Pleural Effusion and Empyema

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Pleural Effusion and Empyema

Chapter Objectives

After reading this chapter, you will be able to:

• List the anatomic alterations of the lungs associated with pleural diseases.

• Describe the causes of pleural diseases.

• List the cardiopulmonary clinical manifestations associated with pleural diseases.

• Describe the general management of pleural diseases.

• Describe the clinical strategies and rationales of the SOAPs presented in the case study.

• Define key terms and complete self-assessment questions at the end of the chapter and on Evolve.

FIGURE 23-1 Right-sided pleural effusion. CL, Collapsed lung (partially collapsed); DD, depressed diaphragm; FA, fluid accumulation. Inset, Atelectasis, a common secondary anatomic alteration of the lungs.

Anatomic Alterations of the Lungs

A number of pleural diseases can cause fluid to accumulate in the pleural space; this fluid is called a pleural effusion, or if infected, an empyema (see Figure 23-1). Similar to free air in the pleural space, fluid accumulation separates the visceral and parietal pleura and compresses the lungs. In severe cases, atelectasis will develop, the great veins may be compressed, and cardiac venous return may be diminished. Pleural effusion and empyema produce a restrictive lung disorder.

The major pathologic or structural changes associated with significant pleural effusion are as follows:

• Lung compression

• Atelectasis

• Compression of the great veins and decreased cardiac venous return

Etiology and Epidemiology

Pleural effusion affects approximately 1.3 million people each year in the United States. Early signs and symptoms include pleuritic chest pain, “chest pressure,” dyspnea, and cough. Chest pain can occur early when there is intense inflammation of the pleural surfaces. “Chest pressure” usually develops until the effusion is in the moderate (500 to 1500 mL) to large (>1500 mL) category. Dyspnea rarely occurs in small effusions unless significant pleurisy is present. A cough is usually directly related to the degree of atelectasis caused by the effusion.

A pleural effusion may be transudative or exudative. A transudate develops when fluid from the pulmonary capillaries moves into the pleural space. The fluid is thin and watery, containing a few blood cells and little protein. The pleural surfaces are not involved in producing the transudate. In contrast, an exudate develops when the pleural surfaces are diseased. The fluid has a high protein content and a great deal of cellular debris. Exudate is usually caused by inflammation, infection, or malignancy. Transudative pleural effusions and exudative pleural effusions are differentiated by comparing the chemistries of the pleural fluid with those of the blood. The pleural effusion is classified as exudative when one or more of the following is found in the pleural fluid:

• Pleural fluid protein >2.9 g/dL (29 g/L)

• Pleural fluid cholesterol >45 mg/dL (1.16 mmol/L)

• Pleural fluid lactate dehydrogenase (LDH) >60% of upper limit for serum

Common Causes of Transudative Pleural Effusion

Congestive Heart Failure

Congestive heart failure is the most common cause of pleural effusion. Both right- and left-sided heart failure can result in pleural effusion. In general, left-sided heart failure is more likely to produce pleural effusion than right-sided heart failure. In right-sided heart failure (cor pulmonale), an increase in the hydrostatic pressure in the systemic circulation can (1) increase the rate of pleural fluid formation and (2) decrease lymphatic drainage from the pleural space because of the elevated systemic venous pressure. In left-sided heart failure, an increase in hydrostatic pressure in the pulmonary circulation can (1) decrease the rate of pleural fluid absorption through the visceral pleura and (2) cause fluid movement through the visceral pleura into the pleural space.

Hepatic Hydrothorax

Occasionally, pleural effusions can develop as a complication of hepatic cirrhosis, particularly when ascitic fluid is present in the abdomen. The pleural effusion in these patients is generally right-sided.

Peritoneal Dialysis

As in the pleural effusion that occurs as a result of abdominal ascites, pleural fluid also may develop as a complication of peritoneal dialysis. When the peritoneal dialysis is stopped, the pleural effusion usually disappears rapidly.

Nephrotic Syndrome

Pleural effusion is commonly seen in patients with nephrotic syndrome. It is generally bilateral. The effusion is a result of the decreased plasma oncotic pressure that develops in patients with this disorder.

Pulmonary Embolism or Infarction

Thirty percent to 50% of patients with pulmonary arterial emboli develop pleural effusion. Two distinct mechanisms are responsible. First, obstruction of the pulmonary vasculature can lead to right-sided heart failure, which in turn can lead to pleural effusion. The second mechanism involves the increased permeability of the capillaries in the visceral pleura that develops in response to the ischemic infarction caused by the pulmonary emboli.

Common Causes of Exudative Pleural Effusion

Malignant Pleural Effusions

About two thirds of malignant pleural effusions occur in women. Malignant pleural effusions are highly associated with breast and gynecologic malignancies.

Malignant Mesotheliomas

Malignant mesotheliomas arise from the mesothelial cells that line the pleural cavities. Individuals with chronic asbestos exposure have a much greater risk for developing mesothelioma. The pleural fluid is exudative and generally contains a mixture of normal mesothelial cells, differentiated and undifferentiated malignant mesothelial cells, and a varying number of lymphocytes and polymorphonuclear leukocytes.

Bacterial Pneumonias

As many as 40% of patients with bacterial pneumonia have an accompanying pleural effusion. Most pleural effusions associated with pneumonia resolve without any specific therapy. Approximately 10%, however, require some sort of therapeutic intervention. If appropriate antibiotic therapy is not instituted, bacteria invade the pleural fluid from the lung parenchyma. Eventually, pus will accumulate in the pleural cavity (empyema). Pleural effusion also can be produced by viruses, Mycoplasma pneumoniae, and Rickettsia, although the pleural effusions are usually small.

Tuberculosis

Pleural effusion may develop from extension of a caseous tubercle into the pleural cavity. It also is possible that the inflammatory reaction that develops in tuberculosis obstructs the lymphatic pores in the parietal pleura. This in turn leads to an accumulation of protein and fluid in the pleural space. Pleural effusion caused by tuberculosis is generally unilateral and small to moderate in size (see Chapter 17).

Fungal Diseases

Patients with fungal diseases occasionally have secondary pleural effusions. Common fungal diseases that may produce pleural effusions are histoplasmosis, coccidioidomycosis, and blastomycosis (see Chapter 18).

Pleural Effusion Resulting from Diseases of the Gastrointestinal Tract

Pleural effusion is sometimes associated with diseases of the gastrointestinal tract such as pancreatitis, subphrenic abscess, intrahepatic abscess, esophageal perforation, abdominal operations, and diaphragmatic hernia.

Pleural Effusion Resulting from Collagen Vascular Diseases

Pleural effusion occasionally develops as a complication of collagen vascular diseases. Such diseases include rheumatoid pleuritis, systemic lupus erythematosus, Sjögren’s syndrome, familial Mediterranean fever, and Wegener’s granulomatosis.

Other Pathologic Fluids That Separate the Parietal from the Visceral Pleura

In addition to transudate and exudate, other pathologic fluids can separate the parietal pleura from the visceral pleura.

Empyema

The accumulation of pus in the pleural cavity is called empyema. Empyema commonly develops as a result of inflammation. Thoracentesis may confirm the diagnosis and determine the specific causative organism. The pus is usually removed by chest tube drainage. Open thoracotomy drainage may occasionally be necessary.

Chylothorax

Chylothorax is the presence of chyle in the pleural cavity. Chyle is a milky liquid produced from the food in the small intestine during digestion. It consists mainly of fat particles in a stable emulsion. Chyle is taken up by fingerlike intestinal lymphatics called lacteals and transported by the thoracic duct to the neck. From the thoracic duct the chyle moves into the venous circulation and mixes with blood. The presence of chyle in the pleural cavity is usually caused by trauma to the neck or thorax or by cancer occluding the thoracic duct.

Hemothorax

The presence of blood in the pleural space is known as a hemothorax. Most of these are caused by penetrating or blunt chest trauma. An iatrogenic hemothorax may develop from trauma caused by the insertion of a central venous or pulmonary artery catheter.

Blood can gain entrance into the pleural space from trauma to the chest wall, diaphragm, lung, or mediastinum. A hematocrit of the pleural fluid should always be obtained if the pleural fluid looks like blood. A hemothorax is said to be present only when the hematocrit of the pleural fluid is at least 50%.

OVERVIEW of the Cardiopulmonary Clinical Manifestations Associated with Pleural Effusion and Empyema

The following clinical manifestations result from the pathologic mechanisms caused (or activated) by Atelectasis (see Figure 9-7)—the major anatomic alteration of the lungs associated with pleural effusion (see Figure 24-1).

CLINICAL DATA OBTAINED AT THE PATIENT’S BEDSIDE

The Physical Examination

Increased Respiratory Rate (Tachypnea)

Several pathophysiologic mechanisms operating simultaneously may lead to an increased ventilatory rate:

• Stimulation of peripheral chemoreceptors (hypoxemia)

• Decreased lung compliance–increased ventilatory rate relationship

• Activation of the deflation receptors

• Activation of the irritant receptors

• Stimulation of J receptors

• Pain, anxiety

Increased Heart Rate (Pulse) and Blood Pressure

Chest Pain, Decreased Chest Expansion

Cough (Dry, Nonproductive)

Chest Assessment Findings

• Tracheal shift

• Decreased tactile and vocal fremitus

• Dull percussion note

• Diminished breath sounds

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