The chest X-ray is the most frequently requested X-ray at the radiology department. A primary indication is to exclude/confirm lung pathology (including overfilling, pneumonia, pneumothorax). In addition, it provides some information on inserted lines and tubes (deep venous lines, tracheal tube, gastric tube), heart/vessels (cardiomegaly, aneurysm), the mediastinum (lymphadenopathy), the ribs/vertebrae and soft tissues (subcutaneous emphysema). When the X-ray is made, the beam travels from the X-ray tube through the body and hits a phosphorus plate/detector. The whiteness (= density) depends on the amount of radiation passing through the tissue. The more X-rays are obstructed (absorbed or scattered) and do not reach the phosphorus plate/detector, the denser (=whiter) the image. Highly absorbent materials, such as metal, will be imaged as dense. Another example: X-rays travel more easily through air-filled lungs (black) than bone (white). The information received on the plate is converted into a digital image, in this case the chest X-ray.

  • Each chest X-ray is evaluated as if you are standing in front of the patient; so the right side of the image is the patient's left side and vice versa.
  • Importantly, the X-ray beam has a divergent property. This means it widens as the distance to the X-ray tube increases. A drawback of this phenomenon is that tissues/structures farther from the plate are imaged larger.

Posterior-anterior (PA) image: 

The X-ray beams pass through the body from posterior to anterior. The patient is standing with his abdomen against the plate. The arms are on the hips (fig. 1).


Figure 1. Technique for posterior-anterior (PA) chest X-ray.

Anterior-posterior (AP) image:

The X-ray beams pass through the body from anterior to posterior. The patient is sitting/lying with his back against the plate (fig. 2).

Figure 2. Technique for anterior-posterior (AP) chest X-ray.

Lateral image:

The X-ray beams pass through the body from right to left according to convention. The patient is standing/sitting with his left chest against the plate. Both arms are lifted into the air to prevent overprojection of the arms (fig. 3). 

Figure 3. Technique for lateral chest X-ray.

Comment: in order to image the heart size as realistically as possible in a lateral image, the left side of the chest is positioned against the plate. Note: Because of the divergent property of the X-ray beams, structures farther from the plate are projected larger. On the AP image, the heart is (relatively) farther away from the plate, complicating evaluation of the heart size. 

TIP: When in doubt or when you are making a PA or AP image, look for the contours of the scapula. The arms are not abducted in an AP image; the scapulae are therefore not fully turned away; compared to a PA image, the scapular contours are more towards medial (see fig. 1 & 2).

The best evaluable images are a PA image and a lateral image. The image should be non-rotated, taken in a position of adequate inspiration and have good penetration.


Adequacy of inspiration can be verified when you can see 10 dorsal ribs, and the 5th and 7th ribs cross the diaphragm at mid-clavicular.  
Tips to distinguish dorsal & ventral: the horizontal ribs are at the dorsal side. 

 Figure 4. Chest X-ray with adequate inspiration.


In a non-rotated image, the spinous processes of the thoracic vertebrae project in the middle between the medial ends of the claviculae.

 Figure 5. Non-rotated chest X-ray.


This refers to the amount of radiation passing through the body. If too much or too little radiation is given, the resulting image will be more dense (= whiter) or lucent (=blacker) than desired. There are now standard settings to optimize imaging. Nevertheless, images are regularly made with suboptimal or poor X-ray penetration (think of chest X-ray in an adipous patient). 
Important: in a chest X-ray with good penetration, one can look through the heart and see the contours of the thoracic vertebrae.

Normal anatomy

The pleural cavity is formed by the visceral pleura (= membrane attached to the lungs) and the parietal pleura (= membrane attached to the surrounding structures). The pleurae outline both lungs and are invisible on a normal chest x-ray (fig. 6).

 Figure 6. The pleural cavity is formed by the visceral pleura and parietal pleura. The pleurae outline both lungs. Sinus pleura: the most caudal part of the pleural cavity.

The lung lobes are separated by interlobar fissures; the place where the visceral pleurae touch each other (fig. 6). The visceral pleura is very thin (< 1 mm) and is visible only when it is thickened or hit tangentially by the X-ray beam.
The major fissure separates the upper lobe from the lower lobe both left and right; on a lateral image it inclines from level Th-4/Th-5 in a ventrocaudal direction to the diaphragm (fig. 7). The major fissures are invisible on the anterior-posterior image (fissures are not hit tangentially by the X-ray beam).
In the right side of the chest, the middle lung lobe is created by the minor fissure, which is largely horizontal but can also be curved.  The minor fissure can be seen on both the anterior-posterior and lateral images (fig. 7).

 Figure 7. The fissures on a lateral chest X-ray and anterior-posterior chest X-ray.

TIP to distinguish the left and right major fissures on the lateral image: the left major fissure ends on the left hemidiaphragm. The left hemidiaphragm is often lower, making it easier to trace the fissure. Also consider the air bubble in the stomach as point of reference of the left hemidiaphragm. 

To refresh your memory, a summary of the borders of the 5 lung lobes is given below.

 Figure 8. Left lower lobe.

 Figure 8. Left upper lobe.

 Figure 8. Right upper lobe.

 Figure 8. Middle lobe.

 Figure 8. Right lower lobe.

About 1% of the population have an additional lung lobe; the lobus venae azygos, also known as the azygos lobe. The azygos lobe is separated from the right upper lobe by the fissura venae azygos. The azygos vein normally runs along the spine parallel to the esophagus. However, if an azygos lobe is present, the vein runs through the upper part of the right lung (fig. 9).

 Figure 9. Lobus venae azygos.

The heart is retrosternal (towards left) with the tip towards left. The heart normally sits somewhat rotated in the chest; the left ventricle/atrium are located more posteriorly than you would expect (fig. 10). On the anterior-posterior image, the contours of the right atrium and left ventricle are visible. The right ventricle contour is visible on the lateral image by its central (anterior) retrosternal position.

 Figure 10. Position of the heart. RA = right atrium, RV = right ventricle, LA = left atrium, LV = left ventricle, VCS = vena cava superior or superior caval vein.

The contours of the hili are created for the most part by the pulmonary arteries (fig. 11). In more than 90% of the people, the left hilus is higher than the right hilus. This is because the left pulmonary artery runs over the left main bronchus, whereas the right pulmonary artery runs under the right main bronchus and separates in the mediastinum. In other people, the hili are at the same level. Note: higher position of the right hilus versus the left hilus is usually pathological (or the result of postoperative changes).

On lateral images, the right anterior pulmonary artery can be seen anteriorly of the trachea. The left pulmonary artery is posterior of the trachea.

 Figure 11. Anatomy of hili on an anterior-posterior chest X-ray (a) and a lateral chest X-ray (b). Note that at both left and right the pulmonary artery is sharply delineated (see yellow dotted lines).

From central to peripheral the airway consists of: trachea, main bronchus, bronchioli and alveoli.
The pulmonary artery carrying the low-oxygen blood originates in the right ventricle and terminates, together with the bronchioli, in the smallest pulmonary radiological unit: the secondary pulmonary lobule (0.5 - 3.0 cm). The alveoli are where the gas exchange takes place (fig. 12).
The secondary pulmonary lobule is surrounded by a thin fibrous wall: the interlobular septa. In the interlobular septa are the pulmonary veins (transporting the high-oxygen blood to the left atrium) and the lymph vessels. 

Figure 12. Secondary pulmonary lobule.


The following points may be used as a guide to assess a chest X-ray. 
(Note: some terms are explained later in the Pathology section)

  1. Technique: how was the image made? (Supine, standing, AP, PA). What is the technique? (Rotation, inspiration). Has everything been imaged?
  2. Artificial lines (if present): position of drains/deep venous lines/tracheal tubes/gastric tube?
  3. Mediastinum: widened? (including aortic pathology, space-occupying lesion/lymphadenopathy) Free air? (pseudomediastinum) Position of trachea/bronchi? (when displaced: think of atelectasis) 
  4. Lung hili: are the hili sharp? Can all be explained by vessels? (Think of a mass/lymphadenopathy) Lungs: Symmetric lung vessel markings? Normal tapering towards peripheral? 
  5. Heart: are the heart contours sharp? Can you see through the heart? Enlarged heart? 
  6. Pleura: pleural thickening? Pneumothorax?
  7. Subdiaphragmal: free air? (fig. 13) Intestinal pathology? Hiatal hernia? 
  8. Soft tissues: subcutaneous emphysema? Are there (superimposed) abnormalities of skin, breasts and other body parts? (fig. 13)
  9. Bone: ribs intact? Fracture/vertrebral collapse? Bone lesions?

 Figure 13. Extrapulmonary abnormalities. A lock of hair may simulate lung pathology (a) Extensive subdiaphragmal free air in a patient with gastric perforation (b).

Additional tips:

  • Review all previous tests. This may provide significant clarification, especially in situations where interpretation is complex. Always ask yourself the question: what has changed? (‘find the differences')
  • When in doubt whether a density is real or has been created by superimposition of multiple (physiological) structures, examine the other direction. If the density is visible on both the anterior-posterior and the lateral image, chances are this is a real finding. 
  • Note that if the imaged abnormality is large, people tend to stop looking. If your evaluation is unsystematic, chances are you will miss other abnormalities (this phenomenon is termed by some the “instant happiness syndrome”).
  • Do not underestimate the evaluation of the chest X-ray. Abnormalities are often not obvious and can be very subtle. Try to see as many chest X-ray tests as possible in your medical career, because your frame of references is worth its weight in gold in evaluation.


  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax


In atelectasis, lung tissue loses its volume.
The lung lobes are separated by the fissures. When a lung lobe collapses, the borders (= fissures) of the lung lobe in question will move. Collapsed lung tissue has lost its air content and folds together, like an emptied balloon.
This ‘empty balloon’ causes the pulmonary vessels and bronchi in this area to move close together, also termed ‘crowding'.  This often results in increased density (=whiter). The surrounding lung tissue tries to fill the empty space causing hyperinflation, so-called "compensatory hyperinflation". 
Other evidence of atelectasis includes displacement of surrounding structures, such as surgery clips, pulmonary abnormalities, trachea and the mediastinum. Also the ribs may move closer together. 

Etiology of various forms of atelectasis: tumor/foreign body/mucus (postobstructive atelectasis) (fig. 14), lobectomy (postoperative atelectasis), pleural fluid (compression atelectasis), trauma/neuromuscular disorder/infection (restrictive movement).

 Figure 14. Atelectasis of right lower lobe. Increased volume of entire left lung with shift of the mediastinum and trachea (see black arrows). This is secondary to a subtotal closure of the right intermediate bronchus with an intrabronchial tumor (histology: carcinoid).

In summary:
Displacement of the fissures strongly suggests atelectasis. Other indications include: crowding of lung tissue, compensatory hyperinflation of surrounding lung tissue and displacement of surrounding structures (vacuum effect!)
Important: atelectasis is not a disease in itself, but should be regarded as a manifestation of underlying lung disease.


  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax



  • infiltrate = abnormal vague density in the lungs.   
  • consolidation = the air-filled alveoli are replaced by fluid, blood, pus, mucus, edema or another substance. 
  • pneumonia (lung infection) = infection (air replaced by pus) of the alveoli, therefore a form of consolidation.

In practice, the above terms are regularly used interchangeably.

Two characteristics of pneumonia are discussed below.

Silhouette sign

Anatomical borders are visible on X-ray because of differences in capacity to absorb X-rays. The degree of absorption determines density (=whiteness). E.g. bone has a higher absorption capacity than fat and will therefore have a denser aspect (see fig. 15).

Figure 15. X-ray densities.

The heart absorbs more X-rays than the lungs; this creates the anatomical contour of the heart. If two structures have the same density, it will be difficult to distinguish them. Example: in lung edema (consequence: increased X-ray absorption in the lungs), the heart contour/diaphragmatic dome will be less easily distinguished due to the lack of difference in density. This phenomenon, the loss of radiographic contour, is termed the silhouette sign (fig. 16).

 Figure 16. Retrocardial consolidation in the left lower lobe. The medial side of the left hemidiaphragm is no longer sharply delineated (silhouette sign). The consolidation also creates limited volume loss; the left hemidiaphragm has been displaced towards cranial (atelectasis).

Silhouette sign may occur in various locations. Each location is in itself associated with specific lung lobe pathology.
Summary of lung lobes + location of silhouette sign (fig. 17): 

  • left lower lobe: left hemidiaphragm + descending aorta 
  • left upper lobe: aortic arch
  • lingula: left heart contour
  • right lower lobe: right hemidiaphragm
  • middle lobe: right heart contour
  • right upper lobe: right paratracheal  

Figure 17. Location of silhouette sign (yellow dotted lines) in the various lung lobes. RUL = right upper lobe, ML = middle lobe, RLL = right lower lobe, LUL = left upper lobe, LLL = left lower lobe.

Air bronchogram

The trachea and the two main bronchi are clearly visible on a chest X-ray because of the difference in absorption capacity of air and mediastinal fat.  More towards peripheral, the air-filled bronchi have thin walls and are surrounded by air-filled alveoli. The result is that the peripheral bronchi are invisible on a chest X-ray (silhouette sign!). The linear lines visible on a normal chest X-ray are vessels; these fluid-filled structures contrast well with surrounding air. 
In summary: in a normal chest X-ray, anatomical borders of the peripheral bronchi are invisible. 

However, due to pathologic changes bronchi can sometimes be distinguished. When the alveoli are filled with fluid (blood, pus, mucus, edema, cells) rather than air, a density difference develops between the alveoli and bronchi.  Fluid in the alveoli contrasts with the air-filled bronchi, making the ‘invisible’ bronchi visible. This phenomenon is termed an air bronchogram (fig. 18). The presence of an air bronchogram suggests pulmonary pathology.
Air bronchograms may be present in all pathology leading to lung tissue consolidation (including pneumonia, lung edema and ARDS (acute respiratory distress syndrome)).

 Figure 18. Air bronchograms in bilateral pneumonia.

Consider: tumors in the bronchus may produce a postobstructive infiltrate. Would you expect an air bronchogram in that case?

Answer: no. Air bronchograms require an open airway. If a bronchus tumor prevents air from passing the tumor, the postobstructive infiltrate will not cause an air bronchogram.

  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax

Interstitial lung diseases

Alveolar / interstitium:
For the sake of convenience, we will subdivide the lung into 2 components; the alveoli (the ‘air bags') and the supporting interstitium (structures surrounding vessels, lymph vessels, bronchi), see fig. 19.

Figure 19. The secondary lobule.

The interstitium can then be subdivided into the peribronchovascular/centrilobular/intralobular/interlobular/subpleural interstitium. This course will not go into the details of this subclassification. 

Air absorbs virtually no X-rays and therefore the normally air-filled alveoli cannot be differentiated on a chest X-ray (fig. 20).

Figure 20. X-ray densities (=whiteness).

All the alveoli together produce a lucent (= black) area. The branching pulmonary vessels are dense (=white). The structures surrounding the vessels/lymph vessels/bronchi are the interstitium and are normally (in healthy persons) invisible on a chest X-ray. 
In alveolar disease, the alveoli are filled with materials that produce a fluid density.  The material type (blood, pus, mucus, edema, cells) cannot be ascertained on a chest X-ray. Irrespective of the content, the filled alveoli will always surround the interstitium with a dense area, visible on a chest X-ray as a cloud-like consolidation (fig. 21). An alveolar disease is often an acute disorder (think especially of lung edema in heart failure and pneumonia).

 Figure 21. Alveolar consolidations in heart failure.

Interstitial lung disease has multiple presentations. In healthy people, the pulmonary vessels on a chest X-ray become less and less dense towards peripheral. This is logical, as pulmonary vessels continue to branch into smaller vessels, making them less visible on X-ray.

There are 4 types of pathological interstitial patterns, which can be distinguished accurately on CT scans.

  • Linear pattern. Here we see thickened interlobar septae. The interlobar septae separate the secondary lung lobules from each other and contain the pulmonary veins and lymph vessels. The most common cause is pulmonary edema secondary to heart failure.  The thickened interlobar septae, hit tangentially by the X-ray beam, can be seen on chest X-rays as Kerley A and B lines.

 Figure 22. Linear pattern with Kerley A (central) and B (peripheral) lines. Kerley B lines in right lower lobe in a heart failure patient.

  • Reticular pattern.  A collection of small linear dense lines, forming a net structure.  This network of lines may vary from a fine to crude pattern. Reticular abnormalities are seen in diseases including lung fibrosis and asbestosis.

Figure 23. Reticular pattern. A patient with extensive lung fibrosis.

  • Nodular pattern. We see multiple spherical densities varying from 1 mm to 1 cm.  Based on etiology, 3 subgroups can be distinguished: nodular metastases, nodular pneumoconiosis (= inhaled dust particles) and granulomatous diseases (including sarcoidosis and arthritis). Think also of miliary TBC.

Figure 24. Nodular pattern in sarcoidosis.

  • Reticonodular pattern. A combination of a reticular and a nodular lung pattern.

Figure 25. Reticonodular pattern in patient with a history of recurrent pneumonia and HIV.

TIP: with increased interstitial markings (both locally and diffuse) in combination with irregular markings (=abnormal architecture), consider a chronic problem, e.g. lung fibrosis. If there are vague increased interstitial markings with a regular aspect of the branching vasculature, then an acute disorder is more likely. However, a more reliable method to distinguish between acute and chronic lung disease is to review older tests. 


  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax

Heart failure

In heart failure, cardiac output is reduced, resistance is increased or the fluid volume is excessive (mostly in the left ventricle). As a result, the blood is no longer adequately pumped out from the lungs into the large circulation. 
In healthy situations, gas exchange takes place on the capillary-alveolar level, particularly in the lower lung fields. If gas exchange is inadequate, as in heart failure, the upper fields will be used to compensate in order to improve oxygenation.

Stage I:
On a chest X-ray, the first compensatory response will manifest in so-called redistribution of blood to the upper fields. 
This should be taken into account in supine images: gravity will equally distribute blood supply over the upper and lower fields.  In such cases, the term redistribution would be inappropriate. 

 Figure 26. Redistribution to the upper fields.

Stage II:
If heart failure continues to deteriorate, the high pressure will cause the blood to extrude through the vessels into the interstitium. This is manifested in Kerley lines (= fluid in interlobular septa) and peribronchial cuffing (= fluid around the airways), see fig. 27.

 Figure 27. Thickened interlobular septa and peribronchial cuffing (a) Kerley B lines (b).

Stage III:
The lymphatic system can no longer handle the excess fluid. The fluid will extend into the alveoli (= alveolar lung edema) and the pleural cavity (= pleural fluid).

 Figure 28. Alveolar lung edema.

Alveolar lung edema has several causes, including:

  1. Cardiogenic (heart failure)
  2. Neurogenic (head trauma)
  3. Increased permeability of the pulmonary vascular bed: inhalation/toxic gas, high altitude disease, aspiration, contusion, fat embolism, sepsis.

The most common cause of alveolar edema, however, is heart failure.

Other evidence of heart failure:

  • enlarged heart (CTR ratio > 0.50)
  • acute development & recovery after therapy

Below is an example with a summary of signs of heart failure (fig. 29).

 Figure 29. Signs of heart failure. Note also the (compression) atelectasis retrocardial left secondary to pleural fluid (a). Check-up image after treatment (b).


  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax

Pleural fluid

The pleural cavity is formed by the visceral pleura (= membrane attached to the lungs) and the parietal pleura (= membrane attached to the surrounding structures).
The deepest caudal part of the pleural cavity is posterior and lateral. These angles are termed the costophrenic angles (costa = rib, phrenicus = diaphragm), or sinus pleura (fig. 30).

 Figure 30. Sinus pleura on PA images (a) and lateral images (b).

If there is fluid in the pleural cavity, gravity will cause the fluid to move downward. In a standing chest X-ray, depending on the fluid volume, the costophrenic angle will become vague and eventually develop a markedly rounded contour. In moderate to large volumes of pleural fluid, the fluid level will also have the shape of a half moon, also known as the meniscus sign (fig. 31).

 Figure 31. Meniscus sign in pleural fluid in the left costophrenic angle.

The pleural fluid can also extend along the thoracic wall into the interlobar fissures (= interlobar fluid).


  • the posterior costophrenic angle is more reliable in terms of presence of pleural fluid. On a standing anterior-posterior image, pleural fluid is visible from 175 ml, whereas on a lateral image pleural fluid can be seen from 75 ml in the posterior costophrenic angle.
  • Be aware of the effects of gravity and the movement of fluid when assessing chest X-rays.  Example: pleural fluid in a supine patient may cause a uniform white veiling of the lung fields.

Pleural fluid has many causes and the underlying problem cannot always be ascertained based on chest X-ray or chest CT alone. Pleural puncture will enable a more detailed differentiation. In these procedures, transudative pleural fluid (e.g. in heart failure, pancreatitis, liver cirrhosis) or exudative pleural fluid (e.g. in pneumonia, malignancy, autoimmune disease) is obtained.


  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax


COPD means chronic obstructive pulmonary disease and includes the lung diseases chronic bronchitis and emphysema.  Both forms are associated with expiratory flow limitation.

Lung emphysema:
Lung emphysema is associated with a pathologically enlarged air-filled cavity distal of the terminal bronchioli and destruction of the alveolar walls.  Efficiency of ventilation is significantly compromised. No obvious fibrosis is present in emphysema.
Lung emphysema has multiple subtypes (e.g. centrilobular, panlobular and paraseptal emphysema). Subtypes will not be addressed in this course. 

Emphysema abnormalities on chest X-ray (fig. 32):

  • flattened diaphragmatic domes 
  • enlarged retrosternal space (> 4.4 cm) 
  • barrow-shaped chest
  • saber sheath trachea (coronal narrowing and sagital widening of the trachea)
  • narrow heart contours 
  • obliteration of the costophrenic angles 
  • diaphragmatic tenting (= muscle bands of the diaphragm) 

Vascular abnormalities (signs of lung destruction):

  • reduced vascular markings
  • bulla (= focal area of lung emphysema; enlarged alveolar space of > 1 cm) 
  • abnormal lung lucencies 

 Figure 32. COPD on a PA and lateral chest X-ray.

Chronic bronchitis
Chronic bronchitis is characterized by irritation of the mucous membranes of the bronchi/bronchioli, leading to an inflammatory response and excessive mucus production. Eventually, the lumen may become constricted with an increased risk of infection.
The abnormalities of the chest X-ray are frequently subtle and non-specific. In patients with chronic bronchitis, 40-50% of the cases have a normal chest X-ray.

Chronic bronchitis abnormalities on chest X-ray:

  • mild bronchial wall thickening 
  • non-specific increased markings
  • abnormalities as in lung emphysema (hyperinflation & vascular abnormalities) 


  • The above emphysema and chronic bronchitis processes frequently occur together. 
  • The diagnosis COPD is based on spirometry (limited expiration) and cannot be demonstrated/excluded using chest X-ray alone.


  • Atelectasis
  • Pneumonia
  • Interstitial lung diseases
  • Heart failure 
  • Pleural fluid
  • COPD
  • Pneumothorax


In pneumothorax, air is in the pleural cavity. The visceral pleura (=lung membrane) is separated from the parietal pleura.
A pneumothorax may be subdivided into spontaneous and traumatic.


  • penetrating & non-penetrating thoracic injury 
  • mechanical ventilation. .


  • primary: is seen mostly in young adults (men > women) with a tall and thin posture. There is no underlying pulmonary disease.
  • secondary: in patients with underlying lung disease (e.g. COPD, lung cysts, cavitation, connective tissue diseases).

Findings on chest X-ray (fig. 33):

  • visible visceral pleura, with absent lung markings at peripheral
  • deep lucent costophrenic angle (‘deep sulcus sign'). The air is contained in the anterolateral pleural cavity (particularly in chest X-rays made in supine position). 
  • increased sharpness of heart contours and diaphragmatic domes (increased density difference due to the presence of air). 
  • hydropneumothorax (the air-fluid level is created by air and fluid in the pleural cavity. 
  • trace of pleural fluid (present in 20-40% of the cases).

 Figure 33. Right-sided pneumothorax with an air-fluid level (= hydropneumothorax).

Tension pneumothorax (fig 34):
If the pressure in the pleural cavity exceeds the atmospheric pressure (due to valve action), the term tension pneumothorax is used. This is a life-threatening situation and a relieving drain should be inserted immediately.
Tension pneumothorax can be suggested on a chest X-ray; but clinical correlation is needed for the final diagnosis (poor hemodynamic situation). Caudal displacement of the hemidiaphragm suggests tension pneumothorax. Mediastinal shift towards the healthy lung is non-specific and can also be seen in a marked pneumothorax without tension component.
In short: tension pneumothorax can be regarded as a clinical diagnosis.​

 Figure 34. Left-sided tension pneumothorax with trachea/mediastinal shift and caudal displacement of the left hemidiaphragm.


  • W. R. Webb MD, C. B. Higgins. Thoracic Imaging: Pulmonary and Cardiovascular Radiology (second edition, 2011). 
  • L. R Goodman. Felson's Principles of Chest Roentgenology (third edition, 2011)
  • J.E.Takasugi, J.D. Godwin. Radiology of chronic obstructive pulmonary disease. Radiol Clin North Am. 1998 Jan;36
  • S. Whitley et al. Clark’s Positioning in Radiography (12th Edition)


  • Annelies van der Plas, resident radiology LUMC

24/01/2014 (translated to English: 16/08/2016)

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