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Pleural emphysema: Emphysema – Symptoms and causes


Emphysema and Disorders of the Pleural Cavity

Part of the
Comprehensive Manuals of Surgical Specialties
book series (CMSS)


Bullous emphysema is a disorder in which the lungs contain bullae that are not associated with an intrinsic disease of the airways or with pulmonary scarring from a disease such as tuberculosis. For surgical purposes, a bulla is defined as an emphysematous space, not lined by epithelium, with a roof formed by visceral pleura. Most single bullae that occupy less than one-third of a thoracic cavity and that are situated in otherwise normal lungs do not cause symptoms. A large bulla, however, can compress and compromise the function of the rest of the lung. In addition, a bulla can cause a relaxation of the adjacent lung, thereby decreasing the radial tension on airways and causing an increased resistance to airflow. A bulla can become infected; the lung can bleed into a bulla, occasionally causing life-threatening hemoptysis; and a bulla can rupture, producing a pneumothorax.


Pleural Fluid Pleural Cavity Spontaneous Pneumothorax Parietal Pleura Visceral Pleura 

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Copyright information

© Springer-Verlag New York Inc. 1982

Authors and Affiliations

  1. 1.University of MinnesotaUSA
  2. 2.Minneapolis Veterans Administration Medical CenterMinneapolisUSA
  3. 3.SedonaUSA

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  • Emphysema – Physiopedia

    Pulmonary emphysema, a progressive lung disease, is a form of chronic obstructive pulmonary disease (COPD).  Emphysema is primarily a pathological diagnosis that affects the air spaces distal to the terminal bronchiole. It is characterized by abnormal permanent enlargement of lung air spaces with the destruction of their walls without any fibrosis and destruction of lung parenchyma with loss of elasticity.[1]

    There are three types of emphysema; centriacinar, panacinar, paraseptal. See image 1.

    1. Centriacinar emphysema affects the alveoli and airways in the central acinus, destroying the alveoli in the walls of the respiratory bronchioles and alveolar ducts [2] .
    2. Panacinar emphysema affects the whole acinus [2] .
    3. Paraseptal emphysema is believed to be the basic lesion of pulmonary bullous disease [2].

    Emphysema, as a part of COPD, is an illness that affects a large number of people worldwide. In 2016, the Global Burden of Disease Study reported a prevalence of 251 million cases of COPD globally. Around 90% of COPD deaths occur in low and middle-income countries  .

    The prevalence of emphysema:

    • In United States is approximately 14 million, which includes 14% white male smokers and 3% white male nonsmokers.

    It is slowly increasing in incidence primarily due to the increase in cigarette smoking and environmental pollution. Another contributing factor is decreasing mortality from other causes such as cardiovascular and infectious diseases. Genetic factors also play a significant role in determining the possibility of airflow limitation in patients.

    Emphysema severity is significantly higher in the coal worker pneumoconiosis, and this is independent of smoking status.[1]

    The exact cause of Emphysema is still yet to be distinguished, however research is suggesting the prevalence is strongly related to smoking, air pollutions and in some cases, occupation [3]. Another common association is the deficiency of the enzyme alpha₁-antitrypsin, which is the protein protecting the alveoli [4].

    The prevalence of Emphysema within the smoking population is believed to increase as smoking is a major risk factor associated. It is thought to have a higher incidence in those with a lower socioeconomic background, therefore affecting lifestyle and environment, resulting in the likelihood of respiratory infection [5].

    The alveoli and the small distal airways are primarily affected by the disease, followed by effects in the larger airways [4]. Elastic recoil is usually responsible for splinting the bronchioles open. However, with emphysema, the bronchioles lose their stabilizing function and therefore causing a collapse in the airways resulting in gas to be trapped distally[4].

    There is an erosion in the alveolar septa causing there to be an enlargement of the available air space in the alveoli [4]. There is sometimes a formation of bullae with their thin walls of diminished lung tissue.

    Smoking contributes to the development of the condition initially by activating the inflammatory process [3]. The inhaled irritants cause inflammatory cells to be released from polymorphonuclear leukocytes and alveolar macrophages to move into the lungs [3]. Inflammatory cells are known as proteolytic enzymes, which the lungs are usually protected against due to the action of antiproteases such as the alpha1-antitrypsin [3]. However, the irritants from smoking will have an effect on the alpha1-antitrypsin, reducing its activity. Therefore emphysema develops in this situation when the production and activity of antiprotease are not sufficient to counter the harmful effects of excess protease production [3]. A result of this is the destruction of the alveolar walls and the breakdown of elastic tissue and collagen. The loss of alveolar tissue leads to a reduction in the surface area for gas exchange, which increases the rate of blood flow through the pulmonary capillary system [3].

    CT scan is a common method used to diagnosis emphysema. The observations mainly seen to identify emphysema are a decrease in lung attenuation and a decrease in the number and diameter of pulmonary vessels in the affected area [6].

    Patients diagnosed with emphysema may complain of difficult/laboured breathing and reduced exercise capacity as their predominating symptoms [7]. The loss of the elastic recoil in the lungs leads to irreversible bronchial obstruction and lung hyperinflation, which increases the volume over normal tidal breathing and functional residual capacity [7].

    The main aims of treating patients with Emphysema are to relieve symptoms and to improve quality of life [8][9]. To measure patients’ quality of life, the St George’s Respiratory Questionnaire (SGRQ) and the Guyatt’s Chronic Respiratory Questionnaire (CRQ) are often completed in order to measure the effectiveness of a treatment intervention [8].

    Other outcome measures relevant include:

    6 minute walk test

    Grip strength

    Borg RPE

    30 second sit to stand

    Generally, the diagnosis for Emphysema can be based on clinical, functional and radiographic findings [10]. However, it is thought that mild Emphysema is not well detected on conventional chest radiography, therefore the use of pulmonary function tests (PFT) are often used to try and diagnose the condition [11].

    In order to accurately diagnose Emphysema, the history of the patient’s condition needs to be fully understood [12] . The use of high-resolution CT scans is part of the standard procedure when trying to detect this condition as it is non-invasive and is found to be sensitive in detecting pathological changes related to Emphysema [12].

    Physiotherapy and Other Management[edit | edit source]

    Physiotherapy management for Emphysema is commonly associated with similar management of COPD. The use of a pulmonary rehabilitation programme consisting of exercise and education can be designed by the physiotherapist along with other members of the multi-disciplinary team (MDT) in order to maximise the patients exercise capacity, mobility and also self-confidence [4]. The other MDT members can consist of a respiratory nurse and dietitians, as well as the physiotherapist in the hope to treat each patient like an individual and meet their specific needs by tailoring a programme to suit them [4].

    Pulmonary rehabilitation for patients with severe symptoms and multiple exacerbations reduces dyspnea and hospitalizations. [1]

    As COPD is the umbrella term used for diseases like Emphysema, the prevention strategies are very similar. The most common suggestion for preventing emphysema, and such, is to stop smoking, and to avoid breathing in any harmful pollutants [13].

    1. Pahal P, Avula A, Sharma S. Emphysema. [Updated 2021 Feb 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-.Available: https://www.ncbi.nlm.nih.gov/books/NBK482217/#!po=74.0000(accessed 24.5.2021p
    2. Hochhegger B, Dixon S, Screaton N, Cardinal V, Marchiori S, Binukrishnan S, Holemans J, Gosney J, McCann C, Emphysema and smoking related lung diseases. The British Institute of Radiology 2014; 20 (4).
    3. Mattison S, Christensen M. The pathophysiology of emphysema: Considerations for critical care nursing practice. Intensive and Critical Care Nursing 2006; 22: 329-337.
    4. Hough A. Physiotherapy in respiratory and cardiac care. Hampshire: Cengage Learning EMEA, 2014
    5. ↑ Haas F, Haas SS. The Chronic Bronchitis and Emphysema Handbook. Chichester: John Wiley and Sons, Inc; 2000.
    6. ↑ Newell, J. CT of Emphysema. Radiologic Clinics of North America 2002; 40 (1): 31-42.
    7. 7.07.1 Visca D, Aiello M, Chetta A. Cardiovascular function in pulmonary emphysema. BioMed Research International 2013.
    8. 8.08.1 Harper R, Brazierm JE, Waterhouse JC, Walters SJ, Jones NMB, Howard P.Comparison of outcome measures for patients with chronic obstructive pulmonary disease (COPD) in an outpatient setting. Thorax 1997; 52: 879-887.
    9. ↑ Naunheim KS, Wood DE, Mohsenifar Z, Sternberg AL, Criner GJ, DeCamp MM, Deschamps CC, Martinez FJ, Sciurba FC, Tonascia J, Fishman AP. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the national emphysema treatment trial research group. The Annals of Thoracic Surgery 2006; 82 (2): 421-443.
    10. ↑ Klein JS, Gamsu G, Webb WR, Golden JA, Muller NL. High-resolution CT diagnosis of emphysema in symptomatic patients with normal chest radiographs and isolated low diffusing capacity. Radiology 1992; 182: 817-821.
    11. ↑ Sanders C, Nath PH, Bailey WC. Detection of Emphysema with computed tomography correlation with pulmonary function tests and chest radiography. Investigative Radiology 1988; 23: 262-266.
    12. 12.012.1 Zaporozhan J, Ley S, Eberhardt R, Weinheimer O, Svitlana I, Herth F, Kauczor H-U. Paired inspiratory/expiratory volumetric thin-slice CT scan for emphysema analysis: comparison of different quantitative evaluations and pulmonary function test. American College of Chest Physicians 2005; 128 (5): 3212-3220.
    13. ↑ National Health Service. NHS Choices. http://www.nhs.uk/Conditions/Chronic-obstructive-pulmonary-disease/Pages/Introduction.aspx (accessed 02 June 2015)

    Pulmonary Interstitial Emphysema | Cedars-Sinai

    Not what you’re looking for?

    What is pulmonary interstitial emphysema?

    Pulmonary interstitial emphysema (PIE) is when air gets trapped in the tissue outside of tiny air sacs (alveoli) in the lungs. It affects newborn babies. PIE is fairly common in neonatal intensive care units (NICUs).

    When you breathe, air
    travels in through your mouth and nose to your lungs. The air goes into the
    alveoli. This is where gases get exchanged. Here, the lungs send oxygen to
    the blood. And they release carbon dioxide, a waste product. The oxygen then
    travels through the blood to all the organs of your body.

    Normally, air in the lungs stays in the alveoli. But in some cases, air can escape into the nearby tissue around the tiny sacs. This tissue is called the interstitium. This can happen if the wall of an air sac breaks open. If enough air leaks out, this can cause problems with breathing and blood flow.

    PIE usually affects
    low-weight infants who need a device (ventilator) that helps with breathing.
    These infants often have a lung problem that is caused by preterm birth. PIE
    often affects infants in the first few days of life. It may affect one or
    both lungs.

    PIE is classified by how long it lasts. Acute PIE lasts for less than a week. If it lasts longer, it is called persistent PIE. PIE may also be called diffuse or localized. Diffuse means it occurs in multiple places in the lungs. Localized means it occurs in a single spot.

    What causes pulmonary interstitial emphysema?

    PIE most often happens in preterm
    infants. It occurs when their lungs don’t make enough of a substance called
    surfactant. Surfactant allows alveoli to be more flexible and less likely to break

    Being on a ventilator may cause PIE. During artificial ventilation, a ventilator applies air pressure to the air sacs of your child’s lungs. This helps your child breathe by opening closed-off lung sacs. But in some cases, this extra pressure can create a leak in an air sac.

    Who is at risk for pulmonary interstitial emphysema?

    Babies with a greater risk of PIE are those with the following conditions:

    • Preterm birth, which often leads to respiratory disease
    • The lungs don’t develop correctly
      (pulmonary hypoplasia)
    • Breathing in the first intestinal discharge (meconium) at birth
    • A lung infection (pneumonia)
    • Very fast breathing right after birth (transient tachypnea of the newborn)

    What are the symptoms of pulmonary interstitial

    Signs of PIE often appear within 4
    days of birth. Mild PIE may have no signs. More severe PIE may cause signs of breathing
    trouble, such as:

    • Grunting or other signs of trouble breathing
    • Fast breathing
    • Pale appearance
    • Parts of the body tinted blue (cyanosis) due to low oxygen in the blood

    How is pulmonary interstitial emphysema diagnosed?

    You may be asked about you and your
    child’s health history. This may include information before, during, and after birth.
    Your child will have a physical exam. His or her heart and lungs may be checked. Blood
    tests may be done to look for signs of low levels of oxygen and high levels of carbon

    Your child may likely have an
    imaging test, such as a chest X-ray or a chest CT scan. Leaked air will often appear on
    both of these imaging tests.

    How is pulmonary interstitial emphysema treated?

    PIE is a serious condition. It can
    cause death if not correctly treated. For this reason, treatment is done inside a
    neonatal intensive care unit (NICU).

    Treatment is done to make sure your
    child gets enough oxygen. It also aims to prevent more air leaks. Treatment may

    • Lying your baby on the side with the
      air leak, which helps move more air into the lung that is working well
    • Lowering ventilator pressure if possible, to help prevent more air leaks
    • Using high-frequency oscillatory ventilation, which may lower pressure in the air sacs
    • Giving extra oxygen

    Your child’s vital signs and levels of oxygen in the blood are checked during the treatment. Your child may also need X-rays to check on the status of the air leaks as they heal.

    In most cases, PIE gets better with these treatments, and the leaked air goes away.

    If your child has a severe
    localized case of PIE, the healthcare team may collapse the lung with the air leak for a
    short time. This is so the air sac can heal. This is done by placing a breathing tube
    into the lung without the air leak. Or air flow may be blocked for a short time to the
    lung with the air leak. Your child might need a breathing tube and ventilator support
    during this time.

    In rare cases, a child might need to have part of a lung removed to treat PIE that does not go away.

    Your child may also need treatment for other lung problems that may be causing the PIE.

    What are possible complications of pulmonary interstitial

    PIE can sometimes cause pneumothorax. This is air in the space between the outer lungs and the chest wall. This can make breathing problems worse. Your child may need ventilator support or a chest tube for a large pneumothorax.

    How can I prevent pulmonary interstitial emphysema?

    Preventing preterm birth may help prevent PIE. You can decrease the chance of preterm birth by:

    • Not smoking during pregnancy
    • Not using alcohol or drugs during
    • Getting early and regular prenatal
      care throughout your pregnancy
    • Seeking medical attention at the first signs of preterm labor

    Key points about pulmonary interstitial emphysema

    • Pulmonary interstitial emphysema (PIE)
      is when air gets trapped in the tissue outside air sacs in the lungs.
    • It affects some newborn babies who
      are placed on ventilators, or breathing machines. PIE is fairly common in neonatal
      intensive care units (NICUs).
    • Lung disease caused by preterm birth
      increases a child’s risk of PIE.
    • PIE can cause trouble breathing and
      low oxygen levels in the blood.
    • In most cases of PIE, the air leaks go
      away on their own with supportive care.
    • In rare cases, your child might need a
      lung deflated for a short time to help treat PIE. Surgery may be needed in rare

    Next steps

    Tips to help you get the most from a visit to your healthcare provider:

    • Know the reason for your visit and what you want to happen.
    • Before your visit, write down questions you want answered.
    • Bring someone with you to help you ask questions and remember what your provider
      tells you.
    • At the visit, write down the name of a new diagnosis, and any new medicines,
      treatments, or tests. Also write down any new instructions your provider gives
    • Know why a new medicine or treatment is prescribed, and how it will help you. Also
      know what the side effects are.
    • Ask if your condition can be treated in other ways.
    • Know why a test or procedure is recommended and what the results could mean.
    • Know what to expect if you do not take the medicine or have the test or
    • If you have a follow-up appointment, write down the date, time, and purpose for that
    • Know how you can contact your provider if you have questions.

    Not what you’re looking for?

    Chronic Obstructive Pulmonary Disease: Diagnostic Considerations

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    Homa DM,
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    Redd SC.
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    5. Global Initiative for Obstructive Lung Disease. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease [executive summary]. Updated 2004. Accessed online July 5, 2005, at: http://www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1&intId=996.

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    Respiratory symptoms as predictors of 27 year mortality in a representative sample of British adults. BMJ.

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    The natural history of chronic airflow obstruction. Br Med J.

    14. The Alpha-1-Antitrypsin Deficiency Registry Study Group.
    Survival and FEV1 decline in individuals with severe deficiency of alpha1-antitrypsin. Am J Respir Crit Care Med.

    15. Alpha-1 Foundation. A healthcare provider’s guide to alpha-1 antitrypsin deficiency. Accessed online May 18, 2005, at: http://www.alphaone.org/documents/pdf/11.03_hcpg.pdf.

    16. Hnizdo E,
    Sullivan PA,
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    Association between chronic obstructive pulmonary disease and employment by industry and occupation in the US population: a study of data from the Third National Health and Nutrition Examination Survey. Am J Epidemiol.

    17. Oxman AD,
    Muir DC,
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    Occupational dust exposure and chronic obstructive pulmonary disease. A systematic overview of the evidence. Am Rev Respir Dis.

    18. Balmes J,
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    et al.
    American Thoracic Society statement: occupational contribution to the burden of airway disease. Am J Respir Crit Care Med.

    19. Sandford AJ,
    Silverman EK.
    Chronic obstructive pulmonary disease. 1: susceptibility factors for COPD the genotype–environment interaction. Thorax.

    20. Rennard SI,
    Farmer SG.
    COPD in 2001: a major challenge for medicine, the pharmaceutical industry, and society. Chest.
    2002;121(suppl 5):113S–5.

    21. Scanlon PD,
    Connett JE,
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    Altose MD,
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    Buist AS.
    Smoking cessation and lung function in mild-to-moderate chronic obstructive pulmonary disease. The Lung Health Study. Am J Respir Crit Care Med.
    2000;161(2 pt 1):381–90.

    22. Doherty DE.
    Early detection and management of COPD.What you can do to reduce the impact of this disabling disease. Postgrad Med.

    23. Mannino DM.
    COPD: epidemiology, prevalence, morbidity and mortality, and disease heterogeneity. Chest.
    2002;121(suppl 5):121S–6.

    24. Holleman DR Jr,
    Simel DL.
    Does the clinical examination predict airflow limitation? [published correction appears in JAMA 1995;273:1334]. JAMA.

    25. Rennard SI.
    Overview of causes of COPD. New understanding of pathogenesis and mechanisms can guide future therapy. Postgrad Med.

    26. Straus SE,
    McAlister FA,
    Sackett DL,
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    The accuracy of patient history, wheezing, and laryngeal measurements in diagnosing obstructive airway disease. CARE-COAD1 Group. Clinical Assessment of the Reliability of the Examination–Chronic Obstructive Airways Disease [published correction appears in JAMA2000;284:181]. JAMA.

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    Emphysema – an overview | ScienceDirect Topics

    Animal Models of COPD

    Several excellent reviews of animal models of COPD recognize the challenge to simultaneously generate relevant anatomic and functional lesions of the lung, such as chronic bronchitis, airway remodeling, emphysema, PH, and spontaneous exacerbations, all within a useful experimental timeframe. While no model has achieved these goals, there has been important progress in the field, only made possible by animal modeling of such a complex disease. Most models produce only mild to moderate disease, with the exception of the intratracheal elastase instillation, which induces a rapid and dose-dependent degree of airspace enlargement. Moreover, most rodent models that exhibit pulmonary COPD-like lesions are usually partially reversible upon cessation of the inciting exposure and lack the occurrence of spontaneous exacerbation. These models offer the opportunity to study mechanisms of and develop therapies against the development rather than the progression of COPD-like disease. Nevertheless, even if no animal model recapitulates all aspects of human disease, they do offer the opportunity to identify pathogenic or reparative pathways, which, as stated previously, can then be probed in a translational manner to studies of human samples.

    In addition to cigarette smoke exposure by inhalation, which is the most widely accepted animal model of COPD, other models have been developed, each emphasizing a pathogenic mechanism of COPD development, or a certain phenotype (Table 3). Many of these models have been criticized for their nonphysiological nature, the nonrealistic short timespan that some require to induce lesions which are COPD-like, or their transient nature. However, if interpreted in the appropriate context, they each contributed significant knowledge and advanced our understanding of this complex disease. The cigarette smoking inhalation model itself is not an ideal model, although it has several important advantages in that it utilizes the most common risk factor for COPD development, induces several anatomical lesions that best recapitulate ‘human COPD,’ and can be used in a variety of animal species, including well-characterized inbred strains and transgenic mice. In addition to the long duration of time required to induce a robust phenotype, the main disadvantages of the inhaled cigarette smoke model are related to the development of very subtle lesions of chronic bronchitis or mucus hypersecretion, probably linked to a high intrinsic ratio between bronchial epithelial and goblet cells and low number of submucosal glands seen in rodents. In addition, the methods utilized to generate cigarette smoke exposure are not very well standardized; therefore, the degree of COPD disease, with a relatively mild phenotype of emphysema, small airway remodeling, and PH, varies among laboratories and seldom induces the irreversible disease and/or the severe changes seen in human COPD GOLD stage III/IV. These exposure methods include a variety of commercial smoking machines that will deliver either nose-only exposure or whole-body exposure, both occurring intermittently, 3–5 h per day, once or twice a day, at various dosages (expressed as main- and sidestream percentages, ppm of carbon monoxide, cigarettes per minute per day), and for various durations ranging from acute exposures, measured in hours and days, to chronic exposures, lasting from weeks to months. The serum cotinine levels achieved are fairly similar and do not exceed the levels seen in humans with history of moderate cigarette smoking. Acute cigarette smoke exposures typically provoke measurable innate immune responses and antioxidant, stress, and metabolic responses, while chronic cigarette smoke exposures are required to generate significant adaptive immune host defense responses and changes in morphological and functional parameters. There are several notable differences in species and gender susceptibility to cigarette smoke, rats being relatively more resistant, whereas female mice being more susceptible to its effects. Among mouse strains, the NZWLac/J mice are relatively resistant; the C57BL6/J, A/J, DBA2, and SJ/L are mild to moderately susceptible; and AKR/J being most susceptible to cigarette smoke-induced lung COPD-like injury. There is also strain-specific predilection for COPD phenotypes, for example, lungs exposed to cigarette smoke exhibit predominantly emphysema in the pallid mouse (a strain with low levels of A1AT), more prominent airway inflammation and oxidative stress in C57BL6/J, while displaying more prominent apoptosis in the DBA2/J mouse. In other species, such as rabbit, guinea pig, or hamsters, cigarette smoke models have been mainly used to study small airway remodeling or PH, because their airways have more mucus glands, and extensive pulmonary function and hemodynamic measurements can be easily performed in larger animals. In addition, in ferrets, cigarette smoke can cause airway squamous metaplasia and initiate carcinogenesis, allowing the study of smoking-induced lung cancer.

    Table 3. Select animal models of COPD that target specific pathogenic mechanisms

    Mechanisms Animal models
    Inflammation LPS intratracheal instillation
    Genetically modified mice: TNF-R1 KO, IL1-R KO, SPD KO, TLR4 KO; Nrf2 KO, IL13 overexpression
    Matrix proteolysis Elastase intratracheal instillation (e.g., porcine pancreatic elastase or human neutrophil elastase)
    MMP12 KO
    Impaired tissue repair Adiponectin KO
    Apoptosis VEGF inhibition
    Caspase-3, ceramide-12 or -16 intratracheal instillation
    Genetically modified mice: RTP801, EMAP II overexpression
    Starvation-induced ‘emphysema-like’ air spaces (reversible)
    Premature senescence Genetically modified mice: Sirt1 heterozygous KO, Sirt1 transgenic, Klotho homozygous KO
    Autoimmunity Xenogeneic endothelial cell intraperitoneal administration
    Abnormal bronchial epithelial function Genetically modified mice: CFTR KO (± LPS), β-epithelial Na+ channel – overexpression
    Acute exacerbation Elastase intratracheal instillation plus S. pneumoniae inoculation
    Cigarette smoke model plus

    P. aeruginosa inoculation

    Influenza virus

    Replication-deficient adenoviral construct, poly (I:C)

    The typical endpoints of COPD modeling include airway and airspace morphology and morphometry, lung function testing, as well as systemic manifestations of weight loss and decreased functional performance (exercise studies). In addition, a combination of corroborative biochemical and cellular changes indicative of inflammation, oxidative stress, matrix proteolysis, cellular stress, including apoptosis, autophagy, and senescence, are typically presented to refine the lung injury phenotype. These measurements are performed on fixed, inflated lungs, using standardized inflation pressures, on laser capture microdissected lung structures, on bronchoalveolar lavage fluid samples, lung tissue homogenates, primary cells isolated from lung tissues, plasma, cardiovascular structures, bone marrow, etc. An area of ongoing work has been to unify and standardize lung morphometry (e.g., airway remodeling, airspace enlargement, alveolar wall destruction) performed in animal models of COPD. Airspace size, surface to volume ratio, and mean linear intercept have largely been used to define emphysema. In addition to integrating morphometry results with pulmonary function measurements of lung static compliance and lung volumes, the use of stereoscopic analyses of histological sections, micro-CT, or micro-PET imaging will further improve the accuracy of these methods. Recent advances in these methodologies are very exciting and will provide not only accurate descriptive parameters but also mechanistic insight into the disease. To this end, intravital microscopic techniques have been developed to allow real-time assessment of inflammation and injury of the alveolar structures in intact animals.

    The risk of surgical emphysema post VATS pleural biopsy and IPC


    Introduction: Video Assisted Thoracoscopic Surgical (VATS) pleural biopsies are part of the algorithm to investigate unilateral pleural effusions. Visceral pleural thickening can cause trapped lung, and indwelling pleural catheter (IPC) placement is standard management. The risk of developing surgical emphysema is unknown.

    Aim: To establish the incidence, severity, impact and risk factors for surgical emphysema post VATS pleural biopsy and IPC placement (VATS-IPC).

    Method: We retrospectively analysed consecutive patients undergoing VATS-IPC. Chest radiographs and electronic discharge summaries were reviewed. Surgical emphysema was radiographically graded as: 1 localised to IPC site; 2 ipsilateral chest wall; 3 involvement of neck; 4 involvement of contralateral chest wall.

    Results: Between 2000 and 2018, 176 cases were identified. The median age was 70 [interquartile (IQR) range 64-76] years and 126/176 (72%) were male. Surgical emphysema was identified in 97/176 (55%) cases with grade 4 present in 16/176 (9%).

    In patients with grade ≥2 a malignant diagnosis was more likely (97% versus 83%; p=0.01; OR 5.28(95%CI 1-26). No difference in age or gender was identified across the grades (p=0.47 & p=0.35 respectively). Length of stay (LOS) increased across the grades of severity (p<0.01). In those with Grade 4 disease, the LOS was 12.9[8-18.25]days versus 4[3-7] days in those without surgical emphysema (p<0.01). Grading remained significantly associated with LOS when adjusted for diagnosis, age and gender (p=0.03).

    Conclusion: Severe emphysema occurred in nearly 1 in 10 patients. Severity was associated with a malignant diagnosis and with a significant increase in LOS. Further investigation is warranted to identify other risk factors.


    Cite this article as: European Respiratory Journal 2019; 54: Suppl. 63, PA1079.

    This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).

    • Copyright ©the authors 2019

    B.3 Main CT symptoms of lung pathology in viral lung lesions

    Frosted glass


    A section of partially airy lung tissue, against which the vessels, lumens of the bronchi and their walls are visible.

    Significantly more accurately detected with CT than with RH.

    An area of ​​airless lung tissue with visible air lumens of the bronchi and air cavities (for example, emphysema).Vessels and walls of the bronchi in the zone of compaction are not visible.

    Detected equally accurately with RG and CT.

    Reticular changes

    Cobblestone symptom

    Thin lines of the pathologically altered pulmonary interstitium, forming a network.

    CT symptom. When RH is designated as a mesh (cellular) deformation of the pulmonary pattern.

    Synonym: patchwork symptom. Image of reticular changes against the background of a “ground glass” seal.

    CT symptom.

    Peribronchovascular distribution

    Perilobular changes

    The location of the altered areas of the lung tissue along the bronchi and vessels of the lung.

    Equally detected with RH and CT.

    Lung tissue thickening along the interlobular septa, one of the important signs of organizing pneumonia.

    CT symptom.

    Cortical (subpleural, peripheral) distribution

    Root (central) distribution

    Location of altered areas of lung tissue along the visceral pleura (costal, diaphragmatic, mediastinal, interlobar).

    Equally detected with RH and CT.

    Location of altered areas of lung tissue in the area of ​​the lung root.

    Equally detected with RH and CT.

    Air bronchography symptom

    Halo symptom

    Visibility of air-filled bronchi in compacted lung tissue.Indicates the preservation of bronchial patency.

    CT symptom.

    Synonym: rim symptom.

    Area of ​​”frosted glass” around the consolidation area or area of ​​destruction (necrosis). Usually it has an annular shape.

    CT symptom.

    Reverse halo symptom

    Cavity in the lung or area of ​​consolidation

    Synonym: reverse rim symptom, atoll symptom.

    Consolidation zone around the “ground glass” area. It can be of any shape and size. A characteristic sign of organizing pneumonia. CT symptom.

    Closed pathological space in the lung with thick (> 2 – 3 mm) walls, surrounded by airy lung tissue. The cavity contains gas, liquid, necrotic masses). Usually observed with bacterial infections and neoplasms.

    More precisely detected by CT, especially with small sizes.

    Cyst in the lung

    Focus (s) in the lungs

    Closed pathological space in the lung with thin (<2 mm) walls, filled with gas or liquid. CT symptom.

    Consolidation in lung tissue up to 10 mm in size. They can be single, single (up to 6) and multiple (dissemination).More precisely detected by CT (The term “nodule” is synonymous, but not recommended for use).

    Symptom “tree in the buds”

    Picture of organizing pneumonia

    V- and Y-shaped pathological structures in the lung up to 1 cm in size, representing filled with pathological contents and dilated small bronchi and bronchioles.An important sign of a bronchogenic lower respiratory tract infection.

    CT symptom.

    Variable. Usually a combination of ground-glass patches and consolidation with a reverse rim symptom and typical peribronchovascular and / or subpleural distribution. A set of CT symptoms.

    Thoracic surgery

    About the branch

    The department offers the population in Israel and abroad not only the most modern medical equipment, but also the services of a professional and experienced staff.The operations of the chest and chest cavity organs are performed using the most innovative technologies that are selected individually, taking into account the needs of each patient.

    Who can benefit from our services?

    Services offered by the Department of Chest and Thoracic Surgery are intended for the surgical treatment of lung cancer and / or other lung tumors, malignant or benign, primary or secondary, for the treatment of tumors in the mediastinum and thoracic cavity, esophageal cancer and / or benign tumors esophagus, congenital chest deformities or deformities due to trauma, hyperhidrosis, severe pulmonary emphysema, various lung infections and / or chest infections, etc.


    About 80% of operations in the Department of Chest and Thoracic Surgery are performed using minimally invasive methods (thoracoscopy). This method is more effective and safer than the traditional surgical method with opening the chest and spreading the ribs. In the process of thoracoscopic operations, 2-3 incisions are made between the ribs – one for a video camera and two for the introduction of surgical instruments. However, in more complex cases that do not allow for a minimally invasive procedure, a traditional operation with opening the chest is performed.

    Advantages of minimally invasive method:

    • lower level of pain after surgery
    • Shorter hospital stay with faster return to daily activities
    • method allows to operate on elderly people
    • allows you to operate on severe patients suffering from other concomitant diseases
    • preservation of respiratory function after surgery
    • only small scars remain on the body
    • Significant reduction in postoperative complications
    • higher chances of recovery and better quality of life.

    Treatment methods and procedures

    • Lobectomy (removal of a lobe) of the lung in patients with lung cancer and / or other lung tumors.
    • Pneumonectomy (complete removal of the lung) for patients with lung cancer.
    • Removal of mediastinal tumors.
    • Removal of the esophagus in patients with esophageal cancer.
    • Reduction of lung tissue volume in patients with severe pulmonary emphysema.
    • Removal of blisters from the lung in patients with primary pneumothorax or with pulmonary bullae.
    • Adhesion of the pleura in patients with malignant pleural effusion.
    • Correction of congenital chest deformities.
    • Removal of the affected sections of the chest wall in patients with tumors.
    • Partial removal of the heart lining in patients with pericardial effusion.
    • Implantation of a pacemaker in the left ventricle in patients with severe heart failure.
    • Bilateral cauterization of the sympathetic nerve in patients with hyperhidrosis.
    • Biopsies of the pleura, lymph nodes of the mediastinum, pericardium, diaphragm.
    • Diaphragm fixation in patients with diaphragm paralysis.

    Medical staff

    In the thoracic department of the Shamir Medical Center “Assaf ha-Rofe” at your service – a staff of surgeons with extensive experience in the field of minimally invasive operations on the lungs, esophagus and other organs of the chest. The department of surgery of the chest and organs of the chest cavity works in close cooperation with other departments and units in the medical center, including the pulmonary department, departments of radiology, oncology, gastroenterology, pathology and others.
    The department is headed by Dr. Mikhail Papiashvili, one of the leading thoracic surgeons in Israel, specializing in minimally invasive chest surgery.

    About the medical center “Assaf ha-Rofe”

    Shamir Medical Center Assaf HaRofeh is a public university hospital, the fourth largest in Israel, and the central hospital for the Shfela district.

    The work of outpatient clinics, emergency rooms, inpatient departments and maternity wards is carried out with the participation of clinics and laboratories of various medical specializations.3,400 doctors, researchers, paramedical personnel, nurses and administration personnel provide personalized treatment and state-of-the-art medical care to every patient, whether Israelis or coming from abroad for treatment.

    In Noginsk, doctors rescued a patient with COVID-19 who had 7 cardiac arrest

    A 67-year-old man with confirmed coronavirus infection was admitted to the Noginsk central district hospital.His condition was rapidly deteriorating, so the doctors made an urgent decision to transfer the patient to intensive care.

    “The patient was admitted to us in a serious condition, with respiratory failure of the second degree and lung damage of about 75%. His condition required a connection to a ventilator. The situation was aggravated by the man’s serious concomitant disease – bullous lung disease, ”says Roman Uteshev, anesthesiologist-resuscitator of the infectious diseases hospital at the Noginsk hospital.

    Bullous lung disease, or as it is also called emphysema, is a formidable disease manifested by the appearance in the lungs of areas of pathologically stretched lung tissue filled with air.These air bubbles are called bullae. At first, these bullae are small in size and do not cause inconvenience to the patient. But over time, they grow and can reach 15 centimeters in diameter.

    “Emphysema is a serious disease in itself, and then viral pneumonia was added. Already when the patient was on mechanical ventilation, he began to have spontaneous rupture of bullae. After the large bulla burst, the left lung was practically completely collapsed. Against this background, cardiac arrest occurred, ”says the resuscitator.

    The patient was resuscitated within almost 15 minutes. The doctors then performed an emergency drainage of the left pleural cavity to release air from the lung and expand it. Already during the operation, 6 more cardiac arrests occurred, but the doctors did not give up.

    “It was a very difficult battle. Thanks to the well-coordinated work of our entire team, we managed to stabilize the patient, ”explains the doctor.

    In total, the man spent 4 months in the hospital, including a month on mechanical ventilation.This affected the muscles: atrophy began. Doctors attached the expander to the bed, and the man began to develop muscles, learn to sit down, get up on his feet. At the moment, the man has already been discharged home and continues to recover.

    Thoracic surgery in Germany, cost, treatment

    Thoracic surgery is a surgery of the chest cavity organs. Surgery of the heart and great vessels, as a rule, is a separate area, however, in many large and university hospitals in Germany and around the world there are large departments of cardiothoracic surgery.

    Such a combination is easily explained, because the heart and respiratory organs are not only in anatomical proximity, but also in a complex functional relationship with each other, as well as with other organs of the mediastinum. In the diagnosis and treatment of laryngeal pathology, thoracic surgeons work closely with ENT specialists.

    Departments of thoracic surgery in Germany are equipped with the latest equipment, which makes it possible to diagnose and treat the entire spectrum of diseases of the chest wall, lungs, mediastinum.

    The competence of thoracic surgeons includes:
    • Pathology of the respiratory tract (larynx, trachea and bronchi): stenosis (narrowing), congenital malformations, neoplasms, tracheo-esophageal fistulas
    • Pathology of the chest wall: developmental disorders (keeled and funnel chest), trauma and post-traumatic deformities of the ribs and sternum, disrupting the skeleton of the chest and causing cosmetic defects, tumors
    • Pleural pathology: neoplasms, including pleural mesothelioma, pleural effusion of various etiology? Bullous lung disease and pneumothorax of various etiology
    • Diseases and lesions of lung tissue, for the diagnosis and treatment of which surgical and minimally invasive methods are used
    • Pathology of the cervical and thoracic esophagus: developmental anomalies, cicatricial narrowing, neoplasms
    • Primary and secondary tumors of the chest cavity organs.

    For a complete diagnosis, thoracic surgeons have access to all modern examination methods. After examination with auscultation of the lungs, screening X-ray examination and spirography, according to the indications, various types of tomography are prescribed, allowing you to study in detail and carry out 3D-reconstruction of the intrathoracic organs, find out their spatial relationships and plan the necessary interventions.

    Fibrooptic and video bronchoscopy represent not only the most valuable diagnostic method (examination, taking sputum for analysis and biopsy of mucous membranes and formations), but also ample opportunities for minimally invasive treatment.During bronchoscopy, it is possible to install stents that restore patency and stabilize the trachea and large bronchi, occluders – special devices that temporarily close the bronchus, which is the source of bleeding. Also, by means of a bronchoscope, bougienage (dilation) of cicatricial stenosis of the trachea, laser surgery of small benign neoplasms and granulations are performed. In infectious diseases, lung abscesses, pleural empyema, lingering pneumonia and bronchitis, cystic fibrosis, bacteriological diagnosis is of great importance.

    A laboratory study of any material taken during research, with the determination of the sensitivity of the isolated pathogens to antibacterial drugs, provides an effective prescription and correction of treatment. The multidisciplinary pulmonary treatment teams in Germany include bacteriologists and clinical pharmacologists, which are proven to provide the best results. Videothoracoscopy is a minimally invasive surgical procedure that can perform diagnostic and therapeutic functions.Through several point punctures of the chest wall under general anesthesia, special manipulators are introduced into the pleural cavity, with the help of which you can carefully examine the lung, pleura and some mediastinal organs, take a biopsy, coagulate bullae with bullous emphysema, eliminate the pathological contents of the pleural cavity. In clinics of thoracic surgery in Germany, through a thoracoscopic approach (without a traditional surgical incision), resections of metastases in the lungs, removal of a part of the lung in case of focal lesions, reduction operations for pulmonary emphysema, operations on the thoracic esophagus and many other complex interventions are performed.

    Comprehensive oncological treatment is provided for patients with tumors of the thoracic cavity in institutions such as the Interdisciplinary Thoracic Tumor Center, whose specialists work closely with the Cancer Center at the University Hospital in Freiburg. Timely surgical intervention based on the principles of radicality and minimal trauma, supplemented, if necessary, with chemotherapy, radiation therapy, immunotherapy, followed by comprehensive rehabilitation, provides the highest percentage of radical treatment, the best indicators of the duration and quality of life of patients with tumor diseases.The high level of technology, full-fledged equipment and qualifications of doctors put thoracic surgery in Germany in one of the leading positions in the world. In addition, a stay in German clinics is always comfortable and conducive to recovery. Of course, the treatment of lung and mediastinal diseases in Germany is a reliable choice.

    Pulmonology and thoracic surgery | Treatment | Treatment


    The Department of Chest Surgery at the Medipol University Hospital provides effective treatment of patients through the introduction of modern medical technologies and a high academic level of training of specialists.


    • Lung cancer
    • Cancer of the pleura (mesothelioma)
    • Tumors of the trachea
    • Stenosis (narrowing) of the trachea
    • Thymus tumor
    • Progressive emphysema of the lungs
    • Rupture of the pleural membrane of the lungs (pneumothorax)
    • Accumulation of fluid in the pleural cavity
    • Inflammation of the pleura (empyema)
    • Chest deformity (depressed or convex chest)
    • Compression syndrome of the upper aperture of the chest
    • Injuries to the chest (fractures, bleeding or organ damage due to stab and gunshot wounds, car accident or fall)
    • Protrusion of adjacent organs of the diaphragm
    • Excessive sweating of the palms (hyperhidrosis)

    Excessive sweating of the palms (hyperhidrosis)


    The Department of Pulmonology of the Clinical Hospital of Medipol University provides qualified medical care by experienced specialists of high academic background.

    The Pulmonology Department offers medical services in the following areas:

    • Diagnostics and treatment of lung cancer,
    • Diagnosis and treatment of chronic obstructive pulmonary disease,
    • Asthma Diagnosis and Treatment,
    • Performing an injection skin test for patients with complaints of allergies (itching in the nose, sneezing, shortness of breath),
    • Conducting immunotherapy (antiallergic vaccine therapy) in patients with indications
    • Test-study of the state of pulmonary functions,
    • Hospitalization of patients requiring advanced diagnostics,
    • Providing assistance in smoking cessation.

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    Pulmonologists of St. Petersburg – latest reviews

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