 cm x 0.8 cm lower left lung nodule. A repeat X-Ray is warranted but the result is still unknown.
My question is -
1. Could the atypical chest pain be the result of the lung nodule?
2. Her previous mammogram showed no abnormality, and she conducts her BSE monthly NOS. Could it be that there is some abnormality in the breast instead?
3. What could best explain her condition(s)?
Best regards - Mariam
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Dear Dr. Ahmad:
If the nodule was closely associated with the pleura then the chest pain can be explained.  If the nodule is close to the bronchioles, then there may be pain but more likely would produce a cough or hemoptysis.  Otherwise, if the nodule resides in the parenchyma of the lung there should not be any pain especially at the size you reported.
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Is there any study that shows the effect of exercise on pulmonary pressure after acute pulmonary thrombo embolic (PTE) treatment??  thank you
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I think it is difficult to do as the patient clinically is not fit for exercise due to his\ her symptoms but you can do dobutamine stress test on the heart if tolerance exists so I think indirectly you can be able to measure pulmonary pressure.
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Is there any experience about post TOF pvr with mechanical valve in young boys?
16-22 years old boys
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Yes there is some experience and it seems to be good.
Ann Thorac Surg. 2013 Apr;95(4):1367-71. doi: 10.1016/j.athoracsur.2012.07.008. Epub 2012 Aug 9.
Outcomes of mechanical valves in the pulmonic position in patients with congenital heart disease over a 20-year period.
Shin HJ1, Kim YH, Ko JK, Park IS, Seo DM.
Abstract
BACKGROUND:
Homografts or bioprosthetic valves have been preferred in the pulmonic position in patients with congenital heart disease. However, unsatisfactory long-term results have aroused interest in the use of mechanical valves. In this study, we investigated the long-term outcomes of mechanical valves implanted in the pulmonic position.
METHODS:
The medical records of 37 patients (27 male, 73%) who underwent 38 mechanical pulmonary valve replacements between October 1988 and February 2011 were reviewed, retrospectively. The median age of patients was 13.5 years (range, 7 months to 23 years), and the median number of prior operations per patient was 2 (range, 0 to 5). Tetralogy of Fallot was the most common diagnosis (n=23). The median valve size was 23 mm (range, 17 to 27 mm), and the median follow-up duration after pulmonary valve replacement was 24.6 months (range, 1.3 months to 22.5 years). Events were defined as the following: valve failure, thrombosis, embolism, bleeding, reoperation, and death.
RESULTS:
There was no in-hospital mortality, but there were 2 late deaths (1 heart failure and 1 traffic accident at 10.8 months and 8.7 years postoperatively, respectively). Excluding the traffic accident death, survival rates were 97%, 97%, and 97%, at 1, 5, and 10 years, respectively. Freedom from thromboembolism or bleeding events was 92%, 92%, and 78.8%, at 1, 5 and 10 years, respectively. Two reoperations were performed at 6.8 and 10.2 years postoperatively. Freedom from reoperation was 100%, 100%, and 85.7%, at 1, 5, and 10 years, respectively.
CONCLUSIONS:
Durability of mechanical valve in pulmonic position was excellent. Thromboembolism or bleeding events due to anticoagulation therapy were rare. In growing patients who have undergone prior sternotomies requiring a pulmonary valve replacement, a mechanical valve could be an attractive option.
PMID: 22884602 
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A persistent ventilation tube could lead to bioflim formation over it . Is there a  time limit beyond which it would be advisable to remove it? .
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A persistent grommet could also increase the chances of leaving behind a permanent residual perforation ,isn't it ? 
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prevention and ongoing health and well being.
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I tried inhaled glutathione with good results on perception of dyspnea, in addition to seasonal cycles of immunomodulants (bacterial lysate) + lactic ferments + vit. D + acetylcysteine.
I'd recommend as well 13- or 23-valent vaccine for Streptococcal pneumonia in patients with multiple pneumonia episodes.
I do NOT recommend flu shots.
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Apart from the subcutaneous tumour, is the lung tumour also primary or metastatic? If metastatic, does it still represent actual lung tumour?
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Dear Riva,
Here attached you have three articles about the LLC model.
One article was "already" published in 1974 in the excellent journal Cancer Rwsearch.
A second attachd article shows a nice study using this model and published in PlosOne, which is a good journal.
A third article is a recent review and shows that the LLC model is often use.
There are ~4,000 publications with the LLC model in the PubMed database ...
I would not be too anxious with the LLC model ...
Best regards
Robert
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Lungs are fixed by PFA and embeded in OCT and stored at -80oC. I am using the general protocol of abcam (http://www.abcam.com/protocols/immunostaining-paraffin-frozen-free-floating-protocol) to stain frozen sections of mice lungs and I get auto-fluorescence. 
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Yavuz,
Autofluorescence is always a problem with IF staining.  One of the things that can cause a great deal of autofluorescence is the fixing and permeabilizing agent used, but PFA is a good choice for this, as compared to methanol.  Another common cause of autofluorecence is the presence of RBCs in the sample.  Although this cannot be completely avoided, it can be reduced if you perfuse the animal with saline upon sacrifice before harvesting the tissue.  You can never remove all the RBCs, but perfusing does help. 
If you can't decrease the autofluorescence enough even with settings on your microscope/camera setup, then can you use IHC instead?  If you use adequate peroxide to quence the endogenous peroxidase activity (I use 3% peroxide in methanol--10x the concentration in the abcam protocol) then you can get very clear staining and be able to see the structure in the tissue. 
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This was a symptomatic event where the patient experienced severe central chest pain radiating "like a vice" around the body causing severe pain between the shoulders. Diagnosed by means of positive D-dimer and typical ECG changes such as SInus Tachycardia during the acute event, then ECG observations noted SR, S1Q3-Type with new RBBB.
The patient self administered GTN spray during the acute event, was given S/C heparin thereafter and commenced on oral aspirin 100mg. Seven days later, the patient was prescribed and given two 30 mg doses of oral prednisolone for an unrelated event.
Would evidence of PE still be availalabe given the time frame and susequent medications?
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Hopefully, I have understood my dear colleague's question properly,but in any case offer the following. I believe that one should perform a scan that may be diagnostic for embolization of the chronic type and the information given should be supplemented with additional clinical history directed toward chronic embolization. However, the information provided is sufficient for the initiation of pulmonary scintigraphy with the caveat that its significance is different than it would be in the acute setting. In specific, a negative scan would not rule out an historic embolic event, but, it would rule out massive chronic inter-current embolization. On the other hand, a positive scan could rule in chronic persistent embolization or a persistent unresolved embolism, and any abnormality detected on such a scan that is not characteristic or definitive for embolism would merit better anticoagulant therapy with repeat scanning after as little as three days or possibly one or two weeks. In that latter case, if the abnormality or abnormalities seen on scanning resolve(s) or is in any way improved one has presumptive evidence of ongoing resolution of prior embolization meriting long term anticoagulation, and a workup for potential etiology.
I have arrived at this opinion following many scans in the chronic setting for patients who are sometimes undiagnosed for months, some of whom arrive for scanning with severe respiratory/circulatory compromise in whom the possibility of embolism has been an afterthought. My belief is that the logistics of these situations preclude refusing to perform a scan that may clinch a difficult diagnosis. Or, to say it another way, no harm is done by performing a scan, provided that we interpret it to be consistent with the patient history.
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65 years old lady with gradually pregressive dyspnea....HRCT s/o ILD, rest of the blood parameters are normal. She was started with IV methyl prednisolone followed by oral tablets along with N Acetyl cysteine...but, she is not responding with increasing dyspnea.....today we have added tab azathioprine.  Any suggestion please...
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I suggest to read this article: N Engl J Med 2012;366:1968-77. I know that it is frustrating but as MD, we should avoid to harm our patients. Best regards, G
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Right lung edema has been observed in minimally invasive right thoracotomy mitral valve procedures, requiring extracorporeal membrane oxygenation in some patients. Proposed mechanisms have included right lung manipulation, ischemia/reperfusion, and reexpansion edema.
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I think manipulation and isolation of the lung during MICS mitral is the primary cause. Other anatomical causes are technical issues as described and should be avoided even in standard mitral operations. One approach is to have periodic ventilation of the lung and/or maintain a little PEEP. Less lung is manipulated in Aortic valves and you see less unilateral lung injury which I think is contusion more likely than pure edema. Hope this is helpful to all.
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What is the recent formula that can be used for calculation of lung age in smoking and non smoking people?
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The original paper from Morris & Temple Preventive Medicine 1985 vol 14 pg 655- 662 compared different methods but the authors suggested that the formula based on FEV1 was superior.
Lung age = (2,87x height in inches) - (31,25 x observed FEV1) - 39,375
But Vito has a valid point….
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Considering the increasing epidemiological burden of TB, especially drug resistant TB, should the old TB sanatoria/TB hospitals (many of which are defunct) be upgraded?
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Dear Gyanshankar,
The question and answer are probably different in countries with high or low prevalence and incidence of TB. There is no doubt that the rehabilitated structures could host, isolate, eat, cure and care many patients and together form health actors.
I remember, I was a young pulmonologist thirty years ago in a Sanatorium.
Best Regards.
Jean.