Pleurisy
Pleurisy (also known as pleuritis) is characterized by chest pain that results from inflammation of the pleural surfaces from any cause. The pain originates from the parietal pleura, which derives most of its innervation from the intercostal nerves. The central portion of the diaphragmatic parietal pleura receives phrenic innervation, so that inflammation of the diaphragmatic surfaces causes referred pain to the ipsilateral shoulder. Inspira-tory chest pain, however, is not uniquely pleural and may occur with pericarditis or chest wall disease.
Pleuritic chest pain may result from primary involvement of the pleura by neoplasia, infection, trauma, or inflammation or from secondary spread of one of these processes from subjacent lung tissue. Thus, a common cause of pleuritic chest pain is pneumococcal pneumonia, which typically begins at the lung periphery and spreads to the adjacent pleural surfaces. Many middle-aged and elderly persons who report having experienced pleurisy in the past probably suffered from pneumonia.
Diagnosis
Pleuritic chest pain is typified by intensification on deep inspiration. It is usually sharp in quality, may be present continuously, and is characteristically made worse by movements of the thorax, as well as by coughing, sneezing, or other sudden respiratory movements. If the pain is severe, inability to take a deep breath without aggravating the pain may lead to the sensation of shortness of breath. Often, pleuritic chest pain must be differentiated from chest wall pain of musculoskeletal origin (e.g., localized muscle strain, costochondritis, or rib fracture) and from the pain associated with pericarditis. Superficial tenderness of the chest wall on light palpation favors chest wall pain, but tenderness on deep palpation does not reliably exclude pleuritis. A pleural friction rub heard on auscultation of the chest establishes the presence of a pleural disorder.
A chest radiograph can be useful in suggesting the underlying cause of pleuritic pain. If the chest radiograph shows the presence of effusions, the causes of pleuritic pain are limited to the processes that produce pleural effusion [seePleural Effusion, below]. If the chest radiograph is normal, pleuritic chest pain has a relatively limited differential diagnosis. Major etiologic possibilities include pulmonary embolism, viral pleurisy, and serositis in association with collagen vascular disease, especially systemic lupus erythem-atosus (SLE). Less common causes of pleuritic chest pain include uremia, sickle cell crisis, and pleuropericarditis that occurs after myo-cardial infarction or pericardiotomy (Dressler syndrome). Some patients present with an acute illness characterized by low-grade fever, headache, and myalgia; in many such episodes, the cause cannot be determined but is presumed to be viral. These acute illnesses are usually self-limited, resolving within a few days to 1 to 2 weeks. Coxsackievirus B and other enteroviruses cause an epidemic form of viral pleuritis called epidemic pleurodynia, or Born-holm disease, which often affects multiple family members. Relapses may occur after the patient is asymptomatic for several days.
Treatment
Idiopathic or viral pleuritis can be treated effectively with nonsteroidal anti-inflammatory drugs and, if necessary, narcotic analgesics. However, the diagnosis is one of exclusion, and pulmonary embolism, a potentially lethal condition, is the most important cause to exclude.
Pleural Effusion
Pleural effusion, the abnormal accumulation of liquid in the pleural space, may affect as many as 800,000 persons in the United States each year. The most common causes are congestive heart failure, malignancy, pneumonia, and pulmonary emboli.
Pathophysiology
A number of factors favor pleural effusion, including (1) altered permeability of the pleural membranes; (2) decreased in-travascular oncotic pressure and, once a pleural effusion has formed, increased pleural liquid oncotic pressure; (3) increased hydrostatic pressure in the pleural capillaries as a result of heart failure; (4) greater negativity of pressure in the pleural space (e.g., if the lung is unable to expand normally); (5) lymphatic obstruction; (6) migration of ascitic liquid across the diaphragm; and (7) migration of pulmonary edema liquid across the visceral pleura.1 Pleural effusion produces a restrictive defect that is correlated with the size of the effusion. Because both the air spaces and the pulmonary circulation are compressed and because of pulmonary hypoxic vasoconstriction, there is little shunting and only mild hypoxemia. Removal of a large effusion can result in modest improvement in lung function, but often, the underlying cause of the effusion (e.g., heart failure or lymphangitic carcinoma) causes persistent functional abnormalities. Various mediators are involved in the production of altered permeability and the evolution of pleural effusions. 2,3
Classification and etiology
Various types of liquid may accumulate in the pleural space. Accumulation of serous liquid is referred to as a hydrothorax. If blood accumulates, the condition is referred to as a hemothorax. An effusion composed of lipids is known as a chylothorax. Accumulation of pus is known as a pyothorax, or empyema. Although imaging studies can be helpful, the actual condition can be distinguished only by analysis of the liquid itself.
Hydrothoraces fall into two major categories on the basis of mechanisms of pleural liquid accumulation: transudation and exudation. Transudation of liquid into the pleural space occurs when there is an imbalance between the hydrostatic and the on-cotic pressures governing the normal rates of pleural liquid formation and resorption. The most common cause of a transuda-tive pleural effusion is congestive heart failure. Other causes are constrictive pericarditis, superior vena cava obstruction, and the hypoalbuminemic states associated with cirrhosis and the nephrotic syndrome [see Table 1]. Pulmonary arterial hypertension and right heart failure usually do not by themselves cause pleural effusions.
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Table 1 Causes of Hydrothorax |
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Transudative |
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Congestive heart failure |
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Constrictive pericardial disease |
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Cirrhosis |
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Nephrotic syndrome |
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Superior vena cava obstruction |
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Ascites (transudative) |
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Peritoneal dialysis |
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Exudative or Transudative |
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Hypothyroidism |
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Pulmonary embolism |
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Trapped lung |
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Exudative |
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Infections (i.e., parapneumonic effusion, tuberculosis) |
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Malignant disorders |
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Primary lung cancer |
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Cancer metastases to the lungs or pleura |
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Lymphoma |
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Mesothelioma |
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Collagen vascular diseases and vasculitides |
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Gastrointestinal diseases |
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Pancreatitis and pancreatic pseudocyst |
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Esophageal rupture |
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Abdominal or retroperitoneal abscess |
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Postabdominal surgery |
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Postendoscopic variceal sclerotherapy |
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Miscellaneous |
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Benign asbestos effusion |
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Meigs syndrome |
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Dressler syndrome (after myocardial infarction or pericardiotomy) |
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Post-coronary artery bypass97 |
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Uremia |
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Sarcoidosis and necrotizing sarcoid granulomatosis |
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Radiation therapy |
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Drugs (e.g., nitrofurantoin, dantrolene, methysergide, all-trans-retinoic acid98) |
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Yellow nail syndrome |
Exudation of liquid into the pleural space results from any process that disrupts the integrity of the endothelial membrane that lines the pleural capillaries and venules. Obstruction of lymphatic drainage from the pleural space is another mechanism that can cause a protein-rich effusion. Exudative effusions are associated with a broad range of disorders, including a variety of infectious, neoplastic, inflammatory, embolic, and vasculitic diseases. In addition, exudative effusions may be caused by the effects of certain drugs and physical agents [see Table 1 ].
Diagnosis
Clinical Manifestations
A pleural effusion may be suspected on the basis of physical examination. Physical findings include dullness on percussion, diminished or absent breath sounds, decreased fremitus, and egophony at the level of the pleural liquid meniscus.
Imaging Studies
The chest radiograph usually establishes the diagnosis; patients are often further evaluated by other imaging techniques (e.g., ultrasonography and computed tomography).4
Radiography When the patient is in the upright position, liquid collects first in the posterior sulcus, the most inferiorly located recess of the pleural space. Blunting of the normally sharp posterior costophrenic angle on a lateral chest radiograph indicates the presence of at least 25 to 50 ml of pleural liquid. As additional liquid accumulates (approximately 150 ml total), the lateral costophrenic angle on a posteroanterior radiograph becomes obliterated. Greater amounts of pleural liquid displace the lung centrally and produce a characteristic homogeneous opacity that forms a concave meniscus with the chest wall [see Figure 1 ].
A massive pleural effusion may opacify an entire hemithorax and displace mediastinal structures to the opposite side of the chest [see Figure 2]. Large effusions may reduce venous return and thus cardiac output, creating hemodynamic compromise. The displacement force that is exerted is proportional to the height of the effusion. A contralateral shift of the mediastinum in a patient with massive pleural effusion may go undetected if there is ipsilateral atelectasis of the lung or if the mediastinum is fixed by an invasive tumor or fibrosis. A mediastinal shift toward the side of the effusion indicates almost complete atelecta-sis of the underlying lung, most often resulting from an obstructing tumor of the mainstem bronchus.
When intense pleural inflammation leads to the formation of adhesions between the visceral and parietal surfaces, localized effusions may collect in the resultant pockets. These loculated effusions may form along any part of the pleural surface and at times may be mistaken for infiltrates or masses within the lung parenchyma [see Figure 3]. A radiographic sign that favors the diagnosis of pleural loculation is the oblique angle formed by the chest wall and the margin of the pleural density. A subpleural lung nodule, in contrast, usually forms an acute angle with the chest wall.
An atypical presentation of pleural effusion is the subpul-monary collection of liquid [see Figure 3]. For unknown reasons, sizable amounts of pleural liquid sometimes collect between the diaphragm and the base of the lung without significantly distorting the contour of the inferior lung margin. In a patient with a subpulmonary effusion, it is possible to mistake the superior border of the effusion for the diaphragmatic silhouette, prompting a needless search for causes of an elevated hemidiaphragm. Several radiographic findings suggest the correct diagnosis. First, the contour of the base of the lung is slightly altered by a subpulmonary effusion; the normal domelike curve formed by the diaphragm is replaced by a hockey stick-like shape, with lat-eralization of the apex of the dome. Second, on the left side, the distance between the base of the lung and the gastric gas bubble is increased. The diagnosis of a subpulmonary effusion is confirmed by a lateral decubitus chest radiograph, which will show layering of the effusion along the lateral chest wall.
Figure 1 This chest radiograph demonstrates the typical configuration of a pleural effusion as seen on posteroanterior projection. The pleural liquid forms a meniscus with the left lateral chest wall.
Figure 2 (a) A massive hydrothorax resulting from a subpleural adenocarcinoma of the lung with a malignant pleural effusion is present in this patient. The heart and mediastinum are deviated to the right. Compression of the heart and increased intrathoracic pressure cause a reduction in venous return and resulting tachycardia (heart rate, 120 beats/min). (b) The heart and mediastinum return to the midline after evacuation of liquid; heart rate falls to 80 beats/min.
In patients with congestive heart failure, pleural liquid may collect between the two visceral pleural surfaces that line the in-terlobar fissures [see Figure 4]. Interlobar effusions, which may be mistaken for tumors of the lung parenchyma, disappear with effective treatment of the heart failure and thus have been called vanishing tumors, or pseudotumors. Interlobar effusions have a characteristic lenticular shape, with the tapered ends oriented in the plane of the fissure.
In some cases of pleural effusion, the only radiograph available for interpretation is an anteroposterior chest radiograph obtained with the patient in the supine position. In this position, a free-flowing pleural effusion spreads along the posterior costal surfaces. The radiograph shows a uniform increase in the opacity of the involved hemithorax, but normal lung markings are visible through the opacity [see Figure 5].
On lateral decubitus radiographs, small amounts of pleural liquid can be identified if the patient is positioned carefully. Free-flowing effusions can be distinguished from loculated effusions or thickened pleural tissue by comparing the pleural density with its appearance on a radiograph taken with the patient in the upright position.
Ultrasonography Ultrasonography is also a very sensitive test for detecting pleural effusions. It is particularly effective in cases of loculated pleural effusions because it can identify the precise site on the chest wall where a needle can be introduced to aspirate a sample.
Computed tomography CT scanning is helpful in distinguishing a pleural mass from a loculated effusion and distinguishing a hydropneumothorax from a lung abscess. CT scanning performed with contrast usually shows parietal pleural thickening in patients with exudates and enhancement of the parietal pleura in patients with empyema.5
