Regardless of cause, excess fluid accumulates in the pleural space when production exceeds resorption. Systemic diseases increasing visceral fluid hydrostatic pressures or decreasing plasma oncotic pressure cause thin, transudative pleural effusions. Thicker, exudative effusions (protein concentrations greater than or equal to 50% of serum) result from diseases, usually inflammatory, involving the pleural surfaces themselves. Inflammation increases the permeability of mesothelial cells and the permeability of pleural capillaries to protein, and may decrease parietal lymph resorption.

Underlying cardiac, hepatic, or renal diseases usually cause transudative effusions. Ventilatory function may be impaired directly by the underlying disease (e.g., pulmonary edema). A large pleural effusion also partially uncouples the lung from the muscles of inspiration, deforms the diaphragm and chest wall, and compresses the lung. Consequently, worsening tachypnea, cyanosis, and retractions with diminished breath sounds and dullness to percussion usually accompany large transudative effusions (see Hydrothorax). Dyspnea associated with transudation into the pleural space, in the absence of inflammation, may be related to mechanical inefficiencies caused by mechanical uncoupling of the lungs and the muscles of respiration and by compression of lung neurogenic receptors connected to vagal and sympathetic fibers within the lung.

Classic findings of early pleuritis are pain in the chest or shoulder (implying that the parietal pleura of the central diaphragm is involved), guarding of the affected side, upper quadrant abdominal pain (pleura on costal diaphragm involved), a pleural friction rub, and grunting, shallow respirations. Pain fibers are present in the parietal but not the visceral pleura. Therefore, pleuritic pain reflects extension of inflammation to the chest wall early in the course of the thoracic process. Because inflammatory effusions cause pain and are exudative, the presence of pain indicates that the effusion quite likely is an exudate. An inflammatory effusion that is becoming large reduces these signs quickly, except for cough and rapid, shallow respirations and, occasionally, chest wall hyperesthesia. Later, the child has fever, cough, and dyspnea. Thus, a child with a large inflammatory effusion appears ill, with fever and dyspnea. Children with immunodeficiencies and those on corticosteroids may have large pleural effusions with few clinical findings. In immunocompetent children, if the inflammation is triggered by an infection with anaerobic bacteria, the findings of pleural involvement may be less dramatic than is typical for infections caused by pathogens such as Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, or Streptococcus pyogenes (group A beta-hemolytic streptococcus). Whether the effusion is exudative or transudative, intercostal spaces may bulge outward and the mediastinum may be pushed to the contralateral side, if the effusion is massive. There can be “e” to “a” changes on auscultation; breath sounds are diminished in intensity and often are “tubular” or resembling the sound of a drummer’s brush sliding across a drum.

Important conditions in the differential diagnosis of pleuritic chest pain in children include costochondritis, chest pain associated with asthma or gastroesophageal reflux, herpes zoster, and occult trauma.

If the air leak is small and the child has little antecedent lung disease, the only symptom of a pneumothorax may be chest pain. The mechanism for this pain is unclear. If the pneumothorax is large or the child has severe underlying disease, pain, cough, dyspnea, and cyanosis may be present. Breath sounds usually are reduced on the side of accumulation of air in the pleural space. If very large, the trachea and cardiac impulse are displaced contralaterally. In a small infant, a large pneumothorax causes subcostal fullness.

The most common and important process involving the pleura in children, a pleural effusion, usually is detected first on the chest radiograph. Skillful use of chest radiography, with occasional help from thoracic ultrasound and computed tomography (CT), allows identification of pleural disease, characterization of an effusion as free or loculated, and distinction between intrapleural processes and peripheral parenchymal disease of the lung.

The usual chest radiographic projections used to evaluate pleural disease are the posteroanterior or anteroposterior, lateral and lateral decubitus (Box 243.1).

Ultrasound has proven to be the imaging modality of choice in pediatrics in localizing pleural fluid and in evaluating peripheral densities abutting the pleura. If a pleural effusion likely is present but decubitus views suggest that it is not free in the pleural space, thoracic ultrasound may identify a loculation that can be aspirated under direct ultrasound guidance. Even when a CT image suggests that a pleural fluid accumulation is homogeneous, the ultrasound often correctly shows that the pleural process is variegated and that large quantities of fluid cannot be removed from one thoracentesis. In these cases, the ultrasound image may show areas of pleural thickening, with fibrinous adhesions separating areas containing relatively thin fluid from others filled with thick pus. Other advantages of ultrasound for use in children are that it is portable and that it does not require separation from parents or a controlled breathing pattern.

If the hemithorax is partially opacified, obtaining lateral decubitus radiographs is preferable first. If the entire hemithorax is opacified, ultrasound is the first imaging choice.

CT scan images offer the promise of more precise portrayal of pleural disease. However, they can be misleading when used to image inflammatory processes like parapneumonic effusions. They show the effusion in worrisome detail that often hastens consideration of unnecessary invasive remedies (see Fibrothorax). CT scans do help in distinguishing between lung abscesses touching the visceral pleura and loculated pus in the pleural space. Lung abscesses rarely require more than antibiotic therapy, and not tube thoracostomy or débridement. Pus in the pleural space, which often requires drainage or débridement, makes an obtuse angle with the chest wall, and an abscess makes an acute angle. CT scans also help detail parenchymal and hilar adenopathy and calcifications accompanying pleural inflammation and may, therefore, help clarify the etiology of the effusion in puzzling cases. High resolution CT scanning should provide more detailed images of how pleural processes affect the parietal pleura and intercostal muscles. Magnetic resonance imaging (MRI), though useful in other aspects of thoracic imaging, particularly of the mediastinum, usually is not required to evaluate pediatric pleural disease because primary and metastatic malignancies of the pleura are such uncommon findings in children. Digitally stored images, created using x-rays because of their image enlargement and clarification capabilities, should prove useful when evaluating pneumothoraces, in particular.