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Anatomic emphysema: Emphysema – Symptoms and causes

Quantitative Emphysema Distribution in Anatomic and Non-anatomic Lung Regions

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. 2015 Jun;12(3):257-66.

doi: 10.3109/15412555.2014.933950.

Epub 2014 Sep 17.

Michael Owsijewitsch 
1
, Julia Ley-Zaporozhan, Jan-Martin Kuhnigk, Annette Kopp-Schneider, Ralf Eberhardt, Monika Eichinger, Claus Peter Heussel, Hans-Ulrich Kauczor, Sebastian Ley

Affiliations

Affiliation

  • 1 1Department of Diagnostic and Interventional Radiology, University Hospital Heidelberg , Heidelberg , Germany.
  • PMID:

    25230093

  • DOI:

    10.3109/15412555.2014.933950

Michael Owsijewitsch et al.

COPD.

2015 Jun.

. 2015 Jun;12(3):257-66.

doi: 10.3109/15412555.2014.933950.

Epub 2014 Sep 17.

Authors

Michael Owsijewitsch 
1
, Julia Ley-Zaporozhan, Jan-Martin Kuhnigk, Annette Kopp-Schneider, Ralf Eberhardt, Monika Eichinger, Claus Peter Heussel, Hans-Ulrich Kauczor, Sebastian Ley

Affiliation

  • 1 1Department of Diagnostic and Interventional Radiology, University Hospital Heidelberg , Heidelberg , Germany.
  • PMID:

    25230093

  • DOI:

    10.3109/15412555.2014.933950

Abstract


Purpose:

The change of emphysema distribution with increasing COPD severity is not yet assessed. Especially, involvement of the upper aspect of the lower lobe is unknown. The primary aim was to quantitatively determine regional distribution of emphysema in anatomically (lung lobes) and non-anatomically defined lung regions (upper/lower lung halves as well as core and rind regions) in a cohort covering equally all COPD severity stages using CT.


Material and methods:

Basically 100 CT data sets were quantitatively evaluated for regional distribution of emphysema. Emphysema characteristics (emphysema index, mean lung density and 15th percentile of the attenuation values of lung voxels) were compared (t-test) in: upper lobes vs. upper halves, lower lobes vs. lower halves, core vs. rind region.


Results:

In patients with ≤ GOLD II, a significantly higher emphysema burden was found in the upper lobes as compared to upper halves. In subjects with GOLD III/IV the differences were not significant for all emphysema characteristics. A high difference between lobes and halves in subjects with ≤ GOLD II was found, in contrast to low difference in higher GOLD stages.


Conclusions:

Lobar segmentation provides improved characterization of cranio-caudal emphysema distribution compared to a non-anatomic approach in subjects up to GOLD stage II.


Keywords:

CT; emphysema quantitation; regional distribution.

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Emphysema – Physiopedia

Original Editors – Students from Glasgow Caledonian University’s Cardiorespiratory Therapeutics Project.

Top ContributorsValentina Mazzoni, Lucinda hampton, Kim Jackson, Esraa Mohamed Abdullzaher, WikiSysop, Admin, Uchechukwu Chukwuemeka, 127. 0.0.1, Evan Thomas and Michelle Lee

Contents

  • 1 Definition/Description
  • 2 Epidemiology
  • 3 Aetiology
  • 4 Pathophysiology
  • 5 Investigations
  • 6 Clinical Manifestations
  • 7 Outcome Measures
  • 8 Diagnostic Procedures
  • 9 Physiotherapy and Other Management
  • 10 Prevention
  • 11 References

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. 1.01.11.2 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. 2.02.12.2 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. 3.03.13.23.33.43.5 Mattison S, Christensen M. The pathophysiology of emphysema: Considerations for critical care nursing practice. Intensive and Critical Care Nursing 2006; 22: 329-337.
  4. 4.04.14.24.34.44.5 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)

Spontaneous mediastinal emphysema

Mediastinal emphysema, or pneumomediastinum, is a pathological condition consisting in air infiltration of mediastinal tissue [4].

It is believed that spontaneous mediastinal emphysema (SES) is a rare, independent disease characterized by a benign course and occurring without specific causes, it mainly affects young men [9, 19, 23, 36].

The first mention of SES is dated 1617, when the midwife of the Queen of France, Louise Bourgeois, in her memoirs, described a sudden swelling of the neck during childbirth [12]. This pathological condition was first described by Rene Laennec in 1819.in the treatise “About listening with a stethoscope” [24]. SES as an independent disease was first reported by Louis Hamman [5, 10, 19, 23, 25] in 1939. He described gross crepitus, synchronous with heart contractions, which is auscultated along the left edge of the sternum in the third to sixth intercostal space, not excluding and other areas, in a sitting position. This clinical symptom is called Hamman’s symptom.

The pathophysiology of this disease, based on experiments on laboratory animals, has been described in 1944 M. Macklin and S. Macklin [5, 10, 23, 25]. In an animal experiment, they showed that SES occurs as a result of a sharp decrease in the pressure gradient between the alveoli and the interstitial tissue of the lungs, which leads to rupture of the alveoli. The described mechanism, combined with pathological changes in the alveolar-capillary membrane and/or interstitial lung tissue, can lead to alveolar rupture into the interstitial space [31]. The breakthrough of the alveolus into the pulmonary interstitium leads to the accumulation of air in it, which propagates along the pressure gradient, perivascularly and peribronchially, centripetally to the hilum of the lungs, and then into the mediastinum (Macklin effect) [20]. This is because the pressure in the mediastinum is lower than at the periphery of the lungs. Most authors agree that the disease occurs as a result of rupture of the terminal alveoli located at the root of the segment (lobe) of the lung and adjacent to the loose tissue surrounding the vessels and bronchi [5, 16, 23]. Once in the mediastinum, air can spread to the cellular spaces of the neck, soft tissues of the chest, into the cavity of the heart shirt, and even (depending on the amount) into the retroperitoneal cellular space [8].

The frequency of SES in hospitalized patients varies, according to various data, from 1:3578 [16] to 1:44 511 [25].

There are various trigger mechanisms or factors contributing to the occurrence of SES. I. Macia et al. [25] consider it appropriate to divide these factors into: predisposing – bad habits and / or diseases in history, which create conditions favorable for the development of the disease, and provoking – conditions that immediately precede the onset of SES.

Many authors consider such pulmonary diseases as predisposing factors as bronchial asthma [5, 9, 16, 19, 25, 29], inflammatory diseases of the upper respiratory tract [5, 19], idiopathic fibrosing lung diseases [9], chronic obstructive diseases lungs [9]. Of the diseases listed above, according to publications in the world literature, only bronchial asthma is considered as a predisposing factor in the development of SES by almost all authors [5, 9, 16, 19, 25, 29, 35, 36]. J. Chapdelaine et al. [11] established this disease in history in almost 50% of patients, A. Newcomb and C. Clarke [29] – in 39% of patients with SES. It should be noted that in the world literature, authors rarely associate the development of SES with bullous emphysema. A.G. Vysotsky [2] described 4 cases of pneumomediastinum as complications of local bullous emphysema. I.I. Platov and V.S. Moiseev [4] believe that the development of SES is associated with the same reasons that lead to the development of spontaneous pneumothorax, namely bullous disease, cystic formations of the lungs of congenital origin, and respiratory inflammatory diseases.

Some authors believe that smoking is a predisposing factor in the development of the disease [9, 25]. J. Macia et al. [25] compared the number of smokers with SES with the number of smokers among the population of Catalonia (Spain), which amounted to 34.1 and 37.5%, respectively. I. Abolnik et al. [6] noted that the number of smokers among SES patients differed slightly from those in the general population.

Many provoking factors have been described that can directly cause the development of the disease. The Valsalva test, intense coughing, sneezing, severe vomiting, hysterical crying, childbirth, defecation, physical activity, bronchospasm, spirometry, playing wind instruments, blowing up balloons, and using inhaled drugs should be singled out [1, 5, 9, 10, 18, 23, 25, 26, 28, 32].

In the communication of M. Caceres et al. [9] dominating among the provoking factors was vomiting, which preceded the onset of the disease in 36% of cases, the second most frequent was an attack of bronchial asthma, this condition was observed in 21% of patients. Cough is also one of the frequent trigger factors, and according to various data, it precedes SES in 7.3% [25] and in 40% of cases [28]. The occurrence of SES on the background of diabetic ketoacidosis [36], chemotherapy [34], and Hodgkin’s disease [21] has also been described.

However, it is not always possible to identify predisposing and/or provoking factors, SES often occurs at rest [9].

The variety of symptoms of the clinical manifestation of SES has been reported by many authors [25, 36]. Most often, there is a triad of clinical symptoms – retrosternal pain (which is the most frequent and constant symptom), difficulty in breathing, neck swelling [1, 5, 15, 16, 19, 25, 29, 35, 36]. I. Abolnik et al. [6] noted the presence of chest pain in 88% of patients with SES, I. Macia et al. [25] – in 85%, M. Gerazounis et al. [16] – in 72.7%, G. Koullias et al. [23] – in 66.6%, M. Caceres et al. [9] – in 54% of patients. The patient may also complain of pain in the throat, back, shoulder, lower back, weakness, dysphagia, odynophagia, rhinophony, change in voice timbre. Some authors also include cough as a symptom of the disease, although it is also a factor provoking the onset of SES [23]. M. Caceres et al. and G. Koullias et al. singled out cough as one of the symptoms of the disease, it was noted in 41 and 32% of their own observations of SES and was, respectively, the second and third most common symptom after retrosternal pain [9, 23].

Of the clinical symptoms of the disease, detected during physical examination, subcutaneous emphysema of the soft tissues of the neck and/or chest is most often noted [1, 2, 5, 7, 16, 25, 36]. Depending on the amount of air that has entered the mediastinal tissue, soft tissue emphysema can spread to the face and lower chest, but this is rare [5]. In the communication of I. Macia et al. [25] in 95% of patients with SES, palpation revealed subcutaneous emphysema of soft tissues, in 66% – neck and in 29% of patients – chest wall. J. Jougon et al. [19] stated the presence of this symptom in 100% of SES patients. M. Gerazounis et al. [16] described the presence of rhinophony (twang) in 5 patients, which was noted together with emphysema of the soft tissues of the neck and developed as a result of air dissection of the tissues of the retropharyngeal cellular space. This symptom is quite rare, but there are observations in which it is the first manifestation of SES and the main clinical symptom of the disease [17].

Hamman’s symptom cannot be called specific for SES, since, according to Yu.V. Haleva [5], such crepitus can also be heard in left-sided pneumothorax without mediastinal emphysema, as well as in bullous emphysema of the reed segments, pneumoperitoneum with a high diaphragm, and stomach dilation. The prevalence of Hamman’s symptom in patients with SES, according to different sources, varies from 0 to 56% [6, 9, 10, 15, 23, 25, 29, 36].

With pneumomediastinum, patients may also have a decrease in cardiac dullness, deafness of heart sounds during auscultation. I. Abolnik et al. [6] noted the presence of a paradoxical pulse in 2 patients with SES. Most patients may have one or more symptoms, but sometimes an objective examination fails to reveal a single symptom [5].

The main methods for diagnosing SES are chest X-ray in frontal and lateral projections, chest CT and radiopaque examination of the esophagus.

A. Yellin et al. [36] pointed out the need to perform radiography (as a routine method of primary diagnosis) in all young patients with chest pain of unknown origin and difficulty breathing. According to many authors, this research method turned out to be informative in the vast majority of patients with SES [6, 16, 23, 36], while they emphasize the need to perform the study in two projections – frontal and lateral, because with a small accumulation of gas in the mediastinum with a review X-ray of the chest in the direct projection of the pneumomediastinum may not be detected [23, 25].

When a pneumomediastinum occurs, x-rays show clear bands or gas bubbles surrounding the mediastinal organs, elevating the mediastinal pleura, and often extending to the neck and/or chest wall [14].

S. Bejvan and J. Godwin [8] report that on AP radiography, free gas in the mediastinum is often detected along the left contour of the heart and covers the inner surface of the mediastinal pleura, creating a clearly visible pleural line lateral to the pulmonary trunk and aortic arch. On radiographs in the lateral projection, free gas forms lines of enlightenment along the contours of the ascending aorta, the aortic arch and its branches, the pulmonary arteries, and the trachea with the main bronchi [8]. Gas is also localized along the line of attachment of the diaphragm to the sternum, along the thymus and brachiocephalic veins [13].

Polypositional radiography is the main and very effective method of research in this disease, but if there is gas infiltration of the soft tissues of the chest wall, then its information content is reduced to almost zero. In such situations, as well as in case of alertness in relation to diseases with a similar clinical picture and if it is necessary to establish the cause of the disease, if the X-ray method is insufficient, it is advisable to perform chest CT [30]. T. Kaneki et al. [20] noted that radiography failed to detect pneumomediastinum in 30% of patients with SES, the final diagnosis was established by chest CT. G. Koullias et al. [23] performed CT scans after the initial x-ray examination in all 25 patients, although they considered x-rays to be the “gold standard” for diagnosing SES, since both of these diagnostic methods turned out to be informative in relation to pneumomediastinum in 100% of cases. CT is undoubtedly the most effective method for diagnosing pneumomediastinum [20], since it easily detects the presence of gas in the mediastinum and its anatomical localization is well determined in cross sections. However, it should be noted that in terms of ease of implementation and radiation exposure to the patient, this method loses to radiography, and one should not forget about the economic aspect. A. Newcomb and C. Clarke [29] believe that if pneumomediastinum is determined by radiography and there is no suspicion of the presence of any formidable disease as the cause of this pathological condition, then we can limit ourselves to this diagnostic method only.

In some observations of SES, given in the world literature, an X-ray contrast study of the esophagus was performed. This additional diagnostic method was used in situations where it was necessary to exclude the presence of such a dangerous condition as rupture of the esophagus. A water-soluble contrast agent and/or a suspension of barium sulfate is used [15, 16, 19, 36]. D. Weissberg [35] used this research method to rule out rupture of the esophagus if SES was preceded by vomiting.

Additional research methods for this disease include esophagoscopy, bronchoscopy and electrocardiography. These methods are auxiliary and are used to confirm the diagnosis of SES in doubtful situations.

Differential diagnosis of SES is carried out with diseases of the cardiovascular (acute coronary syndrome, pericarditis), respiratory (spontaneous pneumothorax, pulmonary embolism, perforation of the tracheobroncheal tree) and digestive (spontaneous rupture of the esophagus) systems [32].

According to foreign authors [15, 25, 29, 35, 36], the optimal time for inpatient observation and treatment of patients with SES is from 2 to 5 days.

SES responds well to conservative treatment, which includes bed rest, anesthesia and oxygen therapy [6, 9, 15, 23, 29]. At the same time, a rather rapid regression of symptoms is observed, and in most cases, complete resolution of the pneumomediastinum occurs by the 8th day [29, 36]. Usually, soon after the alveoli break into the pulmonary interstitium, they collapse, as the pressure in them decreases and the air flow stops [19]. G. Koullias et al. [23] all patients underwent antibacterial prophylaxis of mediastinitis. They used a third-generation cephalosporin with clindamycin added to therapy for suspected esophageal perforation and when the disease was accompanied by fever and leukocytosis. Very rarely, emphysema of the tissue of the neck, chest and abdominal walls, the face progresses and a tense pneumomediastinum develops. In this case, the mediastinum, according to Sauerbruch, “swells like a ball”, the thin-walled main veins of the mediastinum are compressed with a decrease in cardiac activity, respiratory failure and possible death [3]. In such situations, an upper Tiegel mediastinotomy is indicated with tunneling of the pretracheal tissue to the level of the tracheal bifurcation with drainage of the mediastinum and subsequent aspiration, which ensures mediastinal decompression [4]. J. Moore et al. [27] in infants with tense mediastinal emphysema performed drainage of the mediastinum through a subxiphoid access. For soft tissue and mediastinal decompression in this complication, some authors suggest suprasternal mediastinal puncture and sternotomy [33], supraclavicular puncture [6], and tracheostomy [22]. If, despite these measures, there is an increase in intense mediastinal emphysema, urgent transpleural wide mediastinotomy is required [4].

Single observations of SES recurrence have been described [16, 25]. A. Yellin et al. were the first to describe the recurrence of the disease in the literature. [36], they observed patients for 52 months after discharge from the hospital, the recurrence of mediastinal emphysema in one patient occurred 14 months after the first episode without predisposing causes.

Thus, spontaneous mediastinal emphysema is a disease that affects more often young men of working age. Its occurrence requires differential diagnosis with a number of serious pathological conditions. In rare situations, tension mediastinal emphysema can lead to hemodynamic and respiratory disorders.

Clinical and anatomical conference NIIKK them. A.L. Myasnikova National Medical Research Center of Cardiology of the Ministry of Health of Russia March 1, 2022

A.L. Myasnikov, residents and graduate students held a clinical and anatomical conference, the event was held online. A clinical case of a 92-year-old patient was presented.

Final clinical diagnosis:

I34.0 Acquired mitral heart disease: previous secondary infective endocarditis caused by Str. gallolyticus (2018), against the background of chronic rheumatic heart disease, detachment of the chords of the posterior wall of the mitral valve with the formation of severe primary mitral insufficiency. High pulmonary hypertension. Heart rhythm disturbance: permanent form of atrial fibrillation, tachysystolic variant. Circulatory insufficiency 4 FC according to NYHA.

Operation: transcatheter plasty of the mitral valve using the Mitraclip device with implantation of 2 clips (08/07/2020).

Complications: Circulatory arrest, resuscitation (10.08.2020). Takotsubo stress cardiomyopathy. Posthypoxic encephalopathy. Ischemic stroke in the basin of the right middle cerebral artery (08/10/2020). Coma. Extended IVL. Intracardiac blood shunting syndrome, acute hypoxemic respiratory failure, pulmonary hypertension crisis, acute right ventricular failure (08/13/2020).

Concomitant diseases: coronary artery disease: stenosing atherosclerosis of the coronary arteries (hemodynamically significant stenoses of the PNA, DA). Arterial hypertension of the 3rd degree. Atherosclerosis of the aorta and extracranial brachiocephalic arteries. Stenosing atherosclerosis of intracranial arteries. Transient ischemic attack in the basin of the right middle cerebral artery (2018). Chronic cerebral ischemia. Peptic ulcer of the stomach and duodenum, without exacerbation. Suturing a bleeding gastric ulcer (2016). Bilateral pulmonary embolism (2016).

Post-mortem diagnosis:

Main disease: Acquired mitral heart disease: past secondary infective endocarditis caused by Str. gallolyticus (2018), against the background of chronic rheumatic heart disease with detachment of the chords of the posterior wall of the mitral valve, the formation of severe primary mitral insufficiency and high pulmonary hypertension (according to clinical data).

Operation: transcatheter plasty of the mitral valve using the Mitraclip device with implantation of 2 clips (08/07/2020).

Complications: Prolonged rupture of the surgical atrial septal defect. Takotsubo stress cardiomyopathy. Syndrome of intracardiac blood shunting, pulmonary hypertension crisis, right ventricular failure: pronounced plethora of arteries and veins of the lungs with symptoms of thrombosis, dystelectasis, focal pulmonary emphysema, pronounced congestive venous plethora of the superior and inferior vena cava, right atrium. Ischemic stroke in the basin of the right middle cerebral artery (08/10/2020). Cerebral edema.

Concomitant diseases: Stenosing atherosclerosis of the coronary arteries Atherosclerosis of the aorta and extracranial brachiocephalic arteries.