Pleural Disease, Pneumothorax & Lung Exam Findings

Pleural fluid physiology and why effusions form

Normal turnover. The pleural space holds only a thin film of fluid (roughly 10–20 mL). It filters from systemic capillaries of the parietal pleura and is cleared by lymphatic stomata in the same layer; because lymph flow can rise many-fold, an effusion appears only when formation overwhelms that reserve or drainage is blocked.

Transudates. With an intact capillary wall, a shift in Starling forces pushes out a protein-poor, cell-poor ultrafiltrate. Raised hydrostatic pressure from heart failure is the most common cause of any pleural effusion; these are usually bilateral and, when one-sided, more often right-sided. Low plasma oncotic pressure from nephrotic syndrome, cirrhosis or other hypoalbuminemia does the same. In cirrhosis, negative intrathoracic pressure also draws ascites through small diaphragmatic defects, producing a usually right-sided hepatic hydrothorax. The pleura is healthy, so treatment targets the systemic disorder.

Exudates. Here the pleura or its lymphatics are diseased. Inflammation raises capillary permeability: parapneumonic effusion (the most common exudate), tuberculosis, pulmonary embolism, pancreatitis, rheumatoid arthritis, lupus and post-cardiac-injury pleuritis. Tumor both inflames the pleura and obstructs lymphatic outflow through the stomata and mediastinal nodes; lung carcinoma, breast carcinoma and lymphoma cause most malignant effusions. Meigs syndrome (benign ovarian fibroma, ascites and a right effusion that clear after resection) is the classic benign exception.

Pleuritic pain. Only the parietal pleura senses pain. Its costal portion is supplied by intercostal nerves, giving sharp, localized pain with each breath; its central diaphragmatic portion is supplied by the phrenic nerve (C3–C5), so irritation there is referred to the shoulder. The visceral pleura has autonomic innervation only. A creaking friction rub may be heard while inflamed layers rub together and fades once fluid separates them.

Analyzing pleural fluid

Light criteria. Fluid is an exudate if it meets any one of three thresholds:

The criteria were designed for sensitivity, so a heart-failure effusion concentrated by diuretics can falsely qualify. A serum-minus-pleural albumin gradient above 1.2 g/dL then supports a transudate.

Esophageal rupture. Forceful vomiting (Boerhaave syndrome) tears the distal esophagus, spilling saliva, gastric acid and food into the mediastinum and usually the left pleural space. Expect chest pain, subcutaneous emphysema and pneumomediastinum, with fluid showing salivary amylase, very low pH and sometimes food particles.

Parapneumonic effusion and empyema. Most effusions beside a pneumonia are sterile and resolve with antibiotics. When bacteria invade the pleural space, fibrin and loculations form and neutrophil metabolism drives pH and glucose down. A pH below 7.2, glucose below 60 mg/dL, a positive Gram stain or culture, or frank pus (empyema) marks a complicated effusion that needs chest-tube drainage. Common organisms include S. pneumoniae, S. aureus, the S. anginosus group and oral anaerobes.

Chylothorax. Chyle leaks when the thoracic duct is torn (esophageal or cardiothoracic surgery, trauma) or obstructed (lymphoma is the leading nontraumatic cause; LAM is another). The fluid is milky and lymphocyte-rich, with triglycerides above 110 mg/dL and chylomicrons. The duct crosses from right to left near T5, so injury below that level tends to cause a right-sided chylothorax and injury above it a left-sided one. Pseudochylothorax looks similar but is cholesterol-rich and arises in chronic effusions.

Hemothorax. A true hemothorax has a pleural hematocrit above half the blood hematocrit, usually from trauma to intercostal or internal thoracic vessels or a lacerated lung. A large-bore chest tube prevents clotted hemothorax, fibrothorax and empyema. Blood-tinged fluid is far more common, because a few thousand red cells per μL already color it; malignancy, pulmonary embolism and trauma are typical sources.

Tuberculous and malignant effusions. TB pleurisy is mainly a delayed-type hypersensitivity reaction to few bacilli: a lymphocytic exudate with high adenosine deaminase, scant mesothelial cells and usually negative AFB smears. Pleural biopsy showing caseating granulomas, with culture, has the highest yield. Malignant effusions are also lymphocytic and are often large, bloody and recurrent; cytology is the first test.

Removing more than about 1.5 L at one thoracentesis risks re-expansion pulmonary edema.

Pneumothorax

Physiology. At FRC, the lung's inward elastic recoil and the chest wall's outward spring hold intrapleural pressure near −5 cm H2O. Air entering the pleural space abolishes this seal: the lung collapses toward the hilum and the ipsilateral chest wall springs slightly outward. Supplemental oxygen speeds resorption by washing nitrogen out of capillary blood, steepening the gradient for nitrogen to leave the pleural pocket.

• Primary spontaneous: rupture of apical subpleural blebs in a tall, thin young man without known lung disease, causing sudden pleuritic chest pain and dyspnea, often at rest. Smoking is the main modifiable risk and Marfan syndrome (FBN1) predisposes; alveolar distending forces are greatest at the apex. Recurrence is common.
• Secondary spontaneous: underlying lung disease, with COPD bullae the most common; also cystic fibrosis, Pneumocystis pneumonia in AIDS, LAM, Langerhans cell histiocytosis, TB and necrotizing pneumonia. Little reserve makes these more dangerous.
• Traumatic and iatrogenic: rib fractures, penetrating wounds, subclavian or jugular line placement, thoracentesis, transthoracic needle biopsy and barotrauma from positive-pressure ventilation. A sucking chest wound gets an occlusive dressing taped on three sides.

Tension pneumothorax. A flap valve admits air with every breath but lets none escape, most often with trauma or positive-pressure ventilation. Rising pressure collapses the lung, shifts the mediastinum and trachea to the opposite side and compresses the vena cavae. Venous return falls, producing obstructive shock: hypotension, tachycardia, distended neck veins, absent breath sounds and hyperresonance. Tracheal deviation is a late, unreliable sign.

Every needle or tube passes just over the upper border of a rib: the intercostal vein, artery and nerve (top to bottom) run in the costal groove beneath each rib. Staying lateral to the sternal border spares the internal thoracic artery.

Imaging and routine care. A chest film shows a thin visceral pleural line with no lung markings beyond it; ultrasound shows loss of lung sliding. A small, stable primary pneumothorax can be observed with oxygen; larger ones are aspirated or drained, and recurrences are treated with thoracoscopic pleurodesis or bleb resection plus smoking cessation.

Lung examination findings

Sound transmission. Solid, airless lung with patent bronchi conducts vibration well, so consolidation raises tactile fremitus, turns breath sounds bronchial and produces egophony (spoken "E" heard as "A") and whispered pectoriloquy. Fluid or air between lung and chest wall dampens fremitus and breath sounds; percussion then separates them, dull over fluid and hyperresonant over air. Egophony may also be heard at the upper border of an effusion, where compressed lung behaves like consolidation.

Tracheal position. The trachea moves toward volume loss (obstructive atelectasis from a mucus plug, tumor or foreign body; pneumonectomy; upper-lobe fibrosis) and away from added volume or pressure (tension pneumothorax, massive effusion).

Pleural mesothelioma and asbestos

Exposure. Malignant mesothelioma arises 20–40 or more years after asbestos exposure in shipbuilding, insulation, roofing, plumbing or brake work; amphibole fibers (crocidolite, amosite) are more potent than chrysotile. Smoking does not raise mesothelioma risk, but it multiplies the asbestos-related risk of bronchogenic carcinoma, still the most common cancer in exposed workers. Calcified parietal and diaphragmatic pleural plaques are the most common sign of exposure and are benign, not precursors.

Presentation and pathology. Chest pain, dyspnea and a recurrent, often hemorrhagic effusion accompany a thick tumor rind encasing the lung, and the prognosis is poor. Tumors are epithelioid (most common and most favorable), sarcomatoid (worst) or biphasic.