Pleural Effusions and Pneumothorax

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40 Pleural Effusions and Pneumothorax

Pleural effusions and pneumothoraces occur as a result of structural and mechanical abnormalities of the pleural space. Abnormalities of the pleural space are an important cause of morbidity and mortality in infants and children worldwide, and the number of children who develop clinically significant pleural effusions is increasing. Pleural effusions are the result of excessive fluid accumulation in the pleural space, and pneumothoraces occur as a result of the accumulation of air within the pleural space. To better understand the pathophysiology of pleural effusions and pneumothoraces, it is essential to understand the anatomy of the pleural space. The pleural space is a potential anatomic space, approximately 10 to 20 µm wide, located between the visceral and parietal pleurae. The visceral pleura lines the surface of the lung parenchyma, including the interlobar fissures, and the parietal pleura lines the inner surface of the chest wall, mediastinum, and diaphragm (Figure 40-1). The pleural space contains a small amount of fluid (0.3 mL/kg body weight) that is in equilibrium between the amount of fluid formed (filtered) and the amount removed (absorbed).

Pleural Effusions

Starling forces normally govern the amount of pleural fluid that is formed by the subpleural capillaries of the visceral pleura and the amount that is removed by stomata in the parietal pleura and lymphatic system. If the flow of fluid into the pleural space exceeds the amount absorbed, excess fluid accumulates in the pleural space.

Etiology and Pathogenesis

Pleural effusions are the result of an imbalance of hydrostatic and oncotic pressures between the blood in the pulmonary capillary bed and fluid in the pleural space, an alteration in permeability of the pleural membranes, or inadequate uptake by the lymphatic system. Pleural effusions can be divided into transudates and exudates. Exudative effusions occur from pleural inflammation or lymphatic flow obstruction. Transudative effusions occur when there is an imbalance between the formation and reabsorption of pleural fluid. Pleural fluid analysis determines whether the effusion is transudative or exudative. Because exudative effusions result from inflammation of the pleural membranes and leaky capillaries, large molecules such as cholesterol, lactate dehydrogenase (LDH), and proteins enter the pleural space. Conversely, the protein, LDH, and cholesterol levels in transudates are low because the filtration properties of the pleural membranes are not altered.

Typically, small amounts of protein are filtered into the pleural space and are readily absorbed by the parietal pleura via the lymphatic system. If increased amounts of protein enter the pleural space, especially when accompanied by increased capillary permeability (e.g., in pneumonia), the lymphatic system cannot absorb the excessive protein, and an exudative pleural effusion forms. The most common cause of exudative pleural effusions in children is bacterial pneumonia. Additional causes include connective tissue diseases, metastatic intrathoracic malignancy, subdiaphragmatic abscess, and aspiration pneumonitis. Transudative effusions in children are typically associated with overhydration, atelectasis, nephrotic syndrome, and congestive left heart failure. Correcting the oncotic and hydrostatic pressures usually results in resolution of a transudate; drainage of the fluid is only needed for immediate symptomatic relief.

An exudative pleural effusion that is associated with pneumonia is referred to as a parapneumonic effusion. Parapneumonic effusions result from the spread of inflammatory cells and infecting organisms into the pleural space. Initially, the pleurae become inflamed, and the leakage of proteins and leukocytes into the pleural space forms the effusion. Initially, the fluid is sterile with a low leukocyte count. As a parapneumonic effusion progresses and bacteria leak into the pleural space, the pleural fluid becomes purulent, and the effusion is referred to as an empyema, occurring in approximately 0.6% of childhood pneumonia. Loculations (parietal–visceral pleural adhesions) and septations (fibrous strands) form within parapneumonic effusions as the pleural fluid exudate thickens and deposition of fibrin occurs within the pleural space.

The risk of a child developing an empyema increases in certain underlying diseases, such as immunodeficiencies, malignancy, Down syndrome, congenital heart disease, tuberculosis, and cystic fibrosis (CF). Streptococcus pneumoniae remains the most common pathogen causing parapneumonic effusions. Community-acquired methicillin-resistant Staphylococcus aureus is an increasingly common cause of both parapneumonic effusions and empyemas. Empyemas can also be caused by the rupture of lung abscesses into the pleural space; by bacteria entering the pleural space from trauma, thoracic surgery, mediastinitis; or through the spread of intraabdominal abscesses. Complications associated with parapneumonic effusions and empyemas are infrequent in children but include bronchopleural fistula, lung abscess, and empyema necessitatis (perforation through the chest wall). Boys and girls are affected equally by empyemas, and the morbidity and mortality are highest in children younger than 2 years of age.

Clinical Presentation

The size of the effusion, the underlying cause, and when in the course a child presents all determine the clinical presentation. Children with small pleural effusions may be asymptomatic. As the effusion enlarges, it limits lung inflation, causing a decrease in vital capacity. Furthermore, if present, pleural inflammation is associated with dyspnea, chest tightness, and chest pain that is exaggerated by deep breathing, coughing, and straining; all of these further limit full lung expansion. The pain, resulting from stretching of parietal pleura nerve fibers, is often described as a dull ache that worsens with inspiration. The pain is often localized over the chest wall and is referred to the shoulder or the back. Often the child will attempt to decrease the pain by lying on the affected side in an attempt to splint it during breathing.

On physical examination, a child with a significant pleural effusion can appear ill but is rarely toxic appearing. Most children are tachypneic with shallow breathing to minimize the pain. It is important to look for signs and symptoms of underlying conditions that predispose to the development of pleural effusions. If the child has an empyema, he or she is usually febrile with a cough and malaise. If a child is being appropriately treated for pneumonia and is not improving within 48 hours, a parapneumonic effusion must be suspected. A malignant effusion must be suspected in a child with an effusion accompanied by a mediastinal mass or lymphadenopathy. A history of recurrent serious bacterial infections, failure to thrive, or chronic diarrhea is suggestive of a primary immunodeficiency.

Because of splinting toward the affected side, the child may appear to have mild scoliosis. There can be ipsilateral bulging of the intercostal spaces and contralateral displacement of the heart and trachea. A pleural friction rub caused by roughened pleural surfaces may be the only physical examination finding early in the course of disease, heard during inspiration and exhalation. As the pleural effusion increases and separates the pleural membranes, the plural rub disappears. Diminished thoracic wall excursion, decreased breath sounds, dullness to percussion, and decreased tactile and vocal fremitus can be observed over the affected area in an older child with a moderate effusion. If pneumonia is present, crackles and rhonchi can also be audible. In infants, the physical signs of an effusion are less noticeable. Breath sounds can be deceptively loud and clear throughout both lungs because of the small lung volume in an infant.