Michael A. Jantz
Veena B. Antony
Pleural disease itself is an unusual cause for admission to the intensive care unit (ICU). Conditions potentially requiring ICU admission include a large pleural effusion causing acute respiratory failure, hemothorax producing respiratory or hemodynamic compromise, secondary spontaneous pneumothorax with respiratory failure, empyema with sepsis, and re-expansion pulmonary edema. Pleural complications of disease processes and procedures performed in the ICU are common, however, and the changes in respiratory physiology are additive to that of the underlying lung disease. The development of a pneumothorax in a critically ill patient, particularly in mechanically ventilated patients, may be a life-threatening event. Pleural effusions may be overshadowed by the illness requiring ICU admission in the critically ill patient. Pleural effusions and pneumothoraces may not be detected on chest radiographs because the radiologic appearance may differ in the supine patient.
Pleural Effusions in the Intensive Care Unit
Radiologic Evaluation
In the normal pleural space, air and fluid tend to distribute following gravitational influences, with air initially accumulating between the superior portion of the lung and the apex of the thorax, while fluid accumulates between the inferior margin of the lung and the diaphragm. Pleural air and fluid collections shift location when radiographs are obtained in positions other than the erect position. Because radiographs in critically ill patients are taken in the supine or semierect position, the radiographic appearance of air and fluid in the pleural space may thus change.
In normal humans in the supine position, the radiolucency of the lung base is equal to or greater than that of the lung apex due to the anteroposterior diameter of the lung being greatest at the lung base. In addition, in the supine patient, breast and pectoral tissues will tend to move laterally away from the lung base. A pleural effusion should be suspected when increased homogeneous density is present over the lower lung fields as compared with the upper lung fields. Patient rotation, an off-center x-ray beam, prior lobectomy, or a pleural or chest wall mass may produce a unilateral homogenous density that simulates the appearance of a pleural effusion (1). Cardiomegaly, a prominent epicardial fat pad, and lobar collapse or consolidation may obscure the detection of a pleural effusion on a supine radiograph.
Approximately 175 to 525 mL of pleural fluid will produce blunting of the costophrenic angle on an erect chest radiograph (2). This quantity of pleural fluid can usually be detected on a supine radiograph as an increased density over the lower lung zone. Blunting of the costophrenic angle (meniscus sign), silhouetting of the hemidiaphragm, and apical capping may be seen with larger effusions (3). An apparent elevation of the hemidiaphragm may be secondary to a subpulmonic collection of pleural fluid. A diffuse increase in the radiodensity of the hemithorax, or “veiling,” may be seen with very large effusions in the supine radiograph. Thus, the major radiographic finding of a pleural effusion in the supine patient is an increased homogeneous density over the lower lung field that does not obliterate normal bronchovascular markings, does not demonstrate air bronchograms, and does not produce hilar or mediastinal displacement until the effusion is massive. If a pleural effusion is suspected in the supine patient, obtaining an erect or lateral decubitus radiograph may be helpful.
Because the critically ill patient often has underlying parenchymal lung disease, the diagnosis of pleural effusion can be problematic. Ultrasonography (US) or computed tomography (CT) scanning may be required to confirm or exclude the presence of a pleural effusion. US provides good characterization of pleural disease and has an advantage of being able to be performed at the bedside in critically ill patients who are not stable for transport to the radiology department for CT. Disadvantages include impedance of the ultrasound wave by air in the lung or pleural space, a restricted field of view, inferior evaluation of the lung parenchyma compared to CT, and operator dependence (1). In one study of 74 ICU patients evaluated by both chest radiograph and US, the latter detected a pleural effusion that was not appreciated on chest radiograph in 10 additional patients (29% of patients determined to have a pleural effusion) (4). In another study, US was helpful in making a diagnosis in 27 of 41 (66%) patients and influenced treatment planning in 17 of 41 critically ill patients (41%) (5). US-guided thoracentesis at the bedside was successful in 24 of 25 patients in that same study. Other studies have noted the usefulness of US to safely guide bedside thoracentesis in mechanically ventilated patients (6,7,8). The presence of complex septated, complex nonseptated, and homogeneously echogenic patterns within pleural fluid collections are typically indicative of an exudative pleural effusion (9). Homogeneously echogenic effusions suggest hemorrhagic effusions or empyemas whereas US evidence of fibrin septae suggests a parapneumonic effusion, empyema, hemothorax, or malignant effusion (9).
CT may also be helpful in assessing pleural processes in the critically ill patient, and has the advantages of better lung parenchymal imaging, evaluation of the mediastinum, and ability to distinguish pleural from parenchymal abnormalities (1). On CT, free-flowing pleural fluid produces a sickle-shaped opacity in the most dependent part of the thorax (10). Loculated pleural fluid collections are seen as lenticular or rounded opacities in a fixed position with a relatively homogeneous water density (10). CT may be particularly helpful in the diagnosis and management of loculated pleural effusions (11). The most reliable sign of empyema, the split pleura sign, is usually identified during the organizing phase. Following administration of intravenous contrast, the parietal and visceral pleura will be thickened and enhanced and will be noted to be separated, and the extrapleural fat between the empyema and the chest wall may be increased in size (12,13). In one study, this sign was present in only 68% of patients, however (12). CT may be helpful in assessing inadequately drained fluid collections in patients with persistent fevers or sepsis due to malpositioned chest tubes (14).
Diagnostic Thoracentesis
Pleural effusions are common in the ICU. In one prospective study of 100 consecutive patients admitted to a medical ICU, pleural effusions were found on chest radiographs and/or by US in 62% of patients (4). Patients with a pleural effusion provide the opportunity to diagnose, at least presumptively, the underlying process responsible for the accumulation of pleural fluid. Although disease of any organ system can cause a pleural effusion in critically ill patients, the diagnoses listed in Table 144.1 represent most causes in the ICU.
When a pleural effusion is suspected on physical exam and confirmed radiologically, a diagnostic thoracentesis should be considered to establish the cause of the effusion. Observation alone may be reasonable in situations in which the clinical diagnosis is reasonably secure and a small amount of pleural fluid is present, such as in atelectasis or uncomplicated heart failure (15). Thoracentesis should be performed, however, if the patient's clinical condition changes. When the distance from the pleural fluid line to the inside of the chest wall is less than 1 cm on lateral decubitus radiograph, the risk of thoracentesis probably outweighs the value of pleural fluid analysis. If the underlying disease causing the pleural effusion becomes clinically problematic, the effusion will often increase in size and allow for safe thoracentesis. When sampling of a small-volume pleural effusion is indicated, thoracentesis should be performed with US guidance.
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Table 144.1 Causes of Pleural Effusions in ICU Patients |
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The indications for diagnostic thoracentesis are not different in the ICU patient, and receiving mechanical ventilation is not a contraindication. Establishing the diagnosis quickly in critically ill patients may be more important than in the noncritically ill. The reported incidence of pneumothorax in nonventilated patients ranges from 4% to 30% (16,17,18,19,20). Various risk factors for developing a pneumothorax after thoracentesis have been reported, although operator inexperience, baseline lung disease, and use of positive pressure mechanical ventilation appear to be the most established risk factors. Several earlier studies have demonstrated that the incidence of pneumothorax after blind thoracentesis in mechanically ventilated patients, 5% to 10%, is similar to that of nonventilated patients, and it is thus safe to perform blind thoracentesis in mechanically ventilated patients (21,22,23). If the patient on mechanical ventilation does develop a pneumothorax, however, a significant risk of progression to a life-threatening tension pneumothorax exists. As such, some authors have advocated the routine use of ultrasound guidance for all thoracentesis procedures in mechanically ventilated patients given the observed pneumothorax rates of 0% to 3% with ultrasound guidance in nonventilated patients (20,24), as well as in patients receiving mechanical ventilation (6,7,8). Strong consideration should be given to using US guidance in patients with small or moderate effusions, although large effusions may be sampled relatively safely unless the operator is inexperienced. US or CT guidance should be used to sample loculated pleural fluid collections. There are no absolute contraindications to diagnostic thoracentesis. The major relative contraindications are a bleeding diathesis or anticoagulation. In one study of 207 patients with mild to moderate coagulopathy, defined as a prothrombin time (PT) or partial thromboplastin time (PTT) up to twice normal or a platelet count from 50,000 to 100,000 cells/µL, no increase in bleeding complications was noted (25). Thoracentesis should not be performed through an area of active skin infection.
Therapeutic Thoracentesis and Physiologic Effects
The primary indication for therapeutic thoracentesis or chest tube drainage of a pleural effusion is relief of dyspnea, although pulmonary mechanics and oxygenation may be improved in some patients (26). Contraindications to therapeutic thoracentesis are similar to those of diagnostic thoracentesis. Complications from therapeutic thoracentesis are similar to that of diagnostic thoracentesis, with the additional complications of hypoxemia, re-expansion pulmonary edema, and hypovolemia. An increased risk of pneumothorax compared to diagnostic thoracentesis has been noted with therapeutic thoracentesis in some studies (18,20,27) although not others (19,28)
We would recommend the use of a catheter-over-needle system in performing therapeutic thoracentesis to reduce the risk of developing a pneumothorax. In patients with pleural effusion and ipsilateral shift suggesting endobronchial obstruction or a trapped lung, the risk of re-expansion pulmonary edema may be increased, and the patient may be less likely to experience a beneficial effect. In addition, patients with initial negative pleural pressures and those with more precipitous falls in pleural pressures with fluid removal also likely have trapped lung or endobronchial obstruction and are less likely to benefit from therapeutic thoracentesis (29).
Pleural effusions compress the lung, causing atelectasis, ventilation/perfusion mismatch, and shunt physiology with resultant hypoxemia (30). Pleural fluid tends to enlarge the volume of the hemithorax more than it compresses lung volume. Studies in humans have shown that total lung capacity following thoracentesis increases by only approximately one third of the thoracentesis fluid volume, and forced vital capacity increases by approximately one half of the increase in total lung capacity (31). Studies evaluating gas exchange in nonventilated patients have been mixed. One study found a decrease in PaO2(32), one study found no change in PaO2 (33), and one study showed a mild increase in PaO2 (34). More recent studies have also shown variable results, with one study reporting a small increase in PaO2 and decrease in alveolar-arterial O2 gradient (35), although another noted no change in PaO2, alveolar-arterial O2 gradient or shunt, while the amount of blood flow to low ventilation/perfusion units increased slightly (30).
Despite these mixed results, some patients requiring mechanical ventilation may benefit from pleural fluid drainage. Talmor et al. (26) reported that 19 patients with acute respiratory failure and pleural effusions who had a poor response to positive end-expiratory pressure (PEEP)—defined as the inability to wean FiO2 to 0.5 with PEEP up to 20 cm H2O—benefited from chest tube drainage of the pleural effusions. The PaO2 increased from 125 to 199 mm Hg, and the PaO2/FiO2 ratio increased from 151 to 254. Fourteen patients had a unilateral effusion, and five patients had bilateral effusions necessitating bilateral chest tube placement. More recently, Doelken et al. (36) studied the effects of thoracentesis on respiratory mechanics and gas exchange in eight mechanically ventilated patients. Following removal of 800 to 1,950 mL (mean 1,495 mL), no significant change in PaO2 or dead space ventilation was observed. No significant changes were noted for peak and plateau pressures, dynamic and effective static compliance, respiratory system resistance, and intrinsic PEEP. Mean work performed by the ventilator did significantly decrease, however. Further studies are required to confirm these results, although in patients who are difficult to wean from mechanical ventilation, we would consider a trial of therapeutic thoracentesis.
Abdominal Surgery
Approximately one half of patients undergoing abdominal surgery will develop small unilateral or bilateral pleural effusions 24 to 48 hours following surgery (37,38). The incidence of pleural effusions is higher in procedures involving the upper abdomen, in patients having ascitic fluid at time of surgery, and in patients who have postoperative atelectasis (29). Larger left-sided effusions are common following splenectomy. The effusion after abdominal surgery is usually exudative* with a normal glucose level, pH >7.40, and less than 10,000 nucleated cells/µL (37). Small effusions generally do not require diagnostic thoracentesis and resolve spontaneously without becoming clinical significant. Thoracentesis is indicated to exclude empyema if the effusion is relatively large or loculated or if the possibility of a subdiaphragmatic abscess related to the surgery exists.
Acute Respiratory Distress Syndrome
The presence of pleural effusions in acute respiratory distress syndrome (ARDS) has not been well appreciated or studied. In a retrospective study of 25 patients with ARDS, 36% were found to have pleural effusions (39). All patients had extensive alveolar infiltrates in addition to pleural effusions. Pleural effusions have been observed in animal models of ARDS using α-naphthylthiourea, oleic acid, and ethchlorvynol (40,41). In the oleic acid model, 35% of the excess lung water collected in the pleural spaces (40). Effusions are likely underdiagnosed in ARDS because the patient has bilateral alveolar infiltrates and the radiograph is taken in the supine position. In experimental models of ARDS, the effusions are serous to serosanguineous with a predominance of polymorphonuclear leukocytes (PMNs) (41). These effusions resolve as the ARDS resolves and require no specific therapy.
Atelectasis
Atelectasis is a common cause of small pleural effusions in the ICU due to patients being immobile (4). Atelectasis and small effusions are commonly observed following cardiothoracic or abdominal surgery. Other potential causes include endobronchial obstruction from tumor, foreign body, or mucus plugging as well as extrinsic airway compression from malignancy. With lung collapse, local areas of increased negative pressure are created by the separation of the lung and chest wall. The decrease in pleural pressure favors the movement of fluid into the pleural space, presumably from the surface of the parietal pleura (15).
Pleural effusions from atelectasis are serous transudates with a few mononuclear cells, a glucose concentration equal to serum, and a pH of 7.45 to 7.55. The pleural effusions dissipate over several days when the atelectasis resolves.
Chylothorax
A chylothorax is defined as the accumulation of chyle in the pleural space. The predominant mechanisms of chylothorax formation include disruption of the thoracic duct, extravasation from pleural lymphatics, and transdiaphragmatic efflux from chylous ascites (42). The most common cause of chylothorax is lymphoma, accounting for 37% of chylothoraces in a series of 191 patients (43). The second most frequent cause is surgical trauma, which represented 25% of cases in the same series of 191 patients (43). The incidence of chylothorax following thoracic surgery has been reported to be 0.36% to 0.42% (44,45) and 1.9% following lower neck surgery (46). A higher proportion of chylothoraces are noted following esophagectomy (44,45). Virtually all intrathoracic surgical procedures, including lobectomy, pneumonectomy, and coronary artery bypass grafting, have been reported to cause chylothorax (43). Nonsurgical trauma, including blunt and penetrating injuries to the neck, thorax, and upper abdomen as well as obstruction of the superior vena cava or thrombosis of the left subclavian vein from indwelling central venous catheters, may produce chylothoraces in ICU patients (47).
The patient may be asymptomatic if the effusion is small and unilateral, or may be dyspneic with a large unilateral effusion or bilateral effusions. The pleural fluid is usually milky but can be serous, serosanguineous, or bloody. The fluid may not have a milky appearance if the patient is malnourished or not eating (48). The pleural fluid typically has less than 7,000 nucleated cells/µL which are greater than 80% lymphocytes. The pH is alkaline (7.40–7.80), and the triglyceride levels exceed plasma levels (15). A pleural fluid triglyceride concentration greater than 110 mg/dL makes the diagnosis of chylothorax highly likely, whereas a concentration less than 50 mg/dL makes the diagnosis highly unlikely. With triglyceride concentrations of 50 to 110 mg/dL, lipoprotein electrophoresis is indicated to demonstrate the presence of chylomicrons, which confirms the diagnosis of chylothorax (48).
Up to 2 to 3 L of chyle may drain daily, causing loss of fluid, electrolytes, protein, fat, fat-soluble vitamins, and lymphocytes. Severe nutritional depletion and immunodeficiency may result if these losses are not addressed. In addition to chest tube drainage, initial conservative management consists of intravenous hydration and a nonfat, high-protein, high-calorie diet with medium-chain triglycerides, which are absorbed directly into the portal system, or discontinuing all oral feeding and initiating total parenteral nutrition. If the chylothorax fails to resolve with conservative measures after 7 to 14 days, then surgery with thoracic duct ligation may be considered (44,45), although pleuroperitoneal shunting has also been used.
Congestive Heart Failure
Congestive heart failure (CHF) is the most common cause of all transudative pleural effusions and in one study was the most common cause of pleural effusions in a medical ICU (4). Pleural effusions due to CHF are associated with increases in pulmonary venous pressure. In a study of 37 patients admitted for CHF, the mean pulmonary capillary wedge pressure (PCWP) was higher in patients with pleural effusions than in those without—24.1 versus 17.2 mm Hg, respectively (49). Isolated increases in right heart pressures were not associated with pleural effusions. Patients with chronic obstructive pulmonary disease (COPD) and cor pulmonale, in the absence of left ventricular dysfunction, thus rarely have pleural effusions, and other causes for pleural effusions should be sought in these patients.
Most patients with pleural effusion secondary to CHF have the usual signs and symptoms. The chest radiograph classically demonstrates cardiomegaly and bilateral small to moderate pleural effusions of similar size, with right-sided effusions often being slightly greater than the left. Radiographic evidence of pulmonary edema is usually present, with the severity of pulmonary edema correlating with the presence of effusions. In patients who have been hospitalized, records will usually show intake greater than output for several days, weight gain, an increasing alveolar-arterial O2 gradient, and decreasing compliance in those patients requiring mechanical ventilation. Some patients without a history of CHF may not be suspected of having CHF until intravenous hydration produces pleural effusions and subsequent echocardiograms demonstrate left ventricular dysfunction (4).
Pleural effusions from CHF are transudates and have less than 1,000 nucleated cells/µL, which are mainly mesothelial cells and lymphocytes. Acute diuresis may increase the protein concentration of the pleural fluid and thus change the classification of the fluid from transudative to exudative in 8% to 38% of patients (50). In the afebrile patient with clinical CHF and cardiomegaly with bilateral effusions of relatively equal size on chest radiograph, the diagnosis is reasonably secure and observation is appropriate. In patients who are febrile, have pleuritic chest pain, or are noted on chest radiograph to have effusions of disparate size, unilateral effusions, a larger effusion on the left than the right, or absence of cardiomegaly, thoracentesis should be considered to evaluate for other causes of the effusion(s).
Treatment consists of decreasing preload and improving cardiac output with diuretics, inotropes, and afterload-reducing agents. With appropriate management, the pleural effusions will resolve over days to weeks.
Coronary Artery Bypass Surgery
A small left pleural effusion is virtually always present following coronary artery bypass surgery. The effusion is associated with left lower lobe atelectasis and elevation of the left hemidiaphragm on chest radiograph. A few patients may have moderate to large pleural effusions, which may be bloody (51). These effusions tend to be associated with internal mammary artery grafting, which causes exudation from the bed where the internal mammary artery is harvested.
The pleural fluid is an exudate, may or may not be hemorrhagic, and has a low nucleated cell count, with glucose level similar to serum and a pH greater than 7.40. Rarely, a loculated hemothorax may develop with a trapped lung, resulting in clinically significant restriction (52). If a large effusion that qualifies as a hemothorax is present, the fluid should be drained by chest tube thoracostomy. It is unclear if a large hemorrhagic effusion with a pleural fluid/blood hematocrit less than 50% needs to be drained to avoid later necessity for decortication. Treatment with anti-inflammatory agents and possibly chemical pleurodesis may be required for patients with recurrent nonbloody effusions (51).
Esophageal Rupture
Spontaneous esophageal rupture—Boerhaave syndrome—is a potentially life-threatening event and requires immediate diagnosis and therapy. Esophageal rupture or perforation may rarely occur with blunt thoracic trauma or as a complication of endoscopy and nasogastric/orogastric tube placement. The history in spontaneous esophageal rupture is usually severe retching or vomiting; however, activities that generate a Valsalva maneuver can cause esophageal rupture, and in some patients the perforation may be silent (53). The findings on chest radiograph may vary depending on the time between perforation and obtaining of the chest radiograph, the site of perforation, and integrity of the mediastinal pleura. Mediastinal emphysema is present in less than half of patients and may take 1 to 2 hours to be observed, whereas mediastinal widening may take several hours. Pneumothorax, indicating rupture of the mediastinal pleura, is present in 75% of patients; 70% of pneumothoraces are on the left, 20% are on the right, and 10% are bilateral (54). Pleural effusion, with or without associated pneumothorax, occurs in 75% of patients. A presumptive diagnosis should be confirmed radiographically with an esophagram as soon as possible. Because rapid passage of the contrast in the upright patient may not demonstrate a small perforation, the study should be done with the patient in the appropriate lateral decubitus position.
Pleural fluid findings depend on the degree of perforation and the timing of thoracentesis. Early thoracentesis without mediastinal perforation shows a sterile serous exudate with a predominance of PMNs and a pH greater than 7.30. Amylase of salivary origin appears in the fluid in high concentration following disruption of the mediastinal pleura. With the seeding of the pleural space by anaerobic bacteria, the pH falls rapidly and progressively to approach 6.00. The presence of food particles and squamous epithelial cells in the pleural fluid also suggests esophageal rupture (55). Management is usually operative intervention in conjunction with pleural space drainage and antibiotics. Nonoperative therapy with antibiotics and chest tube drainage alone may be considered in a nontoxic patient with small perforations due to instrumentation.
Esophageal Sclerotherapy
Pleural effusions are found in approximately 50% of patients 48 to 72 hours following esophageal sclerotherapy (56). Effusions may be unilateral or bilateral, with no predilection for side. The effusions tend to be small serous exudates with variable nucleated (38,000–90,000 cells/µL) and red cell counts (126,000 to 160,000 cells/µL) and glucose concentrations similar to serum. The mechanism for development of these effusions is likely extravasation of the sclerosant beyond the esophageal mucosa, resulting in mediastinal and mediastinal pleural inflammation. An effusion that is not associated with fever, chest pain, or signs of perforation is not important clinically, and will usually resolve over several days to weeks without specific therapy. A diagnostic thoracentesis should be performed and an esophagram considered in patients with symptomatic effusions for 24 to 48 hours to exclude empyema and esophageal perforation.
Hemothorax
Hemothorax needs to be differentiated from a hemorrhagic pleural effusion, as the latter can be the result of only a few drops of blood in serous pleural fluid. The arbitrary definition of a hemothorax is a pleural fluid to blood hematocrit ratio greater than 50%. Most hemothoraces result from blunt or penetrating thoracic trauma (57). Hemothorax can also result from invasive procedures, pulmonary infarction, malignancy, and ruptured aortic aneurysms. Anticoagulation therapy or coagulopathy may rarely cause a spontaneous hemothorax. Hemothorax should be suspected in any patient with blunt or penetrating chest trauma with a pleural effusion on chest radiograph. Chest tube thoracostomy with a 28 to 32 French chest tube should be performed in these patients and pleural fluid hematocrit measured. In the patient with suspected iatrogenic or spontaneous hemothorax, thoracentesis should be performed, and if positive, a chest tube should be inserted. Chest tube drainage allows the monitoring of the rate of bleeding, may potentially tamponade the bleeding, and will evacuate the pleural space, thus decreasing the risk of developing empyema or a subsequent fibrothorax (57,58). Indications for surgical exploration vary between clinicians, but general guidelines are hemodynamic instability despite adequate resuscitation, initial drainage greater than 1,500 mL, continued bleeding of greater than 200 mL/hour for 3 consecutive hours, continued bleeding of greater than 1,500 mL/day, and radiographic evidence of significant retained clot (greater than one third of the pleural space).
Hepatic Hydrothorax
Pleural effusions are present in approximately 6% of patients with cirrhosis and clinically apparent ascites (59,60). The effusions result from movement of ascitic fluid through congenital or acquired diaphragmatic defects. Rarely, a hepatic hydrothorax may be found in a patient without clinical ascites but with ascites demonstrated only by US, implying the presence of a large diaphragmatic defect. With a small pleural effusion, the patient may be asymptomatic, whereas with large to massive effusions, the patient may have varying degrees of dyspnea. The chest radiograph usually demonstrates a normal cardiac silhouette and a right-sided pleural effusion in 70% of patients, which can vary from small to massive. Effusions are less commonly isolated to the left pleural space (15%) or are bilateral (15%). The pleural fluid is a serous transudate with a low nucleated cell count and a predominance of mononuclear cells, pH greater than 7.40, a glucose level similar to serum, and an amylase less than serum amylase (15). The diagnosis is substantiated by demonstrating that the pleural fluid and ascitic fluid have similar chemistries. If the diagnosis is still in question, injection of a radionuclide into the ascitic fluid with subsequent detection on chest imaging supports the diagnosis (61).
Treatment of hepatic hydrothorax is directed at resolution of the ascites with sodium restriction, diuretics, and paracentesis. It is not uncommon for the effusion to persist until all of the ascitic fluid is mobilized. If the patient is acutely dyspneic or hypoxemic, therapeutic thoracentesis may be done as a temporizing measure. Chest tube drainage should be avoided, as it can cause infection of the fluid, and the prolonged drainage can lead to volume depletion, protein and lymphocyte depletion, and may precipitate renal failure. Chemical pleurodesis is usually unsuccessful due to rapid movement of ascitic fluid into the pleural space. Transjugular intrahepatic portal systemic shunt (TIPS) has been used to treat symptomatic hepatic hydrothorax refractory to medical management (59,60), as has video-assisted thoracoscopic surgery to patch the diaphragmatic defect followed by pleural abrasion or talc poudrage (62).
Hepatic hydrothorax may occasionally be complicated by spontaneous bacterial empyema (SBE) (63). The formation of SBE is a result of either bacterial translocation from infected ascitic fluid or bacteremia and seeding of a hepatic hydrothorax. The criteria for diagnosing SBE are similar to that for diagnosing spontaneous bacterial peritonitis and include a positive Gram stain, positive pleural fluid culture, or total neutrophil count greater than 500 cells/µL. Treatment of SBE is conservative with antibiotic therapy alone, unless frank pus is present, in which case chest tube thoracostomy should be considered.
Hypoalbuminemia
Many patients admitted to the medical ICU have chronic illnesses and associated hypoalbuminemia. Pleural effusions may be observed when the serum albumin is less than 1.8 g/dL. In one study evaluating the association of pleural effusions with hypoalbuminemia, 3 of 21 (14%) patients with serum albumin less than 2.0 g/dL had pleural effusions (64). Since the normal pleural space has an effective lymphatic drainage system, pleural fluid tends to be the last site of collection of extravascular fluid in patients with low oncotic pressure. It is, therefore, unusual to find a pleural effusion solely due to hypoalbuminemia in the absence of anasarca. The chest radiograph usually shows small to moderate bilateral effusions with a normal heart size. The pleural fluid is a serous transudate with less than 1,000 nucleated cells/µL, predominantly mesothelial cells and lymphocytes. The pH ranges from 7.45 to 7.55, and the glucose level is similar to serum. Diagnosis is presumptive if other causes of transudative effusions are sufficiently excluded. The effusions resolve when the hypoalbuminemia is corrected.
Iatrogenic
Insertion of a central venous catheter or extravascular migration of a central venous catheter can cause a pneumothorax, hemothorax, chylothorax, or transudative pleural effusion (65,66). Extravascular migration of a catheter, occurring in approximately 0.4% to 1.0% of insertions, is more common with insertion into the left subclavian and internal jugular veins due to the horizontal orientation of the left brachiocephalic vein in relation to the superior vena cava (58). The postprocedure chest radiograph should always be assessed for proper catheter placement, with catheter positioning parallel to the long axis of the superior vena cava and tip positioning at the right tracheobronchial angle indicating proper placement (67).
In the conscious patient, acute infusion of intravenous fluid into the mediastinum usually results in chest pain and dyspnea. Depending on the volume and rate of infusion of fluid into the mediastinum, tachypnea, respiratory distress, and cardiac tamponade may occur. The chest radiograph demonstrates the catheter tip in an abnormal position, a widened mediastinum, and unilateral or bilateral effusions. The effusion can have characteristics similar to the infusate (milky if lipid is being given), and may be hemorrhagic and neutrophil predominant due to trauma and inflammation. If a glucose-containing solution is being infused, the pleural fluid to serum glucose ratio is greater than 1.0 (66). The central venous catheter should be removed immediately. Observation is sufficient if the effusion is small. If the effusion is large or causes respiratory distress, thoracentesis or tube thoracostomy should be performed. If a hemothorax is discovered, a chest tube should be placed.
Pancreatitis
Pleural effusions are commonly associated with pancreatitis due to the close proximity of the pancreas to the diaphragm. Pleural effusions have been noted in 3% to 20% of patients with pancreatitis (68). The chest radiograph usually demonstrates a small to moderate left-sided effusion (60%), although effusions may be isolated to the right side (30%) or occur bilaterally (10%) (69). The patient usually presents with abdominal symptoms of pancreatitis. The diagnosis is confirmed by an elevated pleural fluid amylase concentration that is greater than serum, although a normal pleural fluid amylase may be found early in the course of acute pancreatitis. The pleural fluid is an exudate with 10,000 to 50,000 nucleated cells/µL, predominantly PMNs. The pleural fluid pH is usually 7.30 to 7.35, and the glucose level is similar to serum (15).
No specific treatment is necessary for pleural effusions associated with acute pancreatitis. The effusion resolves as the pancreatic inflammation subsides. If the pleural effusion does not resolve in 2 to 3 weeks, pancreatic abscess or pseudocyst should be suspected. Recent studies suggest that the presence of pleural effusions in acute pancreatitis is correlated with increased morbidity and mortality (68,70).
Parapneumonic Effusions and Empyema
Patients with severe community-acquired pneumonia admitted to the ICU and patients who develop nosocomial pneumonia often develop parapneumonic effusions, with progression to empyema being less common. An empyema is defined as the presence of pus in the pleural space, although many clinicians extend the definition to include pleural fluid that has a positive Gram stain for bacteria or a positive bacterial culture. Complicated parapneumonic effusions are defined as pleural effusions that will not respond to antibiotic therapy alone and require drainage for resolution, whereas uncomplicated parapneumonic effusions do not require drainage and respond to antibiotic therapy alone for the underlying pneumonia (71,72,73,74).
The usual presentation is similar to the non-ICU patient with fever, dyspnea, chest pain, purulent sputum, leukocytosis, and a new alveolar infiltrate on chest radiograph. In the elderly, debilitated, or immunosuppressed patient, however, many of these findings may be absent. Although pleural space infections most commonly occur in association with pneumonia, it should also be recognized that pleural space infections may result from thoracic surgery, chest tube placement, penetrating chest trauma, esophageal perforation, mediastinitis, subdiaphragmatic abscesses, spontaneous bacterial peritonitis, and bacteremic seeding of a pre-existing effusion (71).
The pleural fluid protein concentration, nucleated cell count, or percentage of PMNs is not helpful in differentiating a complicated from an uncomplicated effusion. When the effusion is free-flowing, as demonstrated by lateral decubitus views or US, and thoracentesis shows a nonpurulent PMN-predominant exudate with a glucose level greater than 60 mg/dL, lactate dehydrogenase (LDH) less than 1,000 IU/L, and pH greater than 7.20, the patient has a high likelihood of pleural fluid resolution with antibiotics alone over 7 to 14 days (uncomplicated effusion). If pus is aspirated on thoracentesis, the diagnosis of empyema is established and immediate drainage is needed. Most clinicians would also advocate drainage of the effusion if the Gram stain or bacterial culture is positive, regardless of the fluid chemistries. If the pH is less than 7.20 in the absence of a positive Gram stain or culture, or if glucose is less than 40 mg/dL and LDH is greater than 1,000 IU/L, particularly with a loculated effusion, most clinicians would advocate drainage (complicated effusion) (72,73,74,75).
In nonloculated complicated parapneumonic effusions and empyemas, drainage can be accomplished by standard chest tube thoracostomy or image-guided percutaneous catheters. Controversy exists concerning the optimal treatment of multiloculated parapneumonic pleural effusions, and it is beyond the scope of this chapter to discuss each approach in detail. Single chest tubes or multiple blindly placed chest tubes are unlikely to be successful. Potential strategies include image-guided catheters with intrapleural fibrinolytic agents or video-assisted thoracic surgery (VATS) as initial therapy (72,73,74,75,76,77,78,79,80). If these measures fail, then empyemectomy and decortication will be required. In the absence of Gram stain or cultures to direct antibiotic therapy, broad-spectrum antibiotics should be used initially. Empyemas are often mixed infections, including anaerobes, and a regimen that includes coverage for anaerobes should be chosen. Aminoglycosides may have poor clinical activity in empyemas and probably should not be used (81).
Postcardiac Injury Syndrome
Postcardiac injury syndrome (PCIS) is characterized by the onset of fever, pleuropericarditis, and parenchymal infiltrates typically 3 weeks (2 to 86 days) following injury to the myocardium or pericardium (82,83). PCIS has been reported following myocardial infarction, cardiac surgery, blunt chest trauma, and pacemaker implantation. The incidence following myocardial infarction has been estimated at up to 4% and up to 30% following cardiac surgery. Based on available data, it appears that PCIS results from an autoimmune reaction following myocardial or pericardial injury (84).
Pleuritic chest pain is reported by virtually all patients, whereas one half of patients will be noted to have dyspnea, fever, pericardial rub, and rales. Half of the patients have a leukocytosis, and almost all have an elevated erythrocyte sedimentation rate. The chest radiograph is abnormal in most patients, with the most common abnormality being left-sided and bilateral pleural effusions (83). Pulmonary infiltrates are present in 75% of patients and are most commonly seen in the left lower lobe (82). The pleural fluid is a serosanguineous or bloody exudate with pH greater than 7.30 and glucose level greater than 60 mg/dL. Nucleated cells range from 500 to 39,000 cells/µL, with a predominance of PMNs early in the course (15). The finding of pericardial fluid on echocardiogram suggests PCIS. The diagnosis is made clinically after pulmonary embolism and parapneumonic effusion have been excluded. An antimyocardial antibody titer in pleural fluid greater than in serum further supports the diagnosis (85).
PCIS is usually self-limited and may not require treatment if symptoms are minor. PCIS usually responds to aspirin or nonsteroidal anti-inflammatory agents, although some patients may require corticosteroids for resolution. Following treatment, the pleural effusion resolves within 1 to 3 weeks. It is important to not misdiagnose PCIS as a pulmonary embolism, as anticoagulation therapy may lead to pericardial hemorrhage and tamponade.
Pulmonary Embolism
Pleural effusions occur in up to 50% of patients with pulmonary embolism (86). The pathogenesis of pleural effusions in pulmonary embolism includes ischemia and inflammatory mediator-induced increased pleural capillary permeability, imbalance in microvascular and pleural space hydrostatic pressures, pleuropulmonary hemorrhage, and atelectasis. With pulmonary infarction, necrosis and hemorrhage into the lung and pleural space may result. More than 80% of patients with pulmonary infarction will have bloody pleural effusions, while up to 40% of patients without radiographic evidence of infarction will also have hemorrhagic fluid (86). Ipsilateral pleuritic chest pain occurs in most patients with pleural effusions complicating pulmonary embolism. A coexistent pulmonary infiltrate is noted on chest radiograph in approximately half of patients with pulmonary embolism and pleural effusion.
Pleural fluid analysis is variable and may demonstrate either an exudate or a transudate (15,87). A bloody pleural effusion in the absence of chest trauma, recent cardiac injury, asbestos exposure, or malignancy should increase the suspicion of pulmonary embolism (88). The pleural fluid is hemorrhagic in two thirds of patients, although the number of red blood cells exceeds 100,000 cells/µL in less than 20% (15). The nucleated cell count ranges from less than 100 (presumably atelectatic transudates) to 50,000 cells/µL (pulmonary infarction). When thoracentesis is performed near the time of acute symptoms, PMNs are predominant; with later thoracentesis, lymphocytes represent the majority of cells, and eosinophils may be present as well. The effusion from pulmonary embolism is usually apparent (92%) on the initial chest radiograph and reaches a maximum volume during the first 72 hours. In patients who demonstrate progression of effusions after 72 hours of therapy, recurrent embolism, hemothorax secondary to anticoagulation, an infected infarction, or an alternative diagnosis should be considered. The effusions usually resolve in 1 week in the absence of an infiltrate on chest radiograph. When an infiltrate is present, presumably representing a pulmonary infarction, the resolution time is longer, typically 2 to 3 weeks (86).
The association of a pleural effusion with pulmonary embolism does not alter therapy. The presence of a bloody effusion is not a contraindication to full-dose anticoagulation, since hemothorax is a rare complication of heparin therapy for pulmonary embolism (89,90). An enlarging pleural effusion on therapy necessitates thoracentesis to exclude hemothorax, empyema, or another cause. The development of a hemothorax during therapy requires discontinuation of anticoagulation, chest tube thoracostomy, and placement of a vena cava filter.
Uremia
Uremic pleural effusions have been reported in 3% to 5% of patients undergoing chronic dialysis (91). In one study evaluating the cause of pleural effusions in 100 patients requiring long-term hemodialysis, uremic pleurisy accounted for 16% of cases (92). Patients may manifest fever, cough, chest pain, and pleural friction rubs. The chest radiograph usually shows a moderate unilateral effusion, although massive and bilateral pleural effusions have been reported (93,94,95). The pleural effusion is a serosanguineous or bloody exudate, with less than 1,500 nucleated cells/µL, predominantly lymphocytes. The creatinine concentration is high, although the pleural fluid to serum creatinine ratio is less than 1.0, unlike in urinothorax (15). The effusions generally resolve with continued dialysis over several weeks but may recur. Uremic pleuritis may cause pleural fibrosis and restriction, requiring decortication in some patients (96,97).
Pneumothorax in the Intensive Care Unit
Pneumothorax, defined as accumulation of air in the pleural space, represents one form of extra-alveolar air. Other forms of extra-alveolar air include pulmonary interstitial emphysema, pneumomediastinum, pneumopericardium, pneumoperitoneum, pneumoretroperitoneum, and systemic air embolism. Three pathologic processes may give rise to extra-alveolar air: (1) generation by gas-forming micro-organisms during an infectious process, (2) direct introduction following trauma to cutaneous or mucosal barriers, and (3) alveolar rupture due to pressure gradients between alveoli and the surrounding interstitial space (barotrauma) (98).
The mechanisms of spontaneous generation of extra-alveolar air were first delineated by Macklin and Macklin (99). In situations in which intra-alveolar pressure is increased, a gradient is produced between the alveolus and the adjacent vascular sheath, causing the alveoli to rupture at their bases. Following rupture, air is introduced in the perivascular adventitia, resulting in interstitial emphysema. The air then dissects proximally to the lung hilum and mediastinum due to a lower mean pressure in the mediastinum compared to that of the lung parenchyma. Once in the mediastinum, the accumulated air may decompress along paths of least resistance into the subcutaneous tissues or, less commonly, into the pericardium, peritoneum, and retroperitoneum. If mediastinal pressure increases abruptly or if decompression via these routes is not sufficient, the mediastinal parietal may rupture, resulting in pneumothorax. Alternatively, air from ruptured alveoli may dissect to the periphery of the lung and rupture via subpleural blebs through the visceral pleura into the pleural space (100).
Pneumothoraces are classified as spontaneous, which occur without preceding trauma or other obvious causes, and traumatic, which occur as a result of direct or indirect trauma to the chest. Spontaneous pneumothoraces can be subdivided into primary spontaneous, which occur in otherwise healthy patients without clinical lung disease, and secondary spontaneous, which occur in patients with underlying lung disease. Traumatic pneumothoraces can be subdivided into the categories of iatrogenic and related to blunt or penetrating chest trauma. In addition, pneumothoraces can be classified as simple or complicated, with complicated pneumothoraces consisting of tension pneumothorax, hemopneumothorax, pyopneumothorax, and open pneumothorax in which the integrity of the chest wall is disrupted. The potential causes of pneumothoraces in critically ill patients are listed in Table 144.2. We will focus mainly on iatrogenic pneumothoraces and pneumothoraces resulting from barotrauma, as these are the most common causes of pneumothoraces in ICU patients.
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Table 144.2 Causes of Pneumothoraces in ICU Patients |
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Radiologic Evaluation
The radiographic signs of pneumothorax in the supine patient frequently differ from the classic visceral pleural line seen on erect views. In a review of 88 critically ill patients with 112 pneumothoraces, only 22% of pneumothoraces were in the classic apicolateral location (101). In this same study, 30% of pneumothoraces were not detected initially, and of these, half progressed to a tension pneumothorax. The anteromedial position is the most common location for pneumothoraces in the supine patient since this area is the least dependent pleural recess (102). With anteromedial collections of air above the level of the pulmonary hilum, the lucency sharply outlines adjacent vascular structures such as the ascending aorta, superior vena cava, and azygous vein. Below the hilum, the lateral cardiac borders are sharply outlined and paralleled by zones of radiolucency. Increased lucency in the region of the anterior cardiophrenic sulcus may also result from air below the hilar level (102).
In addition to the anteromedial and apicolateral locations, pneumothoraces in supine patients can also occur in the subpulmonic and posteromedial locations (101). A subpulmonic pneumothorax may be recognized as a basilar hyperlucency, most commonly in the left hemithorax (103,104). A pleural line defining the base of the lung may be apparent in some cases, allowing for diagnosis of pneumothorax. Other features that may help in the recognition of a subpulmonic pneumothorax include lucency extending deep into the costophrenic sulcus (deep sulcus sign), depression of the hemidiaphragm, and visualization of an unusually distinct cardiac apex (105,106).
An erect or decubitus radiograph should be obtained if possible to confirm or refute the presence of a pneumothorax. In problematic cases, CT or US can be diagnostic. Several studies have demonstrated the presence of pneumothoraces on CT that were not apparent or not appreciated on conventional radiographs (14,107). Occasionally, a pneumothorax may be confused with a large bulla in patients with COPD and other pulmonary diseases that generate cystic changes. In these instances, a CT may be helpful in making the correct diagnosis (100). If the patient is too unstable to obtain a CT, bedside US can be used to evaluate for the presence of a pneumothorax by determining the presence or absence of “lung sliding.” In patients without pneumothorax, the lung–chest wall interface, which represents a to-and-fro movement synchronized with respiration, can be identified. In one study, the disappearance of lung sliding was 95% sensitive for detecting pneumothorax, although false positives did occur (108).
Primary and Secondary Spontaneous Pneumothorax
Patients with pneumothorax have a decrease in vital capacity and an increase in the alveolar-arterial oxygen gradient, with hypoxemia being present in some patients. The hypoxemia is thought to be secondary to development of both anatomic shunts and areas of low ventilation/perfusion in the atelectatic lung. Patients with primary spontaneous pneumothorax rarely require admission to the ICU, as the contralateral lung can maintain the necessary alveolar ventilation and hypoxemia can be managed with supplemental oxygen. Patients with secondary spontaneous pneumothoraces may need ICU admission because the gas exchange abnormality caused by the pneumothorax is superimposed on pre-existing gas exchange abnormalities and, thus, severe hypoxemia can occur. Patients with secondary spontaneous pneumothoraces are more likely to develop hypercapnic respiratory failure than are patients with primary spontaneous pneumothorax (109,110).
Iatrogenic Pneumothorax
Insertion of central venous catheters (CVC) is the most common cause of iatrogenic pneumothoraces in the ICU. In two studies of mechanical complications of central venous catheters, 1.1% of 534 patients and 1.0% of 713 patients suffered a pneumothorax (111,112). Cannulation of the subclavian vein is associated with a higher risk of pneumothorax than cannulation of the internal jugular vein (113,114). Most pneumothoraces occur at the time of the procedure from direct lung puncture, but delayed pneumothoraces have been noted. Bilateral pneumothoraces have been reported to occur from unilateral cannulation attempts (115). A postprocedure chest radiograph should be obtained following placement of a central venous catheter, regardless of the site cannulated, to assess for pneumothorax and proper catheter tip position.
Cardiopulmonary resuscitation has been reported as a cause of iatrogenic pneumothorax. Pneumothorax in this setting may arise either from barotrauma as a consequence of bag-ventilation or from rib fractures sustained during the resuscitation. Hillman and Albin (116) described three patients who developed subcutaneous emphysema and pneumothoraces, one of whom had bilateral pneumothoraces following cardiopulmonary resuscitation with bag-ventilation. Shulman et al. (117) reported two patients in whom barotrauma was observed following resuscitation. One of the patients was ventilated with an Ambu-bag whereas the other was ventilated with a positive pressure demand valve. Other cases of pneumothorax related to cardiopulmonary resuscitation or malfunctioning valves in self-inflating bags have been reported (118,119).
Based on these observations, a chest radiograph should be obtained on all patients after a successful resuscitation to evaluate for pneumothorax. During cardiopulmonary resuscitation, if the patient is difficult to ventilate, subcutaneous emphysema is noted, or pulseless electrical activity (electromechanical dissociation) is present, the diagnosis of pneumothorax, particularly tension pneumothorax, should be suspected. In a study analyzing postmortem chest radiographs, only 40 of 77 patients had been clinically diagnosed as having a pneumothorax. In this study, procedures most frequently associated with pneumothorax were mechanical ventilation and cardiopulmonary resuscitation. Rib fractures were noted in 23 of the 77 cases (120).
Pneumothoraces may rarely occur following endotracheal intubation, usually due to rupture of the posterior membranous portion of the trachea (121). In a prospective study of translaryngeal intubation in 297 critically ill patients in a teaching hospital, pneumothorax occurred in 1% of patients (122). Pneumothoraces may also result from tracheostomy, either from open procedures or bedside percutaneous dilatational tracheostomy (123). The incidence of pneumothorax after tracheostomy in adults has been reported to be between 0% and 4% (124).
Bronchoscopy in critically ill patients may also cause pneumothoraces. The risk is higher when transbronchial biopsies are obtained, although the degree of increased risk compared to nonventilated patients and the influence of high airway pressures and positive end-expiratory pressure (PEEP) is unknown. It should be recognized that performing bronchoalveolar lavage (BAL) alone may produce a pneumothorax (125,126,127).
Pneumothorax Associated with Mechanical Ventilation
Pneumothorax is a frequent, potentially lethal complication of mechanical ventilation. The pathogenesis of pneumothorax associated with mechanical ventilation—barotrauma—is related to the decompression of extra-alveolar air contained in the mediastinum through the mediastinal pleura or rupture of subpleural blebs through the visceral pleura, as previously described. Conditions associated with an increased risk of pneumothorax while patients undergo mechanical ventilation include ARDS, COPD, asthma, fibrotic lung diseases, aspiration pneumonia, necrotizing pneumonia, and right mainstem bronchus intubation (100).
More recently conducted studies in mechanically ventilated patients with acute lung injury or ARDS have reported pneumothorax occurrence rates between 7% and 42% (128,129,130,131,132,133). The relationship of barotrauma and pneumothoraces to ventilatory pressures in patients with ARDS continues to be debated given earlier studies that suggested a causal relationship. Gammon et al. (128) observed that of 139 patients requiring mechanical ventilation for various diagnoses, the group with pneumothoraces had higher peak inspiratory pressure (PIP) (55 vs. 44 cm H2O) and levels of PEEP (7.7 vs. 3.3 cm H2O). When patients with ARDS and those with other diagnoses were analyzed separately, however, no differences in airway pressures were found between patients with and without pneumothoraces. In a subsequent study by Gammon et al. (129) of 168 patients, trends toward higher airway pressures were observed; however, multivariate analysis revealed that only the presence of ARDS was independently correlated with the development of a pneumothorax. Weg et al. (131), in their study of 725 patients with ARDS, observed no differences in PIP, mean airway pressure, levels of PEEP, or delivered tidal volumes between patients who had a pneumothorax and/or air leak and those who did not. In the study by Amato et al. (132), however, the pneumothorax rate in conventionally ventilated patients with a tidal volume of 12 mL/kg and average plateau pressure of 38 cm H2O was 42% compared to patients ventilated with a lung protective strategy with a tidal volume of 6 mL/kg and average plateau pressure of 24 cm H2O.
The patient requiring mechanical ventilation usually becomes symptomatic after developing a pneumothorax because of the underlying lung parenchymal disease, and this complication should be suspected whenever a sudden clinical deterioration occurs. If conscious, the patient becomes dyspneic and tachypneic and may become dyssynchronous with the ventilator; worsening oxygenation is often seen. Peak inspiratory pressures may increase with a coexisting decrease in lung compliance. A significant percentage of patients will develop a tension pneumothorax. A heightened suspicion for development of a pneumothorax should be maintained in patients who exhibit other forms of barotrauma, such as subcutaneous emphysema, pneumomediastinum, and subpleural air cysts.
Tension Pneumothorax
A tension pneumothorax occurs when intrapleural pressure exceeds atmospheric pressure throughout expiration, and often inspiration as well. This develops when a break in the visceral or parietal pleura produces a one-way valve that is open during inspiration, allowing air to enter the pleural space, but is closed during expiration, preventing the egress of air collecting in the pleural space (92). Tension pneumothoraces most commonly develop as a complication of mechanical ventilation—barotrauma or volutrauma—or as a result of blunt and penetrating thoracic trauma, although tension pneumothoraces can occur in 1% to 4% of patients with spontaneous pneumothoraces (134,135). Attempts at CVC placement in patients receiving positive pressure ventilation may also cause tension pneumothoraces, with delayed presentations having been reported (136). It is important to consider the presence of a tension pneumothorax in the differential diagnosis of a patient with pulseless electrical activity (electromechanical dissociation) undergoing cardiopulmonary resuscitation (CPR).
Tension pneumothorax usually presents as an acute cardiopulmonary emergency beginning with respiratory distress and, if unrecognized and untreated, progresses to cardiovascular collapse and death. Conscious patients with tension pneumothorax appear acutely ill with dyspnea, tachypnea, tachycardia, diaphoresis, and cyanosis. Patients with tension pneumothorax often exhibit decreased ipsilateral breath sounds, hyperresonance to percussion, distended neck veins, tracheal deviation to the contralateral side, and hypotension. Caveats to the aforementioned findings are that severe parenchymal disease or airway obstruction, coupled with the noise generated by ventilator cycling, may cause difficulty in appreciating differences between the hemithoraces, and distension of the neck veins may not be present in patients who are volume depleted. The absence of physical exam findings does not completely exclude the diagnosis of a tension pneumothorax. In the unconscious or critically ill patient, worsening oxygenation may be one of the earliest signs. Increases in airway peak and plateau pressures and decreases in compliance are often observed in mechanically ventilated patients. During hand bagging of the patient, increased pressure requirements to deliver breaths and difficulty in delivering adequate tidal volume may be noted. Increases in pulmonary artery diastolic pressures may be seen in patients who have a Swan-Ganz catheter in place (137).
On the chest radiograph in a patient with tension pneumothorax, in addition to the pneumothorax, there is often shift of the trachea and mediastinum to the contralateral side, ipsilateral diaphragmatic depression, and increased distance between contiguous ribs compared to the unaffected side. It should be emphasized, however, that tension pneumothorax is a clinical diagnosis, and these radiographic findings may be observed in patients without physiologic evidence of a tension pneumothorax. It should also be noted that patients may have cardiopulmonary compromise due to a tension pneumothorax without observing tracheal or mediastinal shift on chest radiograph (138,139).
In one study of 16 ARDS patients with tension pneumothorax, only 5 patients had subtle mediastinal shift (138). Of these 16 patients, 11 had flattening of the diaphragm and 8 had depression of the diaphragm. Diaphragmatic abnormalities may therefore be a more sensitive indicator of tension pneumothorax in patients with ARDS. In 15 of the 16 patients, the location of a loculated tension pneumothorax was subpulmonic or paracardiac. Potential explanations for these observations include the presence of adhesions between the parietal and visceral pleura, as documented in patients with ARDS, which prevent lung collapse and spread of air throughout the pleural space. In addition, the noncompliance of lungs in patients with ARDS may prevent collapse of the ipsilateral lung and compression of the contralateral lung, allowing a small volume of air to significantly increase intrapleural pressure (138,139).
It is important to note that patients with ARDS can develop tension pneumothoraces despite the presence of a chest tube on the ipsilateral side being placed for a previous pneumothorax (138,139,140,141). In the 16 patients reported by Gobien et al. (138) and the 3 patients reported by Ross et al. (139), all patients had a functional ipsilateral chest tube and had localized pneumothoraces. In a study by Heffner et al. (140), 14 patients had recurrent pneumothoraces despite ipsilateral chest tubes, with 9 of the 14 having tension pneumothoraces. In the latter study, 12 of the 14 chest tubes had horizontal as opposed to vertical placement on chest radiograph. The chest tubes in all 9 patients with tension pneumothoraces had horizontal placement. Seven of the 14 patients had subsequent CT scans, with the finding that all 7 chest tubes were placed within interlobar fissures. Thus, chest tubes placed into interlobar or posterior locations may not drain anterior gas loculations, the most common location of pneumothoraces in ARDS patients (101,142), allowing for development of localized tension pneumothoraces. In the patient reported by McConaghy and Kennedy (141), the chest tube was intraparenchymal.
Management of Pneumothoraces and Tension Pneumothoraces
Most critically ill patients in the ICU will have poor cardiopulmonary reserves and may be unable to tolerate a pneumothorax, even in the absence of tension physiology. In nonventilated patients who are hemodynamically stable and have adequate oxygenation and ventilation, simple pneumothoraces that occur as a result of a procedure and are small may reasonably be managed with close observation and monitoring with serial radiographs. Patients with secondary pneumothoraces who require ICU care will usually require chest tube placement because of their poor pulmonary reserve. Patients who are not receiving positive pressure ventilation, but are hemodynamically unstable, should be treated with chest tube thoracostomy, since the additive effects of development of hypoxia or early tension physiology could quickly precipitate cardiopulmonary arrest.
In general, chest tube thoracostomy should be performed in mechanically ventilated patients with a pneumothorax of any size given the significant risk of progression to a tension pneumothorax. Attempts to decrease plateau airway pressures, tidal volumes, and PEEP should be considered if possible after development of a pneumothorax in patients receiving mechanical ventilation. Controlled hypoventilation with the use of neuromuscular blockers or deep sedation may be required in some patients to achieve these goals. For patients with ARDS and recurrent pneumothoraces, the chest tube attempts should be made to place anteriorly where the loculation is most likely to occur. In those patients with recurrent pneumothoraces who are stable for transport to the radiology department, we advocate the use of CT-guided percutaneous drainage, as blind placement of chest tubes into loculi may be difficult (143,144). When extra-alveolar gas is observed in the absence of a pneumothorax, similar attempts to decrease plateau pressure, tidal volume, and PEEP should be considered. No evidence exists that placement of “prophylactic” chest tubes will prevent these patients from suffering a subsequent pneumothorax. These patients should be closely monitored for development of a tension pneumothorax, and equipment to perform an emergent bedside tube thoracostomy should be available.
The development of a tension pneumothorax represents a medical emergency, and the deteriorating patient should be treated based on clinical presentation without waiting for radiographic confirmation. In one series of 74 patients with tension pneumothorax, a diagnosis was made clinically in 45 patients (61%), and these patients had an attributable mortality of 7%. In the remaining 29 patients, diagnosis was delayed between 30 minutes and 8 hours; 31% of these patients died of pneumothorax (145). If a chest tube is not immediately available, a large-bore needle or intravenous catheter should be inserted into the pleural space through the second intercostal space at the midclavicular line. Escape of air from the needle confirms the diagnosis. After decompression, the needle or catheter should be left in place and in communication with the atmosphere until definitive chest tube thoracostomy is performed. As previously mentioned, a high index of suspicion for tension pneumothorax should be maintained for patients who are in cardiac arrest and exhibit pulseless electrical activity.
Bronchopleural Fistula in the Intensive Care Unit
A bronchopleural fistula (BPF) represents a communication between the bronchial tree and the pleural space. Bronchopleural fistulae (BPFs) most commonly result from surgical procedures including pneumonectomy, segmentectomy, and wedge resections of the lung, with an incidence of 1.6% to 6.8% (146). The mortality in patients with BPFs following surgical resection is reported to be between 23% and 71%, usually due to infectious complications (146,147,148). BPFs may also result from blunt or penetrating chest trauma, pulmonary infarction, and as a complication of pulmonary and pleural infections such as tuberculosis, necrotizing pneumonia, lung abscess, or empyema (149,150). Last, BPFs may result as a complication of mechanical ventilation for acute respiratory failure, particularly in patients with ARDS, and, as such, represent a form of barotrauma/volutrauma (149,151). For this discussion, we will focus primarily on BPFs in the setting of patients requiring mechanical ventilation.
BPF in the ventilated patient is defined as an air leak that persists for more than 24 hours following placement of a chest tube. BPFs in patients receiving mechanical ventilation may present acutely with the development of a pneumothorax, with or without tension, or with sudden expectoration of potentially infected material from the pleural space, with flooding of the ipsilateral and contralateral airways leading to respiratory compromise.
Several potential adverse effects of a BPF in the mechanically ventilated patient have been noted. Depending on the size of the fistula, flow resistance through the fistula versus the airways and lung parenchyma, and pressure gradient between the airways and pleural space, air may be redirected from normal intrapulmonary routes to the BPF (152). This can cause loss of effective tidal volume, which may lead to difficulty in oxygenating and ventilating the patient and subsequent development of life-threatening hypoxemia and respiratory acidosis (151). If incomplete lung expansion due to the BPF is present, ventilation/perfusion mismatching and shunt may occur. There may be difficulty in maintaining PEEP with further decrements in oxygenation (153,154). If a high level of chest tube suction is used, the negative pressure may be transmitted to the proximal airways, causing inappropriate ventilator cycling (153,155). Last, BPFs may cause pleural space infection or contamination of the airways.
The amount of air flow through a BPF is typically estimated by subtracting the expired tidal volume from the inspired tidal volume as measured by the ventilator. This method, however, becomes increasingly inaccurate as the size of the leak decreases, particularly when the size of the leak is less than 200 mL/breath (156). More accurate, albeit cumbersome, methods have been developed to quantify the amount of flow through a BPF (157,158,159,160). Air flows through BPFs have been reported up to 22 L/min (157). It has been recognized that the air escaping from a BPF does not flow passively from the airways into the pleural space, but instead participates to some degree in physiologic gas exchange. In two studies evaluating CO2 excretion by BPF in 15 patients, the percent of minute ventilation lost through the BPF ranged from 4% to 53%, with 3% to 44% of CO2 excretion occurring via the BPF (161,162).
The development of a BPF has been regarded as a serious and life-threatening complication of mechanical ventilation. In one of the largest series reported—1,700 consecutive patients receiving mechanical ventilation—Pierson et al. (163) observed that 39 (2.3%) patients developed a BPF. In that study, overall mortality in patients with BPF was 67%. Mortality was higher in patients who developed a BPF late in their illness (94%) than when it occurred within 24 hours of admission (45%). Patients with air leaks greater than 500 mL/breath had a mortality of 100% compared with a mortality of 57% in patients with air leaks less than 500 mL/breath. Mortality was also higher in patients with ARDS than in patients without—81% versus 50%—and in patients with pleural space infections compared to those without said infection—87% versus 54%. A more recent ARDS study by Weg et al. (131), however, suggested that mortality was not different between patients with or without air leaks, 46% versus 39%, respectively. In that study, however, the duration of mechanical ventilation was 4.3 ± 1.3 days, which may not be typical for many patients with BPF, and the subset of patients with BPF was not analyzed separately. It may be that the presence of a BPF is a marker for severity of lung injury and by itself does not directly contribute to mortality.
Management of Bronchopleural Fistulae
Numerous interventions, listed in Table 144.3, have been proposed in the management of BPFs. Many of these are based on the concept of decreasing the pressure gradient between the airways and the pleural space, with decreased air flow through the fistula allowing for earlier closure. Although the various manipulations theoretically make sense, they have not been evaluated in controlled trials. The suggested changes in ventilator settings may actually worsen oxygenation and ventilation in some patients with ARDS. We will discuss those interventions for which some data are available in the following sections. In the absence of difficulty oxygenating or ventilating the patient, it is unknown if active measures to close the BPF affects outcome. Definitive therapy for BPFs includes surgical procedures such as bronchial stump closure with thoracoplasty, myoplasty, or omentoplasty, or completion pneumonectomy (146,148). Unfortunately, most critically ill patients will not be sufficiently stable to undergo these procedures and must be managed medically. Adequate pleural space drainage, antibiotic therapy for pleural space infections, and support of nutritional status is vital in these patients.
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Table 144.3 Potential Options for Management of Bronchopleural Fistula in Mechanically Ventilated Patients |
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Adequate chest tube drainage and full expansion of the lung should be assessed in patients with BPF. An appropriately sized chest tube should be placed, recognizing that air flow through a chest tube is inversely proportional to the length and radius to the fifth power of the tube. It has been suggested that a tube with an internal diameter of 6 mm (18 Fr) is the smallest acceptable size because it will allow a maximum possible flow rate of 15 L/minute at -10 cm H2O (164). Our preference is to use at least a 28 Fr chest tube in these patients. Placement of additional chest tubes or CT-guided percutaneous catheters—if the pleural space is complicated—should be considered if the lung is not fully expanded. As with the chest tube, resistance to flow of air through a chest tube drainage system may need to be considered. In an animal model of BPF, when the size of air leak reached 4 to 5 L/minute, the Thora-Klex and Sentinel Seal systems become clinically impractical. The Pleur-Evac system can handle flow rates up to 34 L/minute, although its use with rates greater than 28 L/min is impractical due to intense bubbling in the control chamber. The Emerson pump, which can be set to deliver chest tube suction greater than -20 cm H2O, is capable of handling air flows up to 35 L/min and is the system of choice for BPFs with extremely high flow rates (164).
Manipulation of the level of chest tube suction may affect BPF air flow, and some authors have suggested using the least amount of suction that maintains lung inflation (151,152). An animal model demonstrated that increasingly negative intrapleural pressures increased air flow in large BPFs but had no effect on small BPFs (165). Roth et al. (160) reported that increasing chest tube suction from 0 to 22.5 cm H2O increased BPF flow in a patient from 24.6 to 26.7 L/minute. In a study of six patients by Powner et al. (158), increasing chest tube suction from 0 to 25 cm H2O increased BPF flow in two patients, had no effect in two patients, and decreased flow in two patients. To decrease air loss through the BPF and applied PEEP, some investigators have applied PEEP to the chest tube (154,166,167), while others have devised systems to synchronously occlude the chest tube during inspiration (168,169). A lack of success using these methods has been noted by other investigators, however (163). These techniques may pose a risk of increasing the size of the pneumothorax or causing a tension pneumothorax; thus, the patient should be closely monitored.
The goals of mechanical ventilation in patients with a BPF are to maintain adequate oxygenation and ventilation while reducing fistula flow. In general, strategies for conventional mechanical ventilation that limit airway pressure and tidal volumes may reduce the amount of air flow escaping through the BPF and allow the fistulous site to heal. As such, it has been recommended to use the lowest possible tidal volume, fewest mechanical breaths per minute, lowest level of PEEP, and shortest inspiratory time.
Alternative methods of mechanical ventilation have been used in a few patients. High-frequency jet ventilation (HFJV) and high-frequency oscillatory ventilation (HFOV) have been used based on the principle that lower airway pressures may be generated in these modes of ventilation and should, therefore, decrease BPF air flow. In one animal model of BPF, an increase in fistula flow was seen with increasing mean airway pressures, and effects on flow were similar whether mean airway pressure was changed by manipulating peak inspiratory pressure, PEEP, or inspiratory:expiratory (I:E) ratios (165). In another animal model, a nonsignificant trend toward increasing BPF flow with increasing peak inspiratory pressures, and a significant increase in BPF flow with increasing PEEP was observed (170).
Several studies comparing HFJV and HFOV with conventional ventilation using animal models have shown less BPF air flow during HFJV and HFOV (171,172,173,174), although one study using HFJV demonstrated no difference (175). In studies reporting blood gases, improved oxygenation was seen during HFJV and HFOV compared with conventional ventilation (172,173,174). Increasing levels of PEEP were also noted to increase BPF flow in two studies (171,175). It is problematic to extrapolate these studies to patients in the ICU because the animal models were cannulated in more proximal bronchi and the lung parenchyma was relatively normal.
HFJV has been used successfully in BPF patients failing conventional therapy (176,177,178,179,180). The two case series comparing the use of HFJV with conventional ventilation have reported disappointing results. In one study, HFJV was of clinical value in only two of the seven patients (159). In that study, no change in the air leak was observed in three patients; one had an unacceptable decline in oxygenation, and one patient disliked the sensation of HFJV and refused further therapy. In the other series of seven patients, no significant decrease in BPF flow was seen, while three patients had an increase in the air leak despite a decrease in peak airway pressures (181). Oxygenation deteriorated in six of the seven patients when switched to HFJV.
Other modes of mechanical ventilation have also been used in patients with BPF. Case reports have reported independent lung ventilation to be of benefit (182,183,184). Case reports of combining independent lung ventilation with high-frequency, low tidal volume ventilation of the affected lung (185) and HFJV of the affected lung have been published (186,187). Differential lung ventilation using a single ventilator and a variable resistance valve attached to one lumen of a bifurcated endotracheal tube has also been described (188,189). Discussion of the techniques of independent lung ventilation and its attendant difficulties is beyond the scope of this chapter, and the reader is referred to other reviews (190,191).
Because many critically ill patients are unable to tolerate a major thoracic procedure, bronchoscopic techniques may provide viable alternatives for closure of BPFs. Endobronchial occlusion of BPFs has been reported with cyanoacrylate-based tissue adhesives (Histoacryl, Bucrylate), fibrin sealants (Tisseal, Hemaseal, thrombin plus fibrinogen or cryoprecipitate), absorbable gelatin sponge (Gelfoam), vascular occlusion coils, doxycycline and blood, Nd:YAG laser, silver nitrate, and lead shot (192,193,194). The agent initially seals the leak by acting as a plug and subsequently induces an inflammatory process with fibrosis and mucosal proliferation, permanently sealing the area. Of these techniques, the uses of cyanoacrylate tissue adhesives and fibrin sealants have been most widely reported. Airway stents may be used to cover and seal the fistula in selected patients depending on the location of the fistula. BPFs due to breakdown of a stump after lobectomy or pneumonectomy, or bronchial dehiscence after lung transplantation or bronchoplastic procedures are the most amenable to successful closure with airway stenting. More recently, the successful closure of BPFs using bronchoscopic placement of endobronchial valves designed for emphysema has been described (195,196,197).
Pleurodesis with various agents has also been tried to effect closure of BPFs. Autologous “blood patch” pleurodesis has been described to be effective in some patients (198,199,200). Pleurodesis with fibrin glue has also been reported (201,202). However, none of these patients was undergoing mechanical ventilation at the time of pleurodesis.
Complications of Thoracentesis and Chest Tube Thoracostomy
Thoracentesis
The most common complication of diagnostic or therapeutic thoracentesis is pneumothorax. The rate of pneumothorax with blind thoracentesis in nonventilated patients has been reported to be between 4% and 30% in prospective studies (16,17,18,19,20). As previously noted, the 5% to 10% rate of pneumothorax in mechanically ventilated patients undergoing blind thoracentesis is similar to that of nonventilated patients (21,22,23). Pneumothorax may be more common following therapeutic thoracentesis than diagnostic thoracentesis, although this was not confirmed in other studies. The incidence of pneumothorax following thoracentesis appears to be less with ultrasound guidance in both nonventilated and mechanically ventilated patients (6,7,8,20,24). Hemothorax has been reported in 0.8% and 1.2% of patients (17,203). Other infrequent complications with an incidence less than 1% include laceration of intercostal vessels, liver and splenic puncture, intra-abdominal hemorrhage, catheter shearing with retained catheter in the pleural space, and systemic air embolism (17,18,203).
Chest Tube Thoracostomy
The complication rate for chest tube placement, excluding recurrent pneumothorax, is low, ranging from 1% to 3% when placed for acute trauma (204,205,206). Reported complications in these studies were empyema (1%–3%), lung parenchyma perforation (0.2%–0.6%), diaphragmatic perforation (0.4%), and subcutaneous placement (0.6%). In an analysis of 126 chest tube placements by pulmonologists at a teaching hospital, the complication rate was 11%, although 10 of the 14 reported complications were related to clotting, kinking, or dislodgment of the chest tube (207). Pulmonary laceration was reported in one patient (0.8%), and subcutaneous placement was noted in one patient (0.8%).
In addition to empyema, chest tube malposition is the most common complication of chest tube thoracostomy. In a study of 77 chest tubes placed emergently in 51 trauma patients, subsequent assessment by CT scanning revealed malpositioning in 20 of the 77 (26%) chest tubes (208). Two chest tubes were subcutaneous, five were intraparenchymal, and nine were intrafissural. Insufficient information was available to determine intraparenchymal versus intrafissural tube placement in four patients. Sixteen of the 20 (80%) chest tube malpositions were associated with persistent pneumothoraces and hemothoraces, including 2 under tension. Of the five intraparenchymal chest tubes documented at CT, only one could be diagnosed by chest radiograph, and only four of the nine intrafissural chest tubes were noted on chest radiograph. Delayed pulmonary perforation by a chest tube has been reported (209), and autopsies have noted perforations that were not clinically suspected (210).
In addition to perforation of the lung, perforation of diaphragm and intra-abdominal organs (spleen, liver, stomach, and colon) has been reported (205,211). These complications are more likely with the use of a trocar. We and others (211) believe that the trocar should never be used. Exploration of the pleural space with a finger should be done prior to tube insertion to confirm placement into the pleural space and to assess for the presence of pleural adhesions and adhesion of the lung to the chest wall, which increases the risk of pulmonary perforation. Other complications include perforation of the right ventricle and right atrium (212,213), cardiogenic shock due to chest tube compression of the right ventricle (214), mediastinal perforation and contralateral hemothorax and pneumothorax (215,216), bleeding from intercostal artery injury (217), and infection at the chest tube site.
Re-expansion Pulmonary Edema
Re-expansion pulmonary edema (RPE) represents one of the most potentially life-threatening complications of therapeutic thoracentesis and chest tube thoracostomy for pleural effusion and pneumothorax. RPE has also been reported following re-expansion of atelectasis from endobronchial obstruction and right mainstem bronchus intubation (218,219,220). Patients developing significant hypoxemia from RPE will often require admission to the ICU. The precise incidence of RPE is unknown. In two series of 400 and 375 cases of spontaneous pneumothorax, no cases of RPE were noted (221,222). Matsuura et al. (223), however, reported that 14% of 146 patients treated for spontaneous pneumothorax developed RPE. In a series of 320 patients with spontaneous pneumothorax, Rozenman et al. (224) observed a 0.9% incidence of RPE, which is likely to best represent the clinical occurrence of RPE. To our knowledge, no studies have been done evaluating the incidence or clinical course of RPE in ICU patients undergoing thoracentesis or chest tube placement. In the study by Matsuura et al. (223), 8 of the 21 patients with RPE were reported as having tension pneumothoraces.
Clinical signs and symptoms include cough, chest tightness or chest pain, dyspnea, tachypnea, tachycardia, and ipsilateral crackles. Patients may produce pink frothy sputum or have frank hemoptysis. The onset of symptoms is immediate or within 1 hour of thoracentesis or chest tube placement in two thirds of patients but may be delayed up to 24 hours (225). Infiltrates are almost always ipsilateral to the side of the pneumothorax or effusion, although contralateral infiltrates alone and bilateral infiltrates have been reported (226). Focal infiltrates corresponding to areas of atelectasis produced by the effusion or pneumothorax have also been reported. RPE has been reported to occur primarily in chronically collapsed lungs. In a review of reported cases by Mahfood et al. (225), however, 8 of 47 (17%) patients and 9 of the 21 (43%) patients in the series of Matsuura et al. (223) had pneumothoraces for less than 24 hours.
Although hypoxemic respiratory failure is a well-recognized complication of RPE, it may not be appreciated that RPE may cause hypotension and cardiovascular collapse. Several case reports have noted severe hypotension with RPE despite adequate oxygenation in some patients (227,228,229,230). In patients in whom a Swan-Ganz catheter was placed, a low cardiac output, a low or normal PCWP, and normal systemic vascular resistance were uniformly observed (227,228,229,230). Hemoconcentration was noted in some patients, suggesting that third-spacing of fluids into the lung accounted for part of the hypotension (230). Many of these patients remained hypotensive despite administration of large amounts of intravenous fluids and vasopressor agents, however, and mortality was 40% (four of ten patients).
Treatment of RPE is mainly supportive, with mechanical ventilation and PEEP being the mainstay of therapy. Diuretics and corticosteroids have been used by some clinicians, although evidence that they are of benefit is lacking. In patients with hypotension, administration of intravenous fluids and vasopressor agents may be necessary. The development of RPE carries a substantial mortality. In a review of 53 reported cases of RPE, Mahfood et al. (225) noted an observed mortality of 20%.
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