Pleural Diseases



Pleural Diseases






11.1 Pneumothorax


The various causes of pneumothorax are summarized in ▶Table 11.1. Spontaneous pneumothorax is differentiated from traumatic, including iatrogenic, pneumothorax.

Small pneumothoraces are often asymptomatic or cause sudden chest pain. Larger pneumothoraces may additionally give rise to dyspnea. A small pneumothorax usually resolves spontaneously within a few days and in general requires no treatment but must be monitored. More rapid absorption of the pleural air is achieved through oxygen insufflation. A chest tube is needed for larger pneumothoraces.

Tension pneumothorax is a special form of pneumothorax (▶Fig. 11.1) in which a valve mechanism caused by the air leak in the visceral pleura allows air to escape from the lung into the pleural space in inspiration but not to return to the lung in expiration. This leads to a progressive pressure increase in the affected hemithorax. Mediastinal displacement toward the unaffected side and a low-riding diaphragm on the affected side are seen on chest radiography. Clinically, there is rapid onset of hypotension, tachycardia, dyspnea, and cyanosis. This dramatic situation stems from several pathophysiologic components4:








Table 11.1 Causes of pneumothorax1,2















Cause


Examples


Spontaneous




  • Primary spontaneous pneumothorax (no underlying pulmonary disease):


    – Bullae or other emphysematous changes


    – Visceral pleura porosity2,3



  • Secondary spontaneous pneumothorax (with underlying pulmonary disease):


    – Airway diseases (chronic obstructive pulmonary disease, cystic fibrosis, asthma)


    – Lung infections (Pneumocystis jirovecii pneumonia, necrotizing pneumonia, tuberculosis)


    – Diffuse parenchymal lung diseases (idiopathic pulmonary fibrosis, sarcoidosis, Langerhans cell histiocytosis, lymphangioleiomyomatosis)


    – Collagen vascular diseases (rheumatoid arthritis, scleroderma, ankylosing spondylitis)


    – Malignant tumors (lung cancer, sarcoma, metastasis)



  • Catamenial pneumothorax (in thoracic endometriosis)


Traumatic




  • Penetrating chest trauma



  • Displaced rib fracture with rupture of the visceral pleura


Iatrogenic




  • Transthoracic lung biopsy



  • Placement of a central venous catheter (subclavian vein)



  • Thoracentesis



  • Transbronchial lung biopsy



  • Pleural biopsy



  • Positive pressure ventilation



  • Chest operations




  • Loss of ipsilateral, negative intrapleural pressure.


  • Mediastinal displacement to the contralateral side with compression of the intrathoracic superior vena cava and kinking at the transition of the inferior vena cava to the right atrium.


  • Reduced venous blood return to the heart because of the two aforementioned mechanisms, in turn giving rise to right heart failure.


  • Onset of atelectasis with an ensuing increase in the pulmonary shunt volume, leading to hypoxemia, which may result in depression of the respiratory center.

Emergency pressure relief of the affected hemithorax through chest tube placement is needed for newly diagnosed tension pneumothorax. Immediate puncture of the pleural space with an adequately long cannula may help bridge the time until a definitive treatment with chest tube is possible.


11.1.1 Imaging Findings

The radiographic findings of pneumothorax will depend on the imaging position (▶Table 11.2).

The most important criterion for a standing radiograph is the ability to identify the visceral pleura, which has separated from the parietal pleura, as a fine linear opacity (▶Fig. 11.3). The
space between this line and the chest wall is a more radiolucent and, in general, avascular area (exception: pneumothorax presenting as a backdrop anterior or posterior to the fully inflated lung lobe). Lung adhesions to the chest wall may occur.






Fig. 11.1 Tension pneumothorax. Radiographs. (a) Baseline findings with atelectasis of the right lung (arrow), mediastinal displacement to the left and prominent pulmonary trunk as sign of right heart strain (arrowhead). (b) Normalization of findings following chest tube placement.


Because the patient is lying down, supine radiographs result in an anterior pleural air collection that hampers direct detection of a visceral pleural line since often the lung abuts the lateral chest wall. Hence, diagnosis is based on indirect signs of air in the pleural space as presented in ▶Table 11.2.








Table 11.2 Projection radiography findings of pneumothorax















Standing PA radiograph


Supine PA radiograph


Visible pleural line


Heart border and mediastinum sharply delineated


Increased radiolucency between lung and chest wall


Increased radiolucency of one lung


Vasculature cannot be identified between the lung and chest wall


More radiolucent, broader and lower costophrenic angle (deep sulcus sign, ▶Fig. 11.2)







Fig. 11.2 Pneumothorax. Radiograph, supine position. Compared with the right side, increased radiolucency of the left lung, more clearly delineated left heart border (arrowhead) and more radiolucent as well as lower left costophrenic angle-deep sulcus sign (arrows). Besides, chest tube on the left.

Computed tomography (CT) has greater sensitivity than radiography for diagnosis of smaller pneumothoraces. It is even able to reliably detect pneumothorax in cases where the radiograph was inconclusive, e.g., because of chest wall emphysema. CT often provides additional information on the etiology of spontaneous pneumothorax and in many cases
contributes to diagnosis and differential diagnosis of pulmonary causes (▶Fig. 11.4). The indications for CT are listed in ▶Table 11.3.



11.2 Pleural Effusion

Pleural effusions are caused by many pathologic conditions (▶Table 11.4). A distinction is made between transudates and exudates on the basis of their origin. Transudates stem from passive filtration of serous fluid into the pleural space, whereas exudates derive from secretion of protein-rich fluid. This distinction can be made through simple laboratory tests of pleural fluid. The effusion is classified as an exudate if at least one of the following criteria is met8:



  • A pleural fluid-to-serum protein ratio greater than 0.5.


  • A pleural fluid-to-serum lactate dehydrogenase level (LDH) ratio greater than 0.6.


  • A pleural fluid LDH of more than two-thirds of maximum normal serum LDH.

Likewise, other fluids (e.g., blood, pus, or chyle) manifest as pleural effusion on imaging.

Cross-sectional imaging, particularly ultrasound, is most sensitive for detection of pleural effusion. Lateral radiographs demonstrate pleural effusions larger than 50 mL, which are initially seen as opacification of the posterior costodiaphragmatic angle. Pleural effusions larger than 100 mL are visible on posteroanterior (PA) radiographs in the lateral costodiaphragmatic angle. Because of geometric projection conditions, pleural effusions appear meniscus-shaped in standing radiographs (▶Fig. 11.6).

In supine radiographs, pleural effusion is located posterior to the lungs and is distributed more or less evenly in the chest cavity, thus causing only diffusely reduced radiolucency of the affected hemithorax. Even several hundred milliliters of pleural effusion can be overlooked in supine radiographs.








Table 11.4 Pathogenesis of pleural effusion9







































Mechanism



Examples


Elevated fluid secretion into the pleural cavity


Increased interstitial fluid in the lung


Congestive left heart failure, pneumonia, pulmonary embolism


Elevated intravascular pressure in the pleura


Congestive left heart failure Congestive right heart failure


Superior vena cava syndrome


Elevated capillary permeability


Pleuritis


Elevated protein content of pleural fluid


Pulmonary edema, hemothorax


Reduced pressure in the pleural space


Atelectasis


Increased fluid in the peritoneum


Ascites, peritoneal dialysis


Rupture of the thoracic duct


Chylothorax


Rupture of thoracic blood vessels


Hematothorax


Reduced pleural fluid absorption


Obstruction of parietal pleura lymph drainage


Malignant tumor, lymphoma


Elevated systemic venous pressure


Congestive right heart failure, superior vena cava syndrome







Fig. 11.6 Right pleural effusion. Radiograph. Meniscus-shaped opacity of the right lateral costophrenic angle.

A subpulmonary pleural effusion occasionally mimics a high-riding diaphragm and can be suspected if the highest point of the diaphragm is located lateral to its middle. Isolated interlobular effusions sometimes present as well-defined oval pulmonary opacities on radiography. These are known as “vanishing tumors” since they tend to migrate and disappear within a few days.



11.3 Pleural Empyema

Pleural empyema is an infection of the pleural cavity usually manifesting as pathologic pleural fluid collection. This is often caused by pneumonia, with the infection spreading secondarily into the pleural space, giving rise to an independent disease process. Less commonly, pathogens use other portals of entry, for example, a perforated lung tumor in the pleural space, following chest injury or as a complication of a surgical procedure. Pleural empyema is distinguished from a noninfected pleural effusion through laboratory analysis of the pleural fluid.10 A summary of the criteria used to differentiate between pleural empyema and noninfected pleural effusion is given in ▶Table 11.5. The most commonly implicated pathogens are gram-negative bacteria as well as Staphylococcus aureus and anaerobes.11 Tuberculosis, too, can give rise to pleural empyema. The continuous development of a chest wall abscess from a pleural empyema is known as “empyema necessitatis” (or “empyema necessitans”), which is often but not exclusively seen in mycobacterial infection.

Pleural empyema consists of three phases10:



  • Exudative phase: In the visceral pleura, the inflammatory process leads to increased capillary permeability, and consecutively to exudation of protein-rich fluid into the pleural space causing an exudative pleural effusion. There is still no sign of pleural thickening.


  • Fibrinopurulent phase: In the later course, inflammatory cells and neutrophils migrate into the pleural fluid, and fibrin is deposited on the pleural surfaces, causing thickening of the visceral and parietal pleura.


  • Organizing phase: Fibroblast activity and capillary neogenesis lead to collagen deposition and ingrowth of granulation tissue on the pleural surfaces, and subsequent pleural fibrosis. This reaction can be very intense and lead to development of extensive pleural thickening.

Treatment is tailored to the cause and stage of pleural empyema. The underlying cause is treated whenever possible. The specific treatment for pleural empyema in the exudative phase usually consists of chest tube placement and appropriate antibiotic treatment. More advanced pleural empyema, in particular in the presence of pleural thickening, requires surgical decortication.








Table 11.5 Differentiation between pleural empyema and noninfected pleural effusion in a fluid sample obtained from thoracentesis.10 One positive criterion suffices for diagnosis of pleural empyema

































Parameter


Pleural empyema


Simple pleural effusion


pH


< 7.2


≥ 7.2


Glucose


< 40 mg/dL


≥ 40 mg/dL


LDHEffusion/LDHserum


> 0.6 or LDH > two-thirds of normal serum level


≤ 0.6 or LDH ≤ two-thirds of normal serum level


Detection of bacteria in culture or on microscopy


+



Purulence


+



Neutrophils in effusion


+



Abbreviation: LDH, lactate dehydrogenase.

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Apr 12, 2020 | Posted by in CARDIOVASCULAR IMAGING | Comments Off on Pleural Diseases

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