Pleural Effusion
The pleural space lies between the lung and chest wall and normally contains a very thin layer of fluid, which serves as a coupling system. A pleural effusion is present when there is an excess quantity of fluid in the pleural space.
Etiology
Pleural fluid accumulates when pleural fluid formation exceeds pleural fluid absorption. Normally, fluid enters the pleural space from the capillaries in the parietal pleura and is removed via the lymphatics situated in the parietal pleura. Fluid can also enter the pleural space from the interstitial spaces of the lung via the visceral pleura or from the peritoneal cavity via small holes in the diaphragm. The lymphatics have the capacity to absorb 20 times more fluid than is normally formed. Accordingly, a pleural effusion may develop when there is excess pleural fluid formation (from the interstitial spaces of the lung, the parietal pleura, or the peritoneal cavity) or when there is decreased fluid removal by the lymphatics.
Diagnostic Approach
When a patient is found to have a pleural effusion, an effort should be made to determine the cause (Fig. 257-1). The first step is to determine whether the effusion is a transudate or an exudate. A transudative pleural effusion occurs when systemic factors that influence the formation and absorption of pleural fluid are altered. The leading causes of transudative pleural effusions in the United States are left ventricular failure and cirrhosis. An exudative pleural effusion occurs when local factors that influence the formation and absorption of pleural fluid are altered. The leading causes of exudative pleural effusions are bacterial pneumonia, malignancy, viral infection, and pulmonary embolism. The primary reason to make this differentiation is that additional diagnostic procedures are indicated with exudative effusions to define the cause of the local disease.
Figure 257-1
Approach to the diagnosis of pleural effusions. CHF, congestive heart failure; CT, computed tomography; LDH, lactate dehydrogenase; PE, pulmonary embolism; TB, tuberculosis; PF, pleural fluid.
Transudative and exudative pleural effusions are distinguished by measuring the lactate dehydrogenase (LDH) and protein levels in the pleural fluid. Exudative pleural effusions meet at least one of the following criteria, whereas transudative pleural effusions meet none:
1. pleural fluid protein/serum protein >0.5
2. pleural fluid LDH/serum LDH >0.6
3. pleural fluid LDH more than two-thirds normal upper limit for serum
The above criteria misidentify ~25% of transudates as exudates. If one or more of the exudative criteria are met and the patient is clinically thought to have a condition producing a transudative effusion, the difference between the protein levels in the serum and the pleural fluid should be measured. If this gradient is greater than 31 g/L (3.1 g/dL), the exudative categorization by the above criteria can be ignored because almost all such patients have a transudative pleural effusion.
If a patient has an exudative pleural effusion, the following tests on the pleural fluid should be obtained: description of the fluid, glucose level, differential cell count, microbiologic studies, and cytology.
Effusion Due to Heart Failure
The most common cause of pleural effusion is left ventricular failure. The effusion occurs because the increased amounts of fluid in the lung interstitial spaces exit in part across the visceral pleura. This overwhelms the capacity of the lymphatics in the parietal pleura to remove fluid. Isolated right-sided pleural effusions are more common than left-sided effusions in heart failure. A diagnostic thoracentesis should be performed if the effusions are not bilateral and comparable in size, if the patient is febrile, or if the patient has pleuritic chest pain, to verify that the patient has a transudative effusion. Otherwise the patient is best treated with diuretics. If the effusion persists despite diuretic therapy, a diagnostic thoracentesis should be performed. A pleural fluid N-terminal pro-brain natriuretic peptide (NT-proBNP) >1500 pg/mL is virtually diagnostic of an effusion secondary to congestive heart failure.
Hepatic Hydrothorax
Pleural effusions occur in ~5% of patients with cirrhosis and ascites. The predominant mechanism is the direct movement of peritoneal fluid through small openings in the diaphragm into the pleural space. The effusion is usually right-sided and frequently is large enough to produce severe dyspnea.
Parapneumonic Effusion
Parapneumonic effusions are associated with bacterial pneumonia, lung abscess, or bronchiectasis and are probably the most common cause of exudative pleural effusion in the United States. Empyema refers to a grossly purulent effusion.
Patients with aerobic bacterial pneumonia and pleural effusion present with an acute febrile illness consisting of chest pain, sputum production, and leukocytosis. Patients with anaerobic infections present with a subacute illness with weight loss, a brisk leukocytosis, mild anemia, and a history of some factor that predisposes them to aspiration.
The possibility of a parapneumonic effusion should be considered whenever a patient with a bacterial pneumonia is initially evaluated. The presence of free pleural fluid can be demonstrated with a lateral decubitus radiograph, computed tomography (CT) of the chest, or ultrasound. If the free fluid separates the lung from the chest wall by >10 mm, a therapeutic thoracentesis should be performed. Factors indicating the likely need for a procedure more invasive than a thoracentesis (in increasing order of importance) include:
loculated pleural fluid
pleural fluid pH < 7.20
pleural fluid glucose < 3.3 mmol/L (<60 mg/dL)
positive Gram stain or culture of the pleural fluid
the presence of gross pus in the pleural space
If the fluid recurs after the initial therapeutic thoracentesis, and if any of the above characteristics are present, a repeat thoracentesis should be performed. If the fluid cannot be completely removed with the therapeutic thoracentesis, consideration should be given to inserting a chest tube and instilling a fibrinolytic (e.g., streptokinase, 250,000 units) or performing thoracoscopy with the breakdown of adhesions. Decortication should be considered when the above are ineffective.
Effusion Secondary to Malignancy
Malignant pleural effusions secondary to metastatic disease are the second most common type of exudative pleural effusion. The three tumors that cause ~75% of all malignant pleural effusions are lung carcinoma, breast carcinoma, and lymphoma. Most patients complain of dyspnea, which is frequently out of proportion to the size of the effusion. The pleural fluid is an exudate, and its glucose level may be reduced if the tumor burden in the pleural space is high.
The diagnosis is usually made via cytology of the pleural fluid. If the initial cytologic examination is negative, then thoracoscopy is the best next procedure if malignancy is strongly suspected. At the time of thoracoscopy, a procedure such as pleural abrasion should be performed to effect a pleurodesis. If thoracoscopy is unavailable, then needle biopsy of the pleura should be performed.
Patients with a malignant pleural effusion are treated symptomatically for the most part, since the presence of the effusion indicates disseminated disease and most malignancies associated with pleural effusion are not curable with chemotherapy. The only symptom that can be attributed to the effusion itself is dyspnea. If the patient's lifestyle is compromised by dyspnea, and if the dyspnea is relieved with a therapeutic thoracentesis, then one of the following procedures should be considered: (1) insertion of a small indwelling catheter; or (2) tube thoracostomy with the instillation of a sclerosing agent such as doxycycline, 500 mg.
Mesothelioma
Malignant mesotheliomas are primary tumors that arise from the mesothelial cells that line the pleural cavities; most are related to asbestos exposure. Patients with mesothelioma present with chest pain and shortness of breath. The chest radiograph reveals a pleural effusion, generalized pleural thickening, and a shrunken hemithorax. Thoracoscopy or open pleural biopsy is usually necessary to establish the diagnosis. Chest pain should be treated with opiates and shortness of breath with oxygen and/or opiates.
Effusion Secondary to Pulmonary Embolization
The diagnosis most commonly overlooked in the differential diagnosis of a patient with an undiagnosed pleural effusion is pulmonary embolism. Dyspnea is the most common symptom. The pleural fluid is almost always an exudate. The diagnosis is established by spiral CT scan or pulmonary arteriography (Chap. 256). Treatment of the patient with a pleural effusion secondary to pulmonary embolism is the same as for any patient with pulmonary emboli. If the pleural effusion increases in size after anticoagulation, the patient probably has recurrent emboli or another complication such as a hemothorax or a pleural infection.
Tuberculous Pleuritis
(See also Chap. 158) In many parts of the world, the most common cause of an exudative pleural effusion is tuberculosis (TB), but tuberculous effusions are relatively uncommon in the United States. Tuberculous pleural effusions are usually associated with primary TB and are thought to be due primarily to a hypersensitivity reaction to tuberculous protein in the pleural space. Patients with tuberculous pleuritis present with fever, weight loss, dyspnea, and/or pleuritic chest pain. The pleural fluid is an exudate with predominantly small lymphocytes. The diagnosis is established by demonstrating high levels of TB markers in the pleural fluid (adenosine deaminase > 40 IU/L, interferon > 140 pg/mL, or positive polymerase chain reaction (PCR) for tuberculous DNA). Alternatively, the diagnosis can be established by culture of the pleural fluid, needle biopsy of the pleura, or thoracoscopy. The recommended treatment of pleural and pulmonary TB is identical (Chap. 158).
Effusion Secondary to Viral Infection
Viral infections are probably responsible for a sizable percentage of undiagnosed exudative pleural effusions. In many series, no diagnosis is established for ~20% of exudative effusions, and these effusions resolve spontaneously with no long-term residua. The importance of these effusions is that one should not be too aggressive in trying to establish a diagnosis for the undiagnosed effusion, particularly if the patient is improving clinically.
AIDS
(See also Chap. 182) Pleural effusions are uncommon in such patients. The most common cause is Kaposi's sarcoma, followed by parapneumonic effusion. Other common causes are TB, cryptococcosis, and primary effusion lymphoma. Pleural effusions are very uncommon with Pneumocystis carinii infection.
Chylothorax
A chylothorax occurs when the thoracic duct is disrupted and chyle accumulates in the pleural space. The most common cause of chylothorax is trauma, but it also may result from tumors in the mediastinum. Patients with chylothorax present with dyspnea, and a large pleural effusion is present on the chest radiograph. Thoracentesis reveals milky fluid, and biochemical analysis reveals a triglyceride level that exceeds 1.2 mmol/L (110 mg/dL). Patients with chylothorax and no obvious trauma should have a lymphangiogram and a mediastinal CT scan to assess the mediastinum for lymph nodes. The treatment of choice for most chylothoraces is insertion of a chest tube plus the administration of octreotide. If these modalities fail, a pleuroperitoneal shunt should be placed unless the patient has chylous ascites. Patients with chylothoraces should not undergo prolonged tube thoracostomy with chest tube drainage because this will lead to malnutrition and immunologic incompetence.
Hemothorax
When a diagnostic thoracentesis reveals bloody pleural fluid, a hematocrit should be obtained on the pleural fluid. If the hematocrit is more than half of that in the peripheral blood, the patient is considered to have a hemothorax. Most hemothoraces are the result of trauma; other causes include rupture of a blood vessel or tumor. Most patients with hemothorax should be treated with tube thoracostomy, which allows continuous quantification of bleeding. If the bleeding emanates from a laceration of the pleura, apposition of the two pleural surfaces is likely to stop the bleeding. If the pleural hemorrhage exceeds 200 mL/h, consideration should be given to thoracoscopy or thoracotomy.
Miscellaneous Causes of Pleural Effusion
There are many other causes of pleural effusion (Table 257-1). Key features of some of these conditions are as follows: If the pleural fluid amylase level is elevated, the diagnosis of esophageal rupture or pancreatic disease is likely. If the patient is febrile, has predominantly polymorphonuclear cells in the pleural fluid, and has no pulmonary parenchymal abnormalities, an intraabdominal abscess should be considered. The diagnosis of an asbestos pleural effusion is one of exclusion. Benign ovarian tumors can produce ascites and a pleural effusion (Meigs' syndrome), as can the ovarian hyperstimulation syndrome. Several drugs can cause pleural effusion; the associated fluid is usually eosinophilic. Pleural effusions commonly occur following coronary artery bypass surgery. Effusions occurring within the first weeks are typically left-sided and bloody, with large numbers of eosinophils, and respond to one or two therapeutic thoracenteses. Effusions occurring after the first few weeks are typically left-sided and clear yellow, with predominantly small lymphocytes, and tend to recur. Other medical manipulations that induce pleural effusions include abdominal surgery; radiation therapy; liver, lung, or heart transplantation; or the intravascular insertion of central lines.
Table 257-1 Differential Diagnoses of Pleural Effusions
Transudative Pleural Effusions
1. Congestive heart failure
2. Cirrhosis
3. Pulmonary embolization
4. Nephrotic syndrome
5. Peritoneal dialysis
6. Superior vena cava obstruction
7. Myxedema
8. Urinothorax
Exudative Pleural Effusions
1. Neoplastic diseases
a. Metastatic disease
b. Mesothelioma
2. Infectious diseases
a. Bacterial infections
b. Tuberculosis
c. Fungal infections
d. Viral infections
e. Parasitic infections
3. Pulmonary embolization
4. Gastrointestinal disease
a. Esophageal perforation
b. Pancreatic disease
c. Intraabdominal abscesses
d. Diaphragmatic hernia
e. After abdominal surgery
f. Endoscopic variceal sclerotherapy
g. After liver transplant
5. Collagen-vascular diseases
a. Rheumatoid pleuritis
b. Systemic lupus erythematosus
c. Drug-induced lupus
d. Immunoblastic lymphadenopathy
e. Sjögren's syndrome
f. Wegener's granulomatosis
g. Churg-Strauss syndrome
6. Post-coronary artery bypass surgery
7. Asbestos exposure
8. Sarcoidosis
9. Uremia
10. Meigs' syndrome
11. Yellow nail syndrome
12. Drug-induced pleural disease
a. Nitrofurantoin
b. Dantrolene
c. Methysergide
d. Bromocriptine
e. Procarbazine
f. Amiodarone
13. Trapped lung
14. Radiation therapy
15. Post-cardiac injury syndrome
16. Hemothorax
17. Iatrogenic injury
18. Ovarian hyperstimulation syndrome
19. Pericardial disease
20. Chylothorax
Pneumothorax
Pneumothorax is the presence of gas in the pleural space. A spontaneous pneumothorax is one that occurs without antecedent trauma to the thorax. A primary spontaneous pneumothorax occurs in the absence of underlying lung disease, while a secondary pneumothorax occurs in its presence. A traumatic pneumothorax results from penetrating or nonpenetrating chest injuries. A tension pneumothorax is a pneumothorax in which the pressure in the pleural space is positive throughout the respiratory cycle.
Primary Spontaneous Pneumothorax
Primary spontaneous pneumothoraces are usually due to rupture of apical pleural blebs, small cystic spaces that lie within or immediately under the visceral pleura. Primary spontaneous pneumothoraces occur almost exclusively in smokers, which suggests that these patients have subclinical lung disease. Approximately one-half of patients with an initial primary spontaneous pneumothorax will have a recurrence. The initial recommended treatment for primary spontaneous pneumothorax is simple aspiration. If the lung does not expand with aspiration, or if the patient has a recurrent pneumothorax, thoracoscopy with stapling of blebs and pleural abrasion is indicated. Thoracoscopy or thoracotomy with pleural abrasion is almost 100% successful in preventing recurrences.
Secondary Pneumothorax
Most secondary pneumothoraces are due to chronic obstructive pulmonary disease, but pneumothoraces have been reported with virtually every lung disease. Pneumothorax in patients with lung disease is more life-threatening than it is in normal individuals because of the lack of pulmonary reserve in these patients. Nearly all patients with secondary pneumothorax should be treated with tube thoracostomy. Most should also be treated with thoracoscopy or thoracotomy with the stapling of blebs and pleural abrasion. If the patient is not a good operative candidate or refuses surgery, then pleurodesis should be attempted by the intrapleural injection of a sclerosing agent such as doxycycline.
Traumatic Pneumothorax
Traumatic pneumothoraces can result from both penetrating and nonpenetrating chest trauma. Traumatic pneumothoraces should be treated with tube thoracostomy unless they are very small. If a hemopneumothorax is present, one chest tube should be placed in the superior part of the hemithorax to evacuate the air, and another should be placed in the inferior part of the hemithorax to remove the blood. Iatrogenic pneumothorax is a type of traumatic pneumothorax that is becoming more common. The leading causes are transthoracic needle aspiration, thoracentesis, and the insertion of central intravenous catheters. Most can be managed with supplemental oxygen or aspiration, but if these are unsuccessful a tube thoracostomy should be performed.
Tension Pneumothorax
This condition usually occurs during mechanical ventilation or resuscitative efforts. The positive pleural pressure is life-threatening both because ventilation is severely compromised and because the positive pressure is transmitted to the mediastinum, which results in decreased venous return to the heart and reduced cardiac output.
Difficulty in ventilation during resuscitation or high peak inspiratory pressures during mechanical ventilation strongly suggests the diagnosis. The diagnosis is made by physical examination showing an enlarged hemithorax with no breath sounds, hyperresonance to percussion, and shift of the mediastinum to the contralateral side. Tension pneumothorax must be treated as a medical emergency. If the tension in the pleural space is not relieved, the patient is likely to die from inadequate cardiac output or marked hypoxemia. A large-bore needle should be inserted into the pleural space through the second anterior intercostal space. If large amounts of gas escape from the needle after insertion, the diagnosis is confirmed. The needle should be left in place until a thoracostomy tube can be inserted.
Disorders of the Mediastinum: Introduction
The mediastinum is the region between the pleural sacs. It is separated into three compartments. The anterior mediastinum extends from the sternum anteriorly to the pericardium and brachiocephalic vessels posteriorly. It contains the thymus gland, the anterior mediastinal lymph nodes, and the internal mammary arteries and veins. The middle mediastinum lies between the anterior and posterior mediastina and contains the heart; the ascending and transverse arches of the aorta; the venae cavae; the brachiocephalic arteries and veins; the phrenic nerves; the trachea, main bronchi, and their contiguous lymph nodes; and the pulmonary arteries and veins. The posterior mediastinum is bounded by the pericardium and trachea anteriorly and the vertebral column posteriorly. It contains the descending thoracic aorta, esophagus, thoracic duct, azygos and hemiazygos veins, and the posterior group of mediastinal lymph nodes.
Mediastinal Masses
The first step in evaluating a mediastinal mass is to place it in one of the three mediastinal compartments, since each has different characteristic lesions. The most common lesions in the anterior mediastinum are thymomas, lymphomas, teratomatous neoplasms, and thyroid masses. The most common masses in the middle mediastinum are vascular masses, lymph node enlargement from metastases or granulomatous disease, and pleuropericardial and bronchogenic cysts. In the posterior mediastinum, neurogenic tumors, meningoceles, meningomyeloceles, gastroenteric cysts, and esophageal diverticula are commonly found.
CT scanning is the most valuable imaging technique for evaluating mediastinal masses and is the only imaging technique that should be done in most instances. Barium studies of the gastrointestinal tract are indicated in many patients with posterior mediastinal lesions, since hernias, diverticula, and achalasia are readily diagnosed in this manner. An 131I scan can efficiently establish the diagnosis of intrathoracic goiter.
A definite diagnosis can be obtained with mediastinoscopy or anterior mediastinotomy in many patients with masses in the anterior or middle mediastinal compartments. A diagnosis can be established without thoracotomy via percutaneous fine-needle aspiration biopsy or endoscopic transesophageal or endobronchial ultrasound-guided biopsy of mediastinal masses in most cases. Alternative ways to establish the diagnosis are video-assisted thoracoscopy, mediastinoscopy, or mediastinotomy. In many cases the diagnosis can be established and the mediastinal mass removed with video-assisted thoracoscopy.
Acute Mediastinitis
Most cases of acute mediastinitis either are due to esophageal perforation or occur after median sternotomy for cardiac surgery. Patients with esophageal rupture are acutely ill with chest pain and dyspnea due to the mediastinal infection. The esophageal rupture can occur spontaneously or as a complication of esophagoscopy or the insertion of a Blakemore tube. Appropriate treatment is exploration of the mediastinum with primary repair of the esophageal tear and drainage of the pleural space and the mediastinum.
The incidence of mediastinitis following median sternotomy is 0.4–5.0%. Patients most commonly present with wound drainage. Other presentations include sepsis or a widened mediastinum. The diagnosis is usually established with mediastinal needle aspiration. Treatment includes immediate drainage, debridement, and parenteral antibiotic therapy, but the mortality still exceeds 20%.
Chronic Mediastinitis
The spectrum of chronic mediastinitis ranges from granulomatous inflammation of the lymph nodes in the mediastinum to fibrosing mediastinitis. Most cases are due to TB or histoplasmosis, but sarcoidosis, silicosis, and other fungal diseases are at times causative. Patients with granulomatous mediastinitis are usually asymptomatic. Those with fibrosing mediastinitis usually have signs of compression of some mediastinal structure such as the superior vena cava or large airways, phrenic or recurrent laryngeal nerve paralysis, or obstruction of the pulmonary artery or proximal pulmonary veins. Other than antituberculous therapy for tuberculous mediastinitis, no medical or surgical therapy has been demonstrated to be effective for mediastinal fibrosis.
Pneumomediastinum
In this condition, there is gas in the interstices of the mediastinum. The three main causes are: (1) alveolar rupture with dissection of air into the mediastinum; (2) perforation or rupture of the esophagus, trachea, or main bronchi; and (3) dissection of air from the neck or the abdomen into the mediastinum. Typically, there is severe substernal chest pain with or without radiation into the neck and arms. The physical examination usually reveals subcutaneous emphysema in the suprasternal notch and Hamman's sign, which is a crunching or clicking noise synchronous with the heartbeat and best heard in the left lateral decubitus position. The diagnosis is confirmed with the chest radiograph. Usually no treatment is required, but the mediastinal air will be absorbed faster if the patient inspires high concentrations of oxygen. If mediastinal structures are compressed, the compression can be relieved with needle aspiration.
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