In healthy humans in the supine position, the radiolucency of the lung base is equal to or greater than that in the lung apex [1]. Furthermore, when in the supine position, breast and pectoral tissue tend to fall laterally away from the lung base. Thus, an effusion should be suspected if there is increased homogeneous density over the lower lung fields compared to the upper lung fields. As the pleural effusion increases, the increased radiodensity involves the upper hemithorax as well. However, failure of chest wall tissue to move laterally, cardiomegaly, prominent epicardial fat pad, and lung collapse or consolidation may obscure a pleural effusion on a supine radiograph. Patient rotation or an off-center X-ray beam can mimic a unilateral homogeneous density. An absent pectoral muscle, prior mastectomy, unilateral hyperlucent lung, scoliosis, previous lobectomy, hypoplastic pulmonary artery, or pleural or chest wall mass may lead to unilateral homogeneous increased density and mimic an effusion.

Approximately 175 to 525 mL of pleural fluid results in blunting of the costophrenic angle on an erect radiograph [2]. This quantity of effusion can be detected on a supine radiograph as an increased density over the lower lung zone. Failure to visualize the hemidiaphragm, absence of the costophrenic angle meniscus, and apical capping are less likely to be seen with effusions of less than 500 mL [1]. The major radiographic finding of a pleural effusion in a supine position is increased homogeneous density over the lower lung field that does not obliterate normal bronchovascular markings, does not show air bronchograms, and does not show hilar or mediastinal displacement until the effusion is massive. If a pleural effusion is suspected in the supine patient, ultrasonography (US) should be performed.

Atelectasis is a common cause of small pleural effusions in comatose, immobile, pain-ridden patients in ICUs [26] and after upper abdominal surgery [27,28]. Other causes include major bronchial obstruction from lung cancer or a mucous plug. Atelectasis causes pleural fluid because of decreased pleural pressure. With alveolar collapse, the lung and chest wall separate further, creating local areas of increased negative pressure. This decrease in pleural pressure favors the movement of fluid into the pleural space, presumably from the parietal pleural surface. The fluid accumulates until the pleural or parietal-pleural interstitial pressure gradient reaches a steady state.

Pleural fluid from atelectasis is a serous transudate with a low number of mononuclear cells, a glucose concentration equivalent to serum, and pH in the range of 7.45 to 7.55. When atelectasis resolves, pleural fluid dissipates during several days.

CHF is the most common cause of transudative pleural effusions and a common cause of pleural effusions in ICUs. Pleural effusions due to CHF are associated with increases in pulmonary venous pressure [29]. Most patients with subacute or chronic elevation in pulmonary venous pressure (pulmonary capillary wedge pressure of at least 24 mm Hg) have evidence of pleural effusion on US or lateral decubitus radiograph. Isolated increases in systemic venous pressure tend not to produce pleural effusions. Thus, patients with chronic obstructive pulmonary disease (COPD) and cor pulmonale rarely have pleural effusions, and the presence of pleural fluid implies another cause.

Most patients with pleural effusions secondary to CHF have the classic signs and symptoms. The chest radiograph shows cardiomegaly and bilateral small-to-moderate pleural effusions of similar size (right slightly greater than left). There is usually radiographic evidence of pulmonary congestion, with the severity of pulmonary edema correlating with the presence of pleural effusion [29].

The effusion is a transudate, with mesothelial cells and lymphocytes accounting for the majority of the less than 1,000 cells per μL [13]. Acute diuresis can raise the pleural fluid protein and lactate dehydrogenase into the range of an exudate [30,31]. In the patient with secure clinical diagnosis of CHF, observation is appropriate. Thoracentesis should be performed if the patient is febrile, has pleural effusions of disparate size, has a unilateral pleural effusion, does not have cardiomegaly, has pleuritic chest pain, or has a PaO₂ inappropriate for the degree of pulmonary edema.

Treatment consists of decreasing venous hypertension and improving cardiac output with diuretics, digitalis, and afterload reduction. In successfully managed heart failure, the effusions resolve during days to weeks after the pulmonary edema has cleared.

Pleural effusions occur in approximately 6% of patients with cirrhosis of the liver and clinical ascites. The effusions result from movement of ascitic fluid through congenital or acquired diaphragmatic defects [32,33,34].

The patient usually has the classic stigmata of cirrhosis and clinically apparent ascites. The usual chest radiograph shows a normal cardiac silhouette and a right-sided pleural effusion, which can vary from small to massive; effusions are less likely isolated to the left pleural space or are bilateral [32,33,34,35]. Rarely, a massive pleural effusion may be found without clinical ascites (demonstrated only by US), implying the presence of a large diaphragmatic defect. The pleural fluid is a serous transudate with a low nucleated cell count and a predominance of mononuclear cells, pH greater than 7.40, and a glucose level similar to that of serum [13]. The fluid can be hemorrhagic due to an underlying coagulopathy or rupture of a diaphragmatic bleb. Demonstrating that pleural and ascitic fluids have similar protein and lactate dehydrogenase concentrations, substantiates the diagnosis [32]. If the diagnosis is problematic, injection of a radionuclide into the ascitic fluid with detection on chest imaging within 1 to 2 hours supports a pleuroperitoneal communication through a diaphragmatic defect [36]; delayed demonstration of the tracer suggests that the pathogenesis of the effusion is via convection through the mesothelium.

Hepatic hydrothorax may be complicated by spontaneous bacterial empyema (SBE), which is analogous to spontaneous bacterial peritonitis. The criteria for diagnosis of SBE are similar to those for the diagnosis of spontaneous bacterial peritonitis. SBE must be considered in the differential diagnosis of the infected cirrhotic patient, even in the absence of clinical ascites [37,38]. The pleural fluid culture and analysis may reveal positive culture, a total neutrophil count of more than 500 cells per μL, and a serum to pleural fluid albumin gradient greater than 1.1. The chest radiograph should not show a pneumonic process. Treatment of SBE is conservative with antibiotics unless purulence is present, in which case tube thoracostomy must be considered.

Treatment of hepatic hydrothorax is directed at resolution of the ascites, using sodium restriction and diuresis. The effusion frequently persists unchanged until all ascites is mobilized. If the patient is acutely dyspneic or in respiratory failure, therapeutic thoracentesis should be done as a temporizing measure. Care should be exercised with paracentesis or thoracentesis because hypovolemia can occur with rapid evacuation of fluid. Chest tube insertion should be avoided as it can cause infection of the fluid, and prolonged drainage can lead to protein and lymphocyte depletion and renal failure. Chemical pleurodesis via a chest tube is often unsuccessful due to rapid movement of ascitic fluid into the pleural space. Treatment options in hepatic hydrothorax refractory to medical management include transjugular intrahepatic portal systemic shunt and video-assisted thoracoscopy to patch the diaphragmatic defect, followed by pleural abrasion or talc poudrage in the properly selected patient [39,40].

Many patients admitted to a medical ICU have a chronic illness and associated hypoalbuminemia. When the serum albumin level falls below 1.8 g per dL, pleural effusions may be observed [41]. Because the normal pleural space has an effective lymphatic drainage system, pleural fluid tends to be the last collection of extravascular fluid that occurs in patients with low oncotic pressure. Therefore, it is unusual to find a pleural effusion solely due to hypoalbuminemia in the absence of anasarca. Patients with hypoalbuminemic pleural effusions tend not to have pulmonary symptoms unless there is underlying lung disease, as the effusions are rarely large. Chest radiograph shows small-to-moderate bilateral effusions and a normal heart size. The pleural fluid is a serous transudate with less than 1,000 nucleated cells per μL, predominantly lymphocytes and mesothelial cells. The pleural fluid glucose level is similar to that of serum, and the pH is in the range of 7.45 to 7.55. Diagnosis is presumptive if other causes of transudative effusions can be excluded. The effusions resolve when hypoalbuminemia is corrected.

Extravascular migration of a central venous catheter can cause pneumothorax, hemothorax, chylothorax, or a transudative pleural effusion [42,43,44]. Its incidence is estimated at less than 1% but may be considerably higher. Malposition of the catheter on placement should be suspected if there is absence of blood return or questionable central venous pressure measurements. The immediate postprocedure chest radiograph should be assessed for proper catheter placement; a catheter placed from the right side should not cross the midline. If the catheter is not in the appropriate vessel, phlebitis, perforation of a vein or the heart, or instillation of fluid into the mediastinum or pleural space can occur. In the alert patient, acute infusion of intravenous fluid into the mediastinum usually results in new-onset chest discomfort and dyspnea. Depending on the volume and the rate at which it is introduced into the mediastinum, tachypnea, worsening respiratory status, and cardiac tamponade may ensue. The chest radiograph shows the catheter tip in an abnormal position [45,46], a widened mediastinum, and evidence of unilateral or bilateral pleural effusions. The effusion can have characteristics similar to those of the infusate (milky if lipid is being given) and may be hemorrhagic and neutrophil-predominant due to trauma and inflammation. The pleural fluid to serum glucose ratio is greater than 1.0 if glucose is being infused [43]. The pleural fluid glucose concentration can fall rapidly after glucose infusion into the pleural space, probably explaining the relatively low glucose concentrations in pleural fluid compared to the infusate [47]. Extravascular migration of a central venous catheter appears to be more common with placement in the external jugular vein, particularly on the left side. Left-sided catheters appear to put the patient at increased risk of perforation because of the horizontal orientation of the left compared to the right brachiocephalic vein. When catheters are introduced from the left side, they should be of adequate length for the tip to rest in the superior vena cava.

Free flow of fluid and proper fluctuation in central venous pressure during the respiratory cycle may not be reliable indicators of intravascular placement. This is probably because intrathoracic pressure changes are transmitted to the mediastinum and, thus, the venous pressure catheter. Aspiration of blood or retrograde flow of blood when the catheter is lowered below the patient’s heart level should confirm intravascular catheter placement. If blood cannot be aspirated and the effusate is aspirated instead, extravascular migration is assured. The central venous catheter should be removed immediately. If there is a small effusion, observation is warranted. If the effusion is large, causing respiratory distress, or a hemothorax is discovered, thoracentesis or tube thoracostomy should be performed.

Community-acquired or nosocomial pneumonia is common in critically ill patients. The classic presentation is fever, chest pain, leukocytosis, purulent sputum, and a new alveolar infiltrate on chest radiograph. In the elderly, debilitated patient, however, many of these findings may not be present. The chest radiograph commonly shows a small-to-large ipsilateral pleural effusion [48,49,50]. When the effusion is free-flowing and anechoic on ultrasound, and thoracentesis shows a nonpurulent, polymorphonuclear (PMN) predominant exudate with a pH of 7.30 or greater, it is highly likely that the effusion will resolve during 7 to 14 days without sequelae with antibiotics alone (uncomplicated effusion). If the chest radiograph or CT demonstrates loculation and pus is aspirated, the diagnosis of empyema is established and immediate drainage is needed. In the free-flowing nonpurulent fluid, if Gram’s stain or culture is positive or pH is less than 7.30, the likelihood of a poor outcome increases, and the pleural space should be drained.

Although a meta-analysis found that low risk patients with fluid pH between 7.20 and 7.30 may be managed without tube drainage, the patient admitted to the ICU typically cannot be considered low risk, and pH values of less than 7.30 should prompt drainage in most cases [51,52,53]. Drainage can be accomplished by standard chest tube or small-bore catheter. When loculations occur, pleural space drainage should be accomplished by placement of image-guided tubes or catheters with fibrinolytics or empyectomy and decortication [54,55]. Most thoracic surgeons routinely begin with thoracoscopy and, if not successful, proceed directly to a standard thoracotomy for empyectomy and decortication [56,57,58,59].

Pleuropulmonary abnormalities are commonly associated with pancreatitis, largely due to the close proximity of the pancreas to the diaphragm. Approximately half of patients with pancreatitis have an abnormal chest radiograph, with pleural effusions in 3% to 17% [60,61]. Mechanisms that may be involved in the pathogenesis of pancreatic pleural effusion include (a) direct contact of pancreatic enzymes with the diaphragm (sympathetic effusion), (b) transfer of ascitic fluid via diaphragmatic defects, (c) communication of a fistulous tract between a pseudocyst and the pleural space, and (d) retroperitoneal movement of fluid into the mediastinum with mediastinitis or rupture into the pleural space [60,62]. Ascitic amylase moves into the pleural space via the previously mentioned mechanisms. The pleural fluid-to-serum amylase ratio is greater than unity in pancreatitis because of slower lymphatic clearance from the pleural space compared with more rapid renal clearance.

The effusion associated with acute pancreatitis is usually small and left-sided (60%), but may be isolated to the right side (30%) or be bilateral (10%) [60]. The patient usually presents with abdominal symptoms of acute pancreatitis. The diagnosis is confirmed by an elevated pleural fluid amylase concentration that is greater than that in serum. A normal pleural fluid amylase may be found early in acute pancreatitis, but increases on serial measurements. The fluid is a PMN-predominant exudate with glucose values approximating those of serum. Leukocyte counts may reach 50,000 cells per μL. The pleural fluid pH is usually 7.30 to 7.35.

No specific treatment is necessary for the pleural effusion of acute pancreatitis; the effusion resolves as the pancreatic inflammation subsides. Drainage of the pleural space does not appear to affect residual pleural damage. If the pleural effusion does not resolve in 2 to 3 weeks, pancreatic abscess or pseudocyst should be excluded.

The presence of a unilateral pleural effusion may suggest pulmonary embolism or obscure the diagnosis by directing attention to a primary lung or cardiac process. Pleural effusions occur in approximately 40% of patients with pulmonary embolism [63]. These effusions result from several different mechanisms including increased pleural capillary permeability, imbalance in microvascular and pleural space hydrostatic pressures, and pleuropulmonary hemorrhage [63,64]. Ischemia from pulmonary vascular obstruction, in addition to release of inflammatory mediators from platelet-rich thrombi, can cause capillary leak into the lung and, subsequently, the pleural space, explaining the usual finding of an exudative effusion.
Transudates, described in approximately 20% of patients with pulmonary embolism, result from atelectasis [64].

With pulmonary infarction, necrosis and hemorrhage into the lung and pleural space may result. More than 80% of patients with infarction have bloody pleural effusions, but more than 35% of patients with pulmonary embolism without radiographic infarction also have hemorrhagic fluid [63]. The presence of a pleural effusion does not alter the signs or symptoms in patients with pulmonary embolism. Chest pain, usually pleuritic, occurs in most patients with pleural effusions complicating pulmonary embolism, and is invariably ipsilateral [63]. The chest radiograph virtually always shows a unilateral effusion that occupies less than one third of the hemithorax [63]. An associated pulmonary infiltrate (infarction) is seen in approximately half of patients with pulmonary embolism and effusion.

Pleural fluid analysis is variable and nondiagnostic [64]. The pleural fluid is hemorrhagic in two thirds of patients, but the number of red blood cells exceeds 100,000 per μL in less than 20% [64]. The nucleated cell count ranges from less than 100 (atelectatic transudates) to greater than 50,000 per μL (pulmonary infarction) [64]. There is a predominance of PMNs when a thoracentesis is performed near the time of the acute injury and of lymphocytes with later thoracentesis. The effusion due to pulmonary embolism is usually (92%) apparent on the initial chest radiograph and reaches a maximum volume during the first 72 hours [63]. Patients with pleural effusions that progress with therapy should be evaluated for recurrent embolism, hemothorax secondary to anticoagulation, an infected infarction, or an alternate diagnosis. When consolidation is absent on chest radiograph, effusions usually resolve in 7 to 10 days; with consolidation, the resolution time is 2 to 3 weeks [64].

The association of pleural effusion with pulmonary embolism does not alter therapy. Furthermore, the presence of a bloody effusion is not a contraindication to full-dose anticoagulation because hemothorax is a rare complication of heparin therapy [65]. An enlarging pleural effusion on therapy necessitates thoracentesis to exclude hemothorax, empyema, or another cause. Active pleural space hemorrhage necessitates discontinuation of anticoagulation, tube thoracostomy, and placement of a vena cava filter.