The potential space between the parietal and visceral pleurae serves as a coupling system between the lung and the chest wall, and normally contains a small amount of fluid A negative pleural pressure is maintained by the dynamic tension between the chest wall and the lung (Chapter 3). Both pleurae have a systemic blood supply and lymphatics, although lymphatic drainage of the pleural space is predominantly via the parietal pleura. Fluid flux through the pleural space is determined by Starling's relationship between microvascular pressures, oncotic pressures, permeability and surface area. Normally, there is net filtration of transudative (protein-poor) fluid into the pleural space that is balanced by resorption via the parietal lymphatics.
Pneumothorax is an important condition that occurs when air enters the pleural space and pleural pressure rises to atmospheric pressure; pneumothorax is discussed in detail in Chapter 35.
Chylothorax is due to accumulation of triglyceride-rich lymph in the pleural space, generally as the result of damage to the thoracic duct causing leakage into the pleural space, for example due to trauma or carcinoma.
Empyema is accumulation of pus.
Pleurisy is a term commonly used to describe the sharp localized pain arising from any disease of the pleura. It is made worse by deep inspiration and coughing.
Most diseases of the pleura present with pleural effusion, which can be detected on chest X-ray (CXR) when more than 300 mL of fluid is present (Fig. 32b). Effusions are due to excessive flui formation or inadequate fluid clearance. Symptoms develop if the fluid is inﬂammatory or if pulmonary mechanics are compromised. Thus, the most common symptoms of a pleural effusion are pleuritic chest pain, dull aching pain, fullness of the chest or dyspnoea. Physical examination reveals decreased breath sounds, dullness to percussion, decreased tactile or vocal fremitus. If there is inflammation there may be a fric- tion rub. Compressive atelectasis (partial lung collapse) may cause bronchial breath sounds. It is useful to categorize pleural effusions as transudative or exudative (Fig. 32a).
Transudative effusions are usually due to an imbalance in Starling's forces across normal pleural membranes, have protein-poor fluid are often bilateral and are not associated with fever, pleuritic pain or tenderness to palpation. The most common cause of a transudative effusion is congestive heart failure. Other causes include cirrhosis with ascites, nephrotic syndrome, pericardial disease or peritoneal dialysis.
Exudative effusions imply disease of the pleura or the adjacent lung and are characterized by an increased protein, lactate dehydrogenase (LDH), cholesterol or white blood cell count (WBC) (Fig. 32a). The differential diagnosis of exudative effusions is broad, including infection, malignancy, autoimmune disease, oesophageal perforation and pancreatitis.
Diagnostic evaluation of pleural effusion should include measurement of pleural aspirate cell count with differential, pH, protein, LDH, cholesterol and glucose. These studies usually distinguish exudates from transudates and will often suggest a specifi diagnosis. For example, extremely low glucose is typical for empyema, malignancy, tuberculosis (Chapter 38), rheumatoid arthritis, systemic lupus evry thematosus (SLE) or oesophageal perforation. If clinically indicated, a specifi diagnosis may be obtained from microbiological stains and culture, cytopathology, amylase, triglycerides and measurement of antinuclear antibody (ANA) titre. Although all patients with SLE have a positive ANA titre in the pleural f uid, it is also present in a significant proportion ( 5%) of other effusions; these may be related to malignancy.
Treatment is for the underlying condition, but persistent or reaccumulating effusions can be drained to dryness (slowly so as to avoid severe pain).
Pneumonia (Chapters 36 and 37) commonly causes parapneumonic pleural effusions. These effusions are usually sterile exudates with a neutrophilic leukocytosis and require only treatment of the pneumonia to resolve. However, if bacteria invade the pleural space, a complicated parapneumonic effusion or empyema will develop. These effusions are characterized by a low pH and extensive fibri deposition causing flui loculation and require adequate open or closed drainage for healing. Streptococcus pneumoniae, Staphylococcus aureus, Gramnegative bacteria and anaerobes commonly cause complicated effusions.
Tuberculosis pleurisy occurs when a subpleural focus of primary infection ruptures into the pleural space, causing a delayed hypersensitivity response. Subsequently, an exudative effusion with a lympho- cytic leukocytosis, a paucity of macrophages and an elevated adenosine deaminase will develop. Patients develop fever, dyspnoea, pleuritic pain and a positive tuberculin response (Chapter 38). Granulomatous inflammatio is seen on pleural biopsy, and culture of pleural tissue has the highest diagnostic yield.
Primary lung malignancies or metastases to the lung may cause pleural effusions by direct invasion or by obstruction of parietal lymphatic drainage. Malignant effusions are mostly exudative (90%), often with a very high LDH, low pH and low glucose. Cytology of the pleural flui has a high diagnostic yield. Symptomatic pleural effusions may respond to therapy for the underlying malignancy, although palliative obliteration of the pleural space (pleurodesis) is often necessary to relieve dyspnoea or chest pain.
Mesothelioma is an uncommon malignancy that originates in the pleura and/or peritoneum (Chapter 33). Over 75% of cases develop 20-30 years after occupational asbestos exposure. Asbestos may also cause benign pleural effusions or calcifie plaques on the parietal pleura in the lower lungs or along the diaphragmatic surface. Mesothelioma typically develops in men aged 50-70 years, presenting with insidi- ous dyspnoea and aching chest pain. CXRs usually show unilateral pleural effusion (Fig. 32b), and computed tomography (CT) shows lumpy f brotic encasement of the pleural space (Fig. 32c). Pleural f uid cytology is not usually diagnostic. Thoracoscopic biopsies have the highest yield. Treatment is generally palliative, including pleurodesis. The prognosis is poor, with a median survival of approximately year.