Pleural Diseases

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Pleural Diseases

Charlie Strange

Chapter Objectives

After reading this chapter you will be able to:

image Describe important anatomic features and physiologic function of the visceral and parietal pleural membranes.

image Describe how pleural effusions occur and the difference between transudative and exudative effusions.

image Identify common causes of transudative and exudative pleural effusions.

image Write definitions of chylothorax, hemothorax, and pneumothorax.

image Describe the impact of moderate to large pleural effusions on lung function.

image State the role of a chest radiograph in recognizing pleural effusions.

image State the purpose of thoracentesis and the potential complications.

image Identify the definitions of spontaneous, secondary, and tension pneumothorax.

image Describe the diagnosis and treatment of pneumothorax.

Key Terms

A spectrum of pleural diseases affects respiratory function. An understanding of pleural anatomy, physiology, and pathology is essential to delivering effective respiratory care. This chapter focuses on the two major disease processes that occur in the pleural space: pleural effusion and pneumothorax.

Pleural Space

Overview and Definitions

Each lung is covered by a thin membrane called the visceral pleura, which adheres closely to the subjacent alveoli of the lung. The visceral pleura dips into the fissures of the lung, allowing the surgeon easy access between the lung lobes and allowing pleural fluid to travel freely between the lobes while remaining in the pleural space.

The ribs and connective tissue of the chest wall are covered on the inner surface by a similar membrane called the parietal pleura. The parietal pleura can be thought of as a sac that covers not only the rib surface (costal pleura) but also the diaphragm (diaphragmatic pleura) and the mediastinum (mediastinal pleura).

The blood vessels and airways that enter the lung connect to the mediastinum at the lung hilum. At this juncture, the visceral pleura meets the mediastinal parietal pleura to form a single, continuous pleural membrane (Figure 25-1).

image
FIGURE 25-1 Anatomy of the pleura.

Because the lung usually is completely inflated, it might be thought that the pleural membranes always touch. However, freeze-fracturing has shown that there is a space between the visceral and parietal pleura that averages 10 to 20 µm in width and is filled with pleural fluid. This thin film of fluid allows the lung to slide over the ribs and allows for a gliding movement that takes little energy and produces little friction.

The average person has approximately 8 ml of pleural fluid per hemithorax.1 The pleural fluid is estimated to have a total protein concentration similar to that of interstitial fluid elsewhere in the body: between 1.3 g/dl and 1.4.2

In humans, the pleural spaces surrounding each lung are completely independent, being separated by the mediastinum. This is not the case in all other mammals. The slaughter of the American buffalo could occur with a single spear or rifle shot because the pleural spaces of the buffalo lung are connected. Consequently, air in the pleural space collapses both lungs. An analogous situation can occur in any patient who has undergone median sternotomy, during which both pleural spaces were entered. Common operations resulting in this condition are lung volume reduction surgery and bilateral lung transplantation.

The pleural space is under negative pressure except during forced expiration. The intact thoracic rib cage provides elastic recoil pressure outward, whereas the intrinsic recoil pressure of the lung is inward toward the lung hilum. The diaphragm further decreases the intrapleural pressure below the atmospheric pressure to allow inspiration to occur. In an upright person, the pressure is more negative at the lung apex than at the lung base because of the weight of the lung and the effects of gravity. The net effect of the negatively pressurized pleural space is that fluid moves into the pleural space from adjacent sites when a communication is present. A patient with ascitic fluid and a diaphragmatic defect preferentially pulls fluid into the chest.

Pleural Effusions

Any abnormal amount of pleural fluid in the pleural space is called pleural effusion. The many causes of pleural effusion are categorized according to etiologic factor and the content of the fluid.3

Pleural fluid enters the pleural space across both the visceral and the parietal pleurae, particularly when the interstitial pressure within either the lung or the chest wall is increased. The main route for pleural fluid removal is small holes within the parietal pleura called stomata, which are large enough to allow a red blood cell to enter and be cleared from the pleural space. The parietal pleural stomata connect with intercostal lymphatic vessels under the ribs that drain posteriorly into the mediastinum. In the mediastinum, these lymphatic vessels enter lymph nodes before draining into the thoracic duct, a large lymphatic channel within the chest, which empties into the left subclavian vein. Abnormalities of increased pleural fluid production or blockade of drainage can cause pleural fluid to accumulate.

Transudative Effusions

Any pleural effusion that forms when the integrity of the pleural space is undamaged is called a transudative pleural effusion. A pleural fluid total protein concentration less than 50% of the serum total protein level and lactate dehydrogenase values in the pleural fluid less than 60% of the serum value indicate the presence of a transudative pleural effusion. In the absence of serum values, an absolute pleural fluid lactate dehydrogenase level less than two-thirds normal for serum suggests the presence of a transudate. These numbers were derived from large patient series in which pleural fluid and serum protein concentrations were measured while the cause of the effusion was being determined and corrected.4

The classification system listed in Box 25-1 is not perfect, and refinements continue to be proposed. For practical purposes, these numbers help narrow the possible causes of pleural fluid formation. Transudative pleural effusions form when hydrostatic and oncotic pressures are abnormal (Figure 25-2).5 The list of diseases that cause transudative pleural effusions is short. These diseases remain relatively easy to diagnose.

Box 25-1   Causes of Pleural Effusion

Transudative pleural effusion

Exudative pleural effusion

Neoplastic disease

Infectious disease

Pulmonary embolism

Gastrointestinal disease

Collagen vascular disease

Drug-induced pleural disease

Miscellaneous diseases and conditions

Hemothorax

Chylothorax

image
FIGURE 25-2 Pleural fluid formation requires both excess fluid formation and decreased elimination. In diseases such as pulmonary arterial hypertension, in which right-sided heart pressure is increased and systemic veins, such as the intercostal veins (A), are pressurized, pleural fluid does not form because pleural fluid formation is not increased, and lymphatic drainage remains intact. However, when left ventricular failure causes pulmonary venule pressure (B) to increase, the addition of interstitial lung water overwhelms the drainage and produces a transudative pleural effusion. Injury to the capillaries (C), as in pneumonia or ARDS, causes fluid to leak into the lung interstitium and pleural space at increased rates. Under these conditions, fibrin can occlude the pleural lymphatic vessels (E) and cause fluid to accumulate. The bronchial microvessels (D) supply the pleura with blood and likely participate to some extent in production of pleural fluid.

Congestive Heart Failure

Elevation of pressure in the left atrium and pulmonary veins is the hallmark of congestive heart failure (CHF). Elevation of pulmonary venous pressure increases the amount of interstitial fluid in the lung. In severe cases, flooding of the alveoli causes pulmonary edema, but in less severe cases, interstitial lung water increases and decompresses into the pleural space. Because systemic venous pressure also is elevated, there is limited capability to remove pleural fluid through the intercostal veins. Pleural fluid must be predominantly removed by the lymphatic vessels. Pleural effusions result when the capacity of pleural lymphatic drainage is overcome.6

CHF is the most common cause of clinical pleural effusions. The effusions can be massive, filling the entire hemithorax and compressing the lung. More commonly, they are small and bilateral. The effusions are rarely drained because outcome is heavily influenced by successful management of the underlying CHF, which also clears the effusions.7

Nephrotic Syndrome

In nephrotic syndrome (also known as nephrosis), the kidneys leak more than 3 g of protein per day into the urine. Because patients become protein depleted, there is insufficient oncotic pressure within the blood to hold appropriate amounts of fluid within the blood vessels. These patients become edematous, and fluid leaks into the lung interstitium and pleural space. Pleural effusions are common but usually are small.

Patients with nephrosis are at increased risk of deep venous thrombosis and pulmonary emboli. In nephrosis, protein S, which keeps blood from clotting, becomes deficient from leaking into the urine. The presence of large or asymmetric pleural effusions should raise the possibility of the presence of pulmonary emboli. Pleural effusions associated with pulmonary emboli usually are exudates and contain large numbers of red blood cells.

Exudative Effusions

An exudative pleural effusion is caused by inflammation in the lung or pleura. This type of pleural effusion has more protein and inflammatory cells present than a transudative effusion. Because therapy for pleural effusion depends on the cause, thoracentesis often is performed to determine the specific biochemical and cellular characteristics of the pleural effusion. Box 25-1 lists the common causes of exudative pleural effusion. These account for approximately 70% of all pleural effusions.

Parapneumonic Effusion

Pleural effusions form in pneumonia because inflammation in the lung increases interstitial lung water and pleural fluid production. Most effusions are small and resolve with resolution of bacterial pneumonia.9 Complicated parapneumonic pleural effusion develops when the pleural fluid has a high enough protein content to clot. The clotting causes fibrin strands to span the visceral and parietal pleurae. The net result is collection of pleural fluid into different loculi within the pleural cavity. These often cannot be drained by a single chest tube.

Progression to empyema is marked by the presence of bacteria within the pleural space, seen as pus or bacteria on Gram stain. Empyema necessitates drainage. Whether complicated parapneumonic effusions necessitate drainage is controversial, although most physicians perform drainage because some of these effusions can progress to empyema.10

Parapneumonic effusions are common causes of persistent fever among patients with pneumonia in the intensive care unit (ICU). Sampling by thoracentesis is commonly performed to exclude empyema. Pleural fluid drainage can improve ventilation if the fluid volume is large.

Postoperative Causes

Various operations involving the chest or upper abdomen produce pleural fluid.12 Effusions following cardiac surgery usually are predominant on the left side and tend to be bloody. These effusions are particularly prevalent after a cutdown of the internal mammary artery for coronary artery bypass.

Small transudative pleural effusions are common when there is any atelectasis in the lung. Upper abdominal operations cause inflammation of the diaphragm and effusion that has been termed sympathetic. Lung surgery in which the lung is unable to fill the thoracic cavity leaves a space under negative pressure, which fills with inflammatory pleural fluid. When the lung is unable to fill the space because of small postoperative size or visceral pleural fibrosis, the resulting pleural effusion can never be completely drained because of the “trapped lung.”

Chylothorax

The thoracic duct is a lymphatic channel that runs from the abdomen through the mediastinum to enter the left subclavian vein. Disruption of the thoracic duct anywhere along its course can cause leakage of chyle into the mediastinum, which may rupture into the pleural space and cause a chylothorax. The most common causes of rupture are malignancy (50%), surgery (20%), and trauma (5%).13 The thoracic duct courses through the right side of the mediastinum in the lower thoracic cavity before crossing to the left side of the mediastinum at T4 to T6. Rupture below this level causes right-sided pleural effusion, whereas rupture above this level causes left-sided pleural effusion.

In a patient who has eaten recently, the effusions are milky white as a result of the presence of chylomicrons (microscopic fat particles) absorbed by abdominal lymphatic vessels. In a fasting patient, these effusions usually are yellow. The effusions may be bloody. A pleural fluid triglyceride concentration greater than 110 mg/dl confirms the diagnosis.14 Computed tomography (CT) should be performed to evaluate the cause of the chylothorax.

Physiologic Importance

Mechanics of Ventilation

Pleural effusions cause lung atelectasis because the capacity of the thorax is limited, and fluid collapses the lung. Spirometry shows restriction. Studies correlating the volume of pleural fluid removed with improvement in forced vital capacity (FVC) show much variability from patient to patient.

image Rule of Thumb

The patient’s vital capacity improves by one-third of the pleural fluid volume removed.16 The remainder of the pleural fluid volume causes diaphragmatic compression and chest wall expansion. Some patients have a delay of 24 to 48 hours before the improvement can be seen as atelectasis resolves. Lack of any improvement suggests that lung consolidation or endobronchial obstruction is present.

Dyspnea is common with small pleural effusions, even when lung mechanics are preserved. The mechanisms are unknown but likely involve activation of stretch receptors or irritant receptors within the airways or nonadrenergic, noncholinergic C fibers in the chest wall or diaphragm. The net result is that dyspnea relief is variable after removal of pleural fluid. Some patients have symptomatic relief after removal of small pleural fluid volumes. Others can have more dyspnea if the fluid is removed in situations such as trapped lung, in which neural activation may increase with fluid withdrawal.

In rare instances, the pleurae thicken with a disease process sufficient to cause fibrothorax. Technically, fibrothorax is any process that causes fibrosis of the thoracic cage that affects pulmonary function. Fibrothorax can be caused by skin (e.g., fibrothorax that occurs rarely in scleroderma), soft tissue, bone (e.g., myositis ossificans, a disease in which muscles calcify), or pleura. Causes of pleural thickening significant enough to produce restriction include severe asbestos pleurisy, rheumatoid pleurisy, complicated trauma, cancer, and empyema.

Diagnostic Tests

Chest Radiography

The chest radiograph is the most common method of detecting a pleural effusion. It is important that, if possible, the chest radiograph be obtained with the patient in an upright position to show a pleural fluid meniscus at the costophrenic angles. When the same patient undergoes radiography in the supine position, the effusion is distributed throughout the posterior part of the chest. The chest radiograph shows a generalized haze, which interferes with the detection of pulmonary infiltrates and quantification of pleural effusion. A lateral decubitus chest radiograph also can help define the presence or absence of pleural effusion.

Ultrasonography and Computed Tomography

Pleural fluid and loculi can be detected easily with ultrasonography of the chest. The sensitivity of ultrasonography for pleural effusions is high, although ultrasonography is an operator-dependent study. Small portable ultrasound machines with high diagnostic accuracy have become available to localize the presence of pleural effusions. Some physicians have begun to use these machines routinely to optimize thoracentesis success.

CT scanning of the chest is the most sensitive study for identification of pleural effusion. A contrast-enhanced scan is essential to delineate the pleural membrane and differentiate peripheral lung consolidation from pleural fluid formation. In addition to showing the size and location of a pleural effusion, a chest CT scan often gives information about the underlying lung parenchyma and the primary process causing the effusion.

Thoracentesis

In thoracentesis, pleural fluid is sampled percutaneously by means of insertion of a needle into the pleural space (Figure 25-3). Administration of adequate local anesthetic ensures a painless procedure if care is taken to place lidocaine at the skin insertion site, along the periosteum of the involved rib, and at the parietal pleura, which is richly innervated with sensory nerve fibers. Diagnostic sampling of pleural fluid for cell counts, cultures, chemistries, and cytologic examination usually can be performed with a single syringe and a small needle. Samples for pleural pH should be kept from contact with room air. Pleural fluid drainage for lung reexpansion generously involves placing a larger catheter into the pleural space for a longer time.

image
FIGURE 25-3 The technique of thoracentesis involves passage of a needle just superior to the rib. If the needle is placed too low on the chest, the diaphragm or organs below the diaphragm can be punctured. Diagnostic thoracentesis can be performed with small amounts of pleural fluid.

Thoracentesis involves the following three major risks: (1) intercostal artery laceration, (2) infection, and (3) pneumothorax.17 Both an artery and a vein course under every rib, and the vessels become increasingly serpiginous with aging. Ensuring needle passage just superior to the rib margin makes bleeding during thoracentesis rare. Ideally, anticoagulants should be stopped before the procedure to lessen bleeding risk.

Because infection can be introduced into the pleural space, a totally sterile procedure is necessary. In some situations, the risk of infection is so high that thoracentesis rarely should be performed. When a lung is surgically removed, the space fills with sterile fluid. An infection introduced into this space usually necessitates open surgical drainage. Any trapped lung also carries a high risk of empyema because of the inability of the visceral and parietal pleurae to meet and contain any infectious process. Needle puncture is one of the most common causes of pneumothorax (see discussion of pneumothorax later in this chapter).

Chest Thoracotomy Tubes

Chest tubes currently are manufactured in various sizes and shapes, ranging from 7 French (F) to 40F catheters. Catheter choice is frequently a matter of physician preference. Larger tubes are less likely to become obstructed and are capable of high airflow rates.

Intercostal placement is designed for the skin and soft tissue to approximate the tube and prevent air from entering the pleural space from the outside. The chest tube is connected to a water-sealed chamber, which usually is contained within a commercially marketed three-bottle system that also regulates pleural pressure and is used to measure pleural fluid volume (Figure 25-4).

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FIGURE 25-4 A-C, The standard three-bottle system is the basis for all commercial chest tube drainage systems. Pleural fluid and pleural air enter compartment C, which serves as a fluid collection trap so that the water-seal fluid volume does not increase (compartment B) and create resistance to air escaping the chest. Air cannot be inspired into the chest because of the water in compartment B. Open entrainment of room air through a submerged tube in compartment A buffers the amount of wall suction applied (−60 cm H2O) to the height of the water column to standardize the pressure (−20 cm H2O) transmitted to the chest.

Pleurodesis

Pleurodesis is the process of fusing the parietal and visceral pleurae with a fibrotic reaction that prevents further pleural fluid formation. Methods to produce pleural symphysis include surgical abrasion and the application of intrapleural chemicals such as doxycycline, minocycline, and talc. Talc has been applied as a powder suspended in sterile saline solution and injected through the chest tube (talc slurry) or dusted through a thoracoscope (talc insufflation). The success of talc pleurodesis, approximately 90%, is higher than that of all alternatives except surgical abrasion.18,19 Pleurodesis is used most commonly in the management of symptomatic pleural effusions caused by cancer. Although pleurodesis of benign effusions, such as effusions occurring with CHF, nephrotic syndrome, and idiopathic chylothorax, have been performed successfully, the procedure is discouraged for pleural effusions that are not malignant. Most pleural effusions are best managed by control of the underlying condition.20

Pleuroperitoneal Shunt and Pleural Catheter

In refractory pleural effusions that cannot be treated adequately with pleurodesis, a small pump can be placed subcutaneously, and tubes are placed in the pleural and peritoneal spaces. The pleuroperitoneal connection has a one-way valve and a pumping mechanism to allow the patient to expel pleural fluid from the negatively pressurized chest to the positively pressurized peritoneum. The pleuroperitoneal shunt is placed as a last resort for refractory pleural effusions for which there is no other treatment. A Pleurx (CareFusion, San Diego, CA) catheter has an adapter for connection to vacuum bottles. It is inserted into the pleural space so that pleural fluid can be removed at home for recurrent effusions. In malignant effusions, pleural drainage lessens over time, and the Pleurx catheter can usually be removed when cancer cells have bridged the pleural space, creating a pleurodesis.

Pneumothorax

Pneumothorax refers to air in the pleural space. Although air can enter the pleural space from outside the body, as occurs in sucking chest wounds, most cases of pneumothorax occur when disruption of the visceral pleura allows air from the lung to enter the pleural space. Pneumothorax is discussed according to etiologic factor because traumatic pneumothorax is managed differently from spontaneous pneumothorax. Spontaneous pneumothorax is of two types:

Chest pain, which is typically sharp and abrupt, occurs in nearly every patient with pneumothorax. Palpation of the chest wall does not worsen the pain, although respiratory efforts may be difficult. Dyspnea occurs in approximately two-thirds of patients when decreases in vital capacity and PO2, probably secondary to airway closure at low lung volumes, cause ventilation/perfusion defects and shunting. When spontaneous pneumothorax is evacuated, hypoxemia may persist in some patients. The following sections describe the diseases that cause pneumothorax and the important treatment differences between them.

Traumatic Pneumothorax

Blunt and Penetrating Chest Trauma

Traumatic pneumothorax can be caused by either blunt or penetrating wounds of the thorax. The common causes of penetrating wounds include gunshots and knife punctures. In many cases, penetrating trauma to the chest can be managed conservatively with a chest tube. The clear indications for entering the chest surgically are uncontrolled bleeding from intercostal or pulmonary arteries and injury to the heart or great vessels. In these situations, the pneumothorax becomes secondary. The chest tube is multifunctional to allow measurement of the rate of bleeding, to allow the lung to be pulled to the parietal pleural surface to tamponade bleeding, and to allow maximum ventilation.

In blunt trauma to the chest, pneumothorax can be the result of a rib fracture that enters the lung parenchyma and allows air to leak into the pleural space. For this type of injury, a chest tube is placed, and the rib fractures necessitate no specific therapy. A more common injury is alveolar rupture, which breaks through the pleural membrane.

Two special injuries that produce pneumothorax are tracheal fracture and esophageal rupture. Tracheal fracture results from severe deceleration injury and often occurs in concert with fractures of the anterior aspect of the first through third ribs. In this case, urgent bronchoscopy is appropriate because tracheal fracture must be corrected surgically. Esophageal rupture produces an air-fluid level in the pleural space. Pleural fluid amylase concentration is elevated from a salivary source.

Large-caliber chest tubes are placed for trauma-related pneumothoraces to allow exit of blood and blood clots, which can be difficult to remove through small-bore catheters. Air leaks from an injured lung can be large. When bleeding is a major component of pleural injury, two chest tubes are used: a posterior chest tube to drain blood that is gravity-dependent and an anterior and apical chest tube to drain air that moves to the lung apex in the absence of pleural disease.

Spontaneous Pneumothorax

Spontaneous pneumothorax is defined as any pneumothorax caused by the escape of air into the pleural space without an obvious cause.

Secondary Spontaneous Pneumothorax

Secondary spontaneous pneumothorax occurs in patients with underlying lung disease. In most cases, the underlying lung disease is chronic obstructive pulmonary disease (COPD) with some component of emphysema. Pneumothorax also can occur with asthma and cystic fibrosis, usually during an exacerbation of disease. Interstitial lung diseases in which lung volumes are spared, such as sarcoidosis, organizing pneumonia, pulmonary Langerhans cell histiocytosis, and lymphangioleiomyomatosis, have a higher incidence than diseases without any component of obstruction, such as idiopathic pulmonary fibrosis.

Depending on the extent of parenchymal lung disease, pneumothorax can be devastating. A Veterans Affairs cooperative study included 185 patients with secondary spontaneous pneumothorax and monitored them for 5 years.24 Although only three patients died of pneumothorax, the mortality rate was 43%.1 Severe underlying lung disease caused most deaths. This finding suggested that most pneumothoraces occur in patients with severe lung dysfunction. The degree of dyspnea is disproportionate to the size of pneumothorax in this group of patients because pulmonary reserve is already diminished. Pneumothorax usually should be evacuated and not observed in this patient cohort.

Catamenial Pneumothorax

Catamenial pneumothorax occurs in conjunction with menstruation and usually is recurrent and right-sided. The reason for the right-sided predominance is unclear. Many patients have endometriosis on the pleural surface, although it may be impossible to see because of hormonal involution during menses. Once the diagnosis is considered, catamenial pneumothorax is not difficult to manage because most patients do not have a recurrence when ovulation is suppressed.

Mini Clini

Subcutaneous Emphysema

Solution

Subcutaneous emphysema occurs when air enters the soft tissues. Although physical examination reveals subcutaneous bubbles, the patient’s family needs to be reassured that the condition is rarely, if ever, physiologically significant. What is important to recognize, however, is that alveolar disruption has occurred, most commonly as the result of barotrauma.

Barotrauma disrupts alveoli and allows air to enter the interstitium of the lung. Rupture of the visceral pleura allows air to produce pneumothorax, or the air can travel along the low-resistance tissue planes of the bronchovascular bundles and through the hilum of the lung to enter the mediastinum. From the mediastinum, air has easy access to the retroperitoneal space, including the scrotum and the neck. The presence of subcutaneous air does not mean that pneumothorax has occurred, although the risk factors for its development are present.

Air under pressure in the pleural space can enter the subcutaneous tissues through the intercostal incision made for chest tube placement. Subcutaneous air often is seen on a chest radiograph after chest tube placement, but the air rarely spreads unless the chest tube is occluded.

In the absence of pneumothorax, there is no way to determine which lung is causing subcutaneous emphysema. For any deterioration in gas exchange, radiographs should be repeated. Because air in the mediastinum can displace the mediastinal parietal pleura, it can be difficult to tell without chest CT whether a small pneumothorax is present. Because patients often are too unstable to be moved, a chest tube sometimes is placed because the potential benefits are greater than the risks.

Complications

Tension Pneumothorax

Tension pneumothorax occurs when air in the pleural space exceeds atmospheric pressure. The radiographic appearance includes mediastinal shift to the contralateral side, diaphragmatic depression, and expansion of the ribs. The lung does not collapse completely if it is involved with a disease process such as acute respiratory distress syndrome (ARDS). Not all patients with radiographic tension have the physiologic changes commonly associated with tension pneumothorax. However, almost all pneumothoraces that occur during mechanical ventilation enlarge if not drained.

As pressure in the thorax increases and mediastinal shift places torsion on the inferior vena cava, venous return to the right side of the heart decreases. Cardiac output decreases, and hypotension with tachycardia results. Hypoxemia occurs as the lung continues to compress because of intrapulmonary shunting through the collapsed lung.

The respiratory therapist (RT) can make the diagnosis of tension pneumothorax. Treatment is emergency decompression of the chest. This procedure usually is done with an 18-gauge intravenous (e.g., Jelco) catheter inserted just over the second rib on the anterior aspect of the chest in the midclavicular line. Catheter placement should elicit a rush of air through the catheter, and this sign confirms the diagnosis. Blood pressure recovery should be rapid, although resolution of hypoxemia depends on complete lung reexpansion and can be delayed. The soft intravenous catheter can be left in place while a more conventional chest tube is inserted.

image Rule of Thumb

Tension pneumothorax is a clinical diagnosis made at the bedside in more than 50% of cases. The clinical signs are diminished breath sounds, hyperresonance to percussion, tachycardia, and hypotension.

In one case series of 74 patients with tension pneumothorax, a clinical diagnosis was made for 45 patients; the associated mortality rate was 7%. In the other cases, the diagnosis was delayed from the onset of clinical signs by 30 minutes to 8 hours, resulting in a 31% mortality rate.25 RTS are in the perfect position to make a timely diagnosis because ventilator alarms give early warnings (e.g., high pressure, lower compliance).

Reexpansion Pulmonary Edema

Reexpansion pulmonary edema occurs in a lung that has been rapidly reinflated from low lung volumes, particularly when the pneumothorax has been long-standing or when the pressure gradient across the lung has become high, as might occur when there is endobronchial obstruction from cancer, mucus, or blood. For many years, it was believed that alveolar edema occurs because intraalveolar pressure becomes negative and pulls fluid from the vasculature. However, the lung fluid has high protein content, a finding that suggests blood vessels have been injured as well.

One proposed mechanism of vascular injury is a phenomenon of reperfusion injury caused by reactive oxygen species. Support for this hypothesis has come from experimental studies that have shown administration of antioxidants before reexpansion decreases the amount of reexpansion pulmonary edema.

Regardless of the cause, lung reexpansion in nonemergency situations should proceed slowly, and transpulmonary pressure should not become excessive. Most physicians who insert a chest tube for a large pneumothorax first place it to water seal without suction. If the lung is not completely inflated on the subsequent chest radiograph, the chest tube is placed to suction. Reexpansion pulmonary edema also occurs after drainage of pleural effusions. As a rule, thoracentesis should be limited to 1000 ml, unless pleural pressures are monitored and not allowed to become less than −20 cm H2O.

Diagnosis

The diagnosis of pneumothorax is established with chest radiography. The diagnosis requires a high-quality film for visualization of a visceral pleural line. In the ICU, 30% of cases of pneumothorax may be missed in retrospect on a chest radiograph. Impediments to diagnosis include a low-quality radiograph, supine position of the patient, concomitant presence of mediastinal air, and subpulmonic or mediastinal position of the pneumothorax. Diagnosis is enhanced with additional upright radiographs or decubitus views.

The size of a pneumothorax is difficult to assess with a chest radiograph because a two-dimensional picture is being taken of a three-dimensional thorax. Size can be confirmed with CT if needed.

image Rule of Thumb

The size of a pneumothorax on a chest radiograph can be estimated with the knowledge that the volume of the lung and thorax is proportional to the cube of their diameters.

For example, on a chest radiograph, the chest measures 8 cm from the spine to the lateral chest wall. A pneumothorax is measured 2 cm from the chest wall:

< ?xml:namespace prefix = "mml" />Volume of the lung=(6cm)3≈216cm3

image

Volume of the hemithorax=(8cm)3=512cm3

image

Lung size=216/512=42%

image

Pneumothorax size≈58%

image

The equation shows the large volume of lung that a pneumothorax can displace despite a “small” distance from the lung to the chest wall. Use of the equation is not as accurate as chest CT because in many pneumothoraces, the lung collapses asymmetrically.

Therapy

Oxygen

Oxygen (O2) should be administered to all patients who have a pneumothorax. Most of the air in a pneumothorax is nitrogen because O2 is readily absorbed. If an air leak is continuing, supplemental O2 rather than nitrogen leaks into the pleural space. After an air leak has been stopped, administration of O2 decreases the blood and tissue partial pressure of nitrogen surrounding the pleural space. Pneumothorax resolution is normally 1.25% of the air per day. O2 speeds recovery by increasing the gradient of nitrogen from the pleural space to the pleural tissues.

Observation

Consensus conferences have recommended observation of patients in stable condition with primary spontaneous pneumothorax and of some patients with small secondary spontaneous pneumothorax before recurrence prevention is administered.26 Small iatrogenic pneumothorax also should be managed with observation. Primary spontaneous pneumothorax often is observed for 4 hours in the emergency department before discharge to home follow-up care as long as no pneumothorax enlargement is found on chest radiographs. Discharged patients should have ready access to emergency care facilities.

Patients with secondary spontaneous pneumothorax should be admitted to the hospital. During observation, it is important to record the respiratory rate and any signs of deteriorating respiratory function. A decrease in oxygen saturation can be an early warning of pneumothorax enlargement. Any deterioration indicates that the pneumothorax must be drained.

Simple Aspiration

Simple aspiration can be used in the emergency department when pneumothorax is first identified. A small catheter is placed into the pleural space, and air is sequentially evacuated with a three-way stopcock until no more air can be removed. If more than 4 L of air is aspirated and no resistance to further aspiration is felt, a chest tube is needed for continuing pleural air leak.

The goal of aspiration is to reexpand the lung. Many patients have a pneumothorax from air leak that subsequently heals between the time of onset and the time treatment is sought in the emergency department. Patients with primary spontaneous pneumothorax who undergo simple aspiration for lung reexpansion and who have a stable chest radiograph 4 hours after aspiration can go home without hospital admission.26,27 Aspiration can decrease the number of patients admitted to the hospital with no increase in complications.27

Chest Tubes

Chest thoracostomy tubes (chest tubes) come in various sizes, ranging from 7F to 40F, and can be connected to a variety of one-way devices (e.g., Heimlich valves) that prevent entry of air into the pleural space from the outside environment. Regardless of chest tube size and the presence of a Heimlich valve or water seal, the effectiveness of chest tube placement for pneumothorax resolution depends more on lung surface healing than on the device used.

Small-Bore Catheter

One simple device is a small-bore 7F catheter with a one-way valve apparatus (Heimlich valve) that prevents air movement back into the chest. Small-bore catheters can be placed with a small skin incision, although they require a trocar for transthoracic placement, and the trocar can injure the lung.

All chest tubes used to drain pneumothorax should be directed to the apex of the lung. Small-bore catheters can be placed in the second intercostal space anteriorly in the midclavicular line or laterally in the chest from the fifth through the seventh intercostal space.

It is difficult to determine whether a Heimlich valve has an ongoing leak unless it is placed to underwater seal. This procedure can be done in the emergency department by placing the Heimlich valve into a cup of water or by placing it in line with a water-seal chamber to see whether an air leak is continuing after lung expansion. Some automated devices also are available that show ongoing air leaks.

Large-Bore Chest Tube

Large-bore chest tubes usually are connected to a commercial equivalent of a three-bottle system to collect any pleural fluid present, to determine whether an air leak is ongoing, and to measure intrapleural pressure (Figure 25-5). Insertion of large-bore catheters is accomplished with local anesthetic and blunt dissection of soft tissue down to the parietal pleura. Dissection should be wide enough to allow insertion of a finger into the pleural space to ensure that no adhesions are holding the lung close to the insertion site and to allow unobstructed entrance of the tube into the pleural space, where it can be directed to the position of choice.

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FIGURE 25-5 A-C, The Pleur-evac (Teleflex, Research Triangle Park, NC) chest tube collection system collects fluid in compartment C so that it does not spill into the water-seal compartment (B). A patent chest tube should cause respiratory variation to be seen on the scale adjacent to compartment B, which measures intrapleural pressure. Compartment B also is the place to see bubbles if an air leak is present. The water level in compartment A controls intrapleural pressure and should be adjusted daily.

Chest tubes are secured with sutures. The insertion distance should be recorded and be checked on subsequent days to ensure that the chest tube does not migrate outward. If the most proximal hole in the tube emerges from the skin, air will enter the tube, and it will appear as if the lung is persistently leaking. Another problem of apparent chest tube leak can occur when the insertion wound is large enough to allow air entry into the pleural space; this usually is accompanied by a sucking sound at the entrance, which can be occluded with petroleum gauze.

A chest radiograph is routinely obtained. However, unless a lateral radiograph also is obtained, confirmation of precise placement often is difficult. In addition, many chest tubes end up in the major fissure, where their function may be suboptimal.

Chest tube removal remains a highly variable practice. Removal of a chest tube as soon as an air leak visually ceases is associated with a 25% rate of recurrence of pneumothorax. The recurrence rate is near zero when chest tubes are removed 48 hours after the air leak no longer is seen in the water-seal chamber.28,29 A common practice of clamping the chest tube, with chest radiographs before and after a 4-hour observation period, can be accompanied by the return of pneumothorax. If symptoms develop during chest tube clamping, the clamp should be removed immediately, and the presence of air leak should be assessed.

Bronchopleural Fistula

Air leaks from the lung through a chest tube can come in many sizes. If a large bronchus is involved in the lung injury, the large air leak is called a bronchopleural fistula (BPF). Many patients with a BPF are receiving mechanical ventilation, and positive airway pressures contribute to the perpetuation of pleural air.

Because a BPF can leak large quantities of air, more than one chest tube may be used to approximate the lung to the chest wall. This maneuver results in tamponade of the site of the air leak and allows pleural healing to occur. Therapy for BPF involves meticulous monitoring of tidal volume, airway pressures, and positive end-expiratory pressure (PEEP); avoidance of auto-PEEP; and consideration of bronchoscopic closure or thoracoscopic surgery.30 Also, endobronchial valves placed by flexible bronchoscopy have shown high rates of success for patients who are not operative candidates.31

Pleurodesis

Patients who have had one pneumothorax are more likely than the general population to have a second. The recurrence rate is greater than 30% among patients with primary spontaneous pneumothorax and approximately 40% among patients with secondary spontaneous pneumothorax. These high recurrence rates indicate that prevention of recurrence of pneumothorax should be undertaken, in particular, for patients in whom pneumothorax may be life-threatening. Preventing recurrence involves production of adhesions between the parietal and the visceral pleura in the involved area and is termed pleurodesis.

The most noninvasive approaches to pleurodesis entail chemical sclerosis of the pleural space through the chest tube after the pleural air leak has ceased. The two most common preparations used at the present time in the United States include 500 mg of doxycycline or 5 g of talc mixed into a 50-ml syringe of sterile saline solution. The agent is injected through the chest tube into the pleural space. The chest tube is then clamped for 2 hours before drainage is allowed.

More invasive methods have included thoracoscopy with pleural poudrage (blowing talc onto the pleural surface under direct visualization), pleural abrasion through a thoracoscope, and thoracotomy with pleurectomy (removing the pleural surface to ensure lung adhesion). More recent recommendations are for pleurodesis to occur after the first secondary spontaneous pneumothorax with thoracoscopic bullae stapling and talc poudrage.28

Because the diseases that produce pneumothorax often involve both lungs, patients may experience sequential events in opposite lungs. In this situation, median sternotomy with bilateral abrasion or pleurectomy can be performed, particularly for patients at considerable risk of development of pneumothorax, such as divers and aviators.

Mini Clini

Bronchopleural Fistula

Solution

The problem is a BPF caused by a large hole in the pleura, which is difficult to manage. The lung surface of patients with underlying emphysema can contain large bullae that do not heal readily when ruptured. Large pleural holes also can develop in patients with necrotizing pneumonia and patients who have undergone surgery on the lung.

The Fanning equation states that humidified airflow through a chest tube is proportional to the chest tube radius to the fifth power. The chest tube radius is the most important determinant of maximal airflow. Airflow through large BPFs has been measured as 16 L/min, a volume impossible to remove through a chest tube smaller than 24F, regardless of the amount of pressure applied.

This patient should receive a second, larger chest tube. The seal of the chest tube at the skin surface should be inspected to ensure that no air is entering the body from the outside. The position of both chest tubes should be confirmed either radiographically or manually to ensure the tubes are in the pleural space. When the lung is expanded, the minute ventilation should decrease because effective alveolar ventilation is improved.

Flow through stopcocks and chest tube collection devices is governed by the same considerations as chest tube size. The manufacturer of the chest tube collection device in your hospital would have the resistance figures necessary to ensure that 16 L/min of airflow can be accommodated.

Mini Clini

Measuring a Large Air Leak

Solution

Although research laboratories can measure airflow through a chest tube with a pneumotachometer, clinical care can be provided by estimating the pleural air leak. The following simple calculations suggest that the excess difference in returned VT (450 to 300 ml) is due to air passing through the chest tube:

30breaths/min(150ml differential=4.5L of pleural ventilation)

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One other problem is that large amounts of CO2 (up to 20%) may be removed through the chest tube.30,32 Removal of CO2 is beneficial because it allows lower VT and respiratory rates for any given PCO2. However, as the air leak closes, CO2 has to be eliminated from the endotracheal tube, necessitating higher minute ventilation. This effect might falsely suggest that ARDS is worsening when the reality is that the air leak is closing.

Nevertheless, when the air leak is measured with every ventilatory change, the mode of ventilation that minimizes air leak is the one most likely to allow pleural healing. Breath-by-breath analysis shows the difference between delivered VT and exhaled VT and approximates the volume of the pleural leak.

PEEP can be a major cause of large BPF and should be turned off. Because there is no such thing as a true plateau pressure when air is exiting through the pleural space, VT should be adjusted to produce the lowest peak airway pressure that can sustain ventilation and oxygenation. The patient should be positioned so that the lung with the air leak is in the bed.33

Auto-PEEP can be impossible to measure if the fistula is large and decompressing the airways. Long expiratory times are preferred. Trials of pressure-controlled and high-frequency jet ventilation are appropriate. In a practical sense, these adjustments are the same ones made to prevent barotrauma in the first place and are limited by the severity of lung injury, which requires more support than would optimally close the air leak.

Mini Clini

Management of Bronchopleural Fistula

Solution

Two ventilatory interventions have been attempted for large BPFs. The first is placement of a double-lumen endotracheal tube, which can carry most ventilation and PEEP on the right lung while underventilating the lung with the fistula to aid in its closure.34 Long-term double-lumen ventilation is difficult for the following reasons: tenuous tube position, the need for continuous paralysis, difficulty with secretion clearance, and high airway resistance through the small endotracheal tube lumens.

The second intervention is application of positive pressure to the chest tube. This back pressure increases resistance across the BPF and allows the remainder of the lung to ventilate better. One simple way to add chest tube resistance is to connect a PEEP valve to the expiratory port of the water-seal chamber.35 PEEP usually is placed at the same level as the ventilator. Inspiratory pressures exceed PEEP, and air flows through the chest tube. However, as expiratory pressures equilibrate, PEEP can be held within the lung, allowing the beneficial effects on oxygenation.

Pressurizing the chest tube entails synchronous closure of the chest tube during inspiration36 and requires specialized equipment, which must be set up under controlled conditions. When used in combination with an in-line PEEP valve, BPF flow can be slowed during both inspiration and expiration.

These techniques usually increase the volume of intrapleural air. The net effect on oxygenation necessitates careful bedside observation because hypoxemia can worsen with any degree of lung collapse. Tension pneumothorax can occur and should be managed expectantly.

Role of the Respiratory Therapist in Pleural Diseases

The RT has important roles in both the diagnosis and the management of pleural disease. Diagnostically, careful palpation and auscultation of the chest by the RT may show the dullness and decreased breath sounds that may prompt suspicion of a pleural effusion and lead the physician to order imaging studies to confirm the presence of a pleural effusion. The RT is in the most proximate position to suggest the diagnosis of pneumothorax because of changing ventilatory function in the ICU. The RT may be called on to assist in performing a thoracentesis or placing a chest tube. Therapeutically, the RT may be called on to assist in setting up the fluid collection chamber after the chest tube is placed or in performing a talc pleurodesis. This broad spectrum of potential roles for the RT makes knowledge of the diagnosis and management of pleural disease essential for the capable RT.

Summary Checklist

• Pleural effusions form when excess pleural fluid is produced by the lung or chest wall in sufficient quantities to overcome the resorptive capacity of the pleural lymphatic vessels.

• Pleural fluid analysis is the key to understanding the specific cause of any pleural effusion.

• Transudates have a pleural fluid total protein level less than 0.5 and lactate dehydrogenase level less than 0.6 of the respective serum values. Common diagnoses include CHF, nephrosis, and cirrhosis.

• Pleural fluid drainage returns approximately one-third of the lung volume as measured by FVC. The other two-thirds of fluid drainage allow the diaphragm to rise and the chest wall to normalize.

• Pneumothorax size is underestimated with a one-dimensional view of the chest. Measurement accuracy requires a three-dimensional perspective.

• The risk factors for pneumothorax and pneumomediastinum are the same. Air ruptures a pleural membrane in pneumothorax, and air passes through the lung hilum in pneumomediastinum.

• O2 therapy speeds resolution of all pneumothoraces by improving nitrogen absorption.

• Chest tube flow depends on tube size, stopcock size, and collection system resistance.

• Breath-by-breath measurement of an air leak can be approximated by the difference between inspired and expired volumes in the absence of endotracheal cuff leaks.

• The type of ventilator that produces the least fistula airflow is the most likely to effect healing.

• Methods to decrease the size of a persistent air leak include lowering tidal volume, lowering respiratory rate, lowering PEEP, and avoiding auto-PEEP. In more severe cases, positioning the affected lung down, double-lumen tube ventilation, adding PEEP valves to the chest tube, inspiratory chest tube occlusion, or thoracic surgery should be considered.

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